Student or educator? Sign up with your school email and get 6 months of Pro free.
CoChat
Sign Up
Cited by 14

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Immortalized human myoblast cell lines for the delivery of therapeutic proteins using encapsulated cell technology

Lathuiliere, Aurelien, Vernet, Remi, Charrier, Emily, Urwyler, Muriel, Von Rohr, Olivier, Belkouch, Marie-Claude, Saingier, Valentin, Bouvarel, Thomas, Guillarme, Davy, Engel, Adrien, Salmon, Patrick, Laumonier, Thomas, Grogg, Julien, Mach, Nicolas·2022·Molecular Therapy - Methods & Clinical Development
DOI 10.1016/j.omtm.2022.07.017PMC PMC9418741
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.omtm.2022.07.017

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Figures

Graphical abstract
Graphical abstract CC BY · PubMed Central
Figure 1 Primary human myoblasts are efficiently immortalized after transduction with lentiviruses encoding for CDK4 and hTERT (A) Primary myoblast cells were transduced with lentiviral vectors encoding the CDK4 and hTERT proteins. Primary and immortalized myoblasts were maintained in culture and proliferation was quantified by determination of population doubling. Each dot represents the mean of two cell counts. (B) Human immortalized myoblasts were expanded and cell differentiation was promoted by removing growth factors from the culture medium. The expression levels of MEF2 and MyHC proteins were quantified by in vitro immunofluorescence to assess the myogenic differentiation process. The image is representative of at least seven images from one biologically independent experiment. Scale bar, 50 μm.
Figure 1 Primary human myoblasts are efficiently immortalized after transduction with lentiviruses encoding for CDK4 and hTERT (A) Primary myoblast cells were transduced with lentiviral vectors encoding the CDK4 and hTERT proteins. Primary and immortalized myoblasts were maintained in culture and proliferation was quantified by determination of population doubling. Each dot represents the mean of two cell counts. (B) Human immortalized myoblasts were expanded and cell differentiation was promoted by removing growth factors from the culture medium. The expression levels of MEF2 and MyHC proteins were quantified by in vitro immunofluorescence to assess the myogenic differentiation process. The image is representative of at least seven images from one biologically independent experiment. Scale bar, 50 μm.CC BY · PubMed Central
Figure 2 Individual immortalized clones demonstrate preserved myogenic characteristics (A) Individual clones were sorted from the immortalized myoblast cell population using single-cell cloning. The proliferation rate of nine selected clones was quantified by determination of population doubling. Each dot represents the mean of two cell counts. (B) Flow cytometry gating strategy to define the percentage of cells expressing myogenic markers (CD56+ CD82+ CD146+). (C) Individual immortalized clones were expanded and cell differentiation was promoted by removing growth factors from the culture medium. The expression levels of MEF2 and MyHC proteins were quantified by in vitro immunofluorescence to assess the myogenic differentiation process. (D) The fusion index was calculated on approximately 200 cells for each individual clone. The immunofluorescence images are representative of at least five images from one biologically independent experiment. Data and errors bars represent mean ± SD from at least five pictures from one independent experiment. The fusion index of each clone was compared with the immortalized population P10 with a one-way ANOVA test. Scale bar, 50 μm.
Figure 2 Individual immortalized clones demonstrate preserved myogenic characteristics (A) Individual clones were sorted from the immortalized myoblast cell population using single-cell cloning. The proliferation rate of nine selected clones was quantified by determination of population doubling. Each dot represents the mean of two cell counts. (B) Flow cytometry gating strategy to define the percentage of cells expressing myogenic markers (CD56+ CD82+ CD146+). (C) Individual immortalized clones were expanded and cell differentiation was promoted by removing growth factors from the culture medium. The expression levels of MEF2 and MyHC proteins were quantified by in vitro immunofluorescence to assess the myogenic differentiation process. (D) The fusion index was calculated on approximately 200 cells for each individual clone. The immunofluorescence images are representative of at least five images from one biologically independent experiment. Data and errors bars represent mean ± SD from at least five pictures from one independent experiment. The fusion index of each clone was compared with the immortalized population P10 with a one-way ANOVA test. Scale bar, 50 μm.CC BY · PubMed Central
Figure 3 Selected immortalized clones can be efficiently transduced for the expression of functional cytokines: example of human GM-CSF (A) Clone no. 2 (parental population) was transduced with lentivirus for the expression of human GM-CSF. Individual clones were then sorted by flow cytometry single-cell sorting and a clone was selected for its huGM-CSF production. The huGM-CSF clone was maintained in culture and proliferation was quantified by determination of population doubling. Each dot represents the mean of two cell counts. (B) Flow cytometry gating strategy to define the percentage of cells expressing myogenic markers (CD56+ CD82+ CD146+). (C) The huGM-CSF clone was expanded and cell differentiation was promoted by removing growth factors from the culture medium. The expression levels of MEF2 and MyHC proteins were quantified by in vitro immunofluorescence to assess the myogenic differentiation process. Scale bar, 50 μm. (D) The fusion index was calculated on around 200 cells. The immunofluorescence images are representative of at least five images from one biologically independent experiment. Data and errors bars represent mean ± SD from at least seven pictures from one independent experiment. The fusion index was compared by a two-tailed unpaired t test. (E) The huGM-CSF secretion by the parental population or by the huGM-CSF clone was quantified by ELISA. Data and error bars represent mean ± SD of n = 2. Lines represent a linear regression, two-way ANOVA with repeated measure. For group effect p = 0.027. No significant effect of time (p = 0.0732). (F) The potency assay for the secreted GM-CSF was evaluated by the LanthaScreen STAT5 TF-1 cellular assay (Thermo Fisher Scientific). Potency capacity was directly correlated with the half maximal effective concentration (EC50) and was determined with a 10-point titration curve. Recombinant GM-CSF was used as a positive control. Data and error bars represent mean ± SD of two experiments.
Figure 3 Selected immortalized clones can be efficiently transduced for the expression of functional cytokines: example of human GM-CSF (A) Clone no. 2 (parental population) was transduced with lentivirus for the expression of human GM-CSF. Individual clones were then sorted by flow cytometry single-cell sorting and a clone was selected for its huGM-CSF production. The huGM-CSF clone was maintained in culture and proliferation was quantified by determination of population doubling. Each dot represents the mean of two cell counts. (B) Flow cytometry gating strategy to define the percentage of cells expressing myogenic markers (CD56+ CD82+ CD146+). (C) The huGM-CSF clone was expanded and cell differentiation was promoted by removing growth factors from the culture medium. The expression levels of MEF2 and MyHC proteins were quantified by in vitro immunofluorescence to assess the myogenic differentiation process. Scale bar, 50 μm. (D) The fusion index was calculated on around 200 cells. The immunofluorescence images are representative of at least five images from one biologically independent experiment. Data and errors bars represent mean ± SD from at least seven pictures from one independent experiment. The fusion index was compared by a two-tailed unpaired t test. (E) The huGM-CSF secretion by the parental population or by the huGM-CSF clone was quantified by ELISA. Data and error bars represent mean ± SD of n = 2. Lines represent a linear regression, two-way ANOVA with repeated measure. For group effect p = 0.027. No significant effect of time (p = 0.0732). (F) The potency assay for the secreted GM-CSF was evaluated by the LanthaScreen STAT5 TF-1 cellular assay (Thermo Fisher Scientific). Potency capacity was directly correlated with the half maximal effective concentration (EC50) and was determined with a 10-point titration curve. Recombinant GM-CSF was used as a positive control. Data and error bars represent mean ± SD of two experiments.CC BY · PubMed Central
Figure 4 In vitro evaluation of encapsulated myoblasts as a delivery system (A) Scheme of the MyoPod capsule depicting the various device components. The huGM-CSF-secreting myoblast clone was encapsulated and kept in culture. Capsules were fixed and processed for histological analysis. Qualitative assessment of survival was then performed by hematoxylin and eosin staining. (B) After 1 week in vitro viable cells were organized in a tissue with aligned nuclei (the right panel is the magnified delimited area). Arrowhead shows aligned nuclei. Arrows point to the yarn that is used as a supporting matrix. Asterisks show the semipermeable membrane. (C) After 3 weeks in vitro, similar observations were made, suggesting a sustained cell survival over time. (D) The huGM-CSF clone was encapsulated and kept in culture for up to 2 years. Regularly (each day during the first week, each 2 weeks, and then each 3 weeks), a 2-h release assessment was performed to evaluate huGM-CSF secretion quantified by ELISA. This experiment used n = 7 capsules. The line represents a linear regression with slope not different from zero, p = 0.0996.
Figure 4 In vitro evaluation of encapsulated myoblasts as a delivery system (A) Scheme of the MyoPod capsule depicting the various device components. The huGM-CSF-secreting myoblast clone was encapsulated and kept in culture. Capsules were fixed and processed for histological analysis. Qualitative assessment of survival was then performed by hematoxylin and eosin staining. (B) After 1 week in vitro viable cells were organized in a tissue with aligned nuclei (the right panel is the magnified delimited area). Arrowhead shows aligned nuclei. Arrows point to the yarn that is used as a supporting matrix. Asterisks show the semipermeable membrane. (C) After 3 weeks in vitro, similar observations were made, suggesting a sustained cell survival over time. (D) The huGM-CSF clone was encapsulated and kept in culture for up to 2 years. Regularly (each day during the first week, each 2 weeks, and then each 3 weeks), a 2-h release assessment was performed to evaluate huGM-CSF secretion quantified by ELISA. This experiment used n = 7 capsules. The line represents a linear regression with slope not different from zero, p = 0.0996.CC BY · PubMed Central
Figure 5 In vivo delivery of huGM-CSF The huGM-CSF-secreting clone was encapsulated. Capsules were implanted into Rag2/IL2rg−/− mice and kept for 1 or 3 weeks in the mice. (A) Histological section of the device after 1 week implantation in the mouse subcutaneous tissue. Hematoxylin and eosin staining demonstrates cell survival inside the MyoPod device. (B) After 3 weeks in vivo, numerous viable myoblastic cells are observed in the inner device chamber (arrowhead). A limited cellular infiltrate is observed in the surrounding subcutaneous tissue (arrow). The asterisk depicts the semipermeable membrane. (C) Capsules were then explanted and, the day after the explantation, a 2-h release was performed to evaluate huGM-CSF secretion quantified by ELISA. One-way ANOVA of n = 2–6 replicates. (D) Serum samples were isolated from implanted mice to quantify huGM-CSF levels. N = 4-5. (E) Evaluation of huGM-CSF secretion by encapsulated cells implanted in an ex vivo human skin model. Each bar represents mean ± SD of n = 3 replicates per time point per condition. (F) Capsules were frozen into liquid nitrogen and, after thawing, huGM-CSF secretion was evaluated by ELISA. Each dot represents mean ± SD of n = 72 replicates.
Figure 5 In vivo delivery of huGM-CSF The huGM-CSF-secreting clone was encapsulated. Capsules were implanted into Rag2/IL2rg−/− mice and kept for 1 or 3 weeks in the mice. (A) Histological section of the device after 1 week implantation in the mouse subcutaneous tissue. Hematoxylin and eosin staining demonstrates cell survival inside the MyoPod device. (B) After 3 weeks in vivo, numerous viable myoblastic cells are observed in the inner device chamber (arrowhead). A limited cellular infiltrate is observed in the surrounding subcutaneous tissue (arrow). The asterisk depicts the semipermeable membrane. (C) Capsules were then explanted and, the day after the explantation, a 2-h release was performed to evaluate huGM-CSF secretion quantified by ELISA. One-way ANOVA of n = 2–6 replicates. (D) Serum samples were isolated from implanted mice to quantify huGM-CSF levels. N = 4-5. (E) Evaluation of huGM-CSF secretion by encapsulated cells implanted in an ex vivo human skin model. Each bar represents mean ± SD of n = 3 replicates per time point per condition. (F) Capsules were frozen into liquid nitrogen and, after thawing, huGM-CSF secretion was evaluated by ELISA. Each dot represents mean ± SD of n = 72 replicates.CC BY · PubMed Central
Figure 6 Novel immortalized myoblasts can be used for the continuous delivery of complex therapeutic macromolecules with preserved functionality (A) Human anti-CD20-expressing myoblasts were encapsulated and kept in culture for up to 40 weeks. Repeated quantification of anti-CD20 levels was performed by ELISA during the course of the experiment. Each point represents the mean of two technical replicates. The line represents a linear regression with a slope not different from zero, p = 0.7246. (B) The specific binding between human anti-CD20 produced by myoblasts and human CD20 was evaluated by a flow cytometry competition assay. Human PBMCs were pre-incubated with different concentrations of either the myoblast-produced anti-CD20 IgG or commercial rituximab and then incubated with a fluorescent-tagged anti-CD20 antibody. The percentage of cells expressing CD20 was then assessed. (C) The functionality of human anti-CD20 produced by myoblasts was evaluated by an antibody-dependent cellular cytotoxicity (ADCC) assay. A mantle cell lymphoma (MCL) cell line expressing CD20 (JeKo-1) pre-exposed to either rituximab or myoblast-produced anti-CD20 were co-cultured with PBMCs for 4 h. The upregulation of the degranulation marker CD107a expression was evaluated on NK cells (CD56+ CD3−, CD14− CD19−) by flow cytometry. (D) The anti-CD20-secreting myoblast cells were encapsulated, implanted into Rag2/IL2rg−/− mice, and kept for 5 months in the mice. Human anti-CD20 was quantified in the mouse serum over the course of the experiment. N = 5. (E) Human anti-CTLA-4-expressing myoblasts were encapsulated and kept in culture for 15 weeks. Repeated quantification of anti-CTLA-4 levels was performed by ELISA during the course of the experiment. Each point represents the mean of six technical replicates. The line represents linear regression with a slope not different from zero, p = 0.8791. (F) The CTLA-4 blockade assay was performed using myoblast-produced supernatant containing anti-CTLA-4. The blockade capacity was directly correlated with the EC50 and determined with an eight-point titration curve. Each point represents the mean ± SD of two technical replicates. (G) RPLC-FL chromatograms of intact commercial ipilimumab and reduced ipilimumab (inset), as well as culture medium, supernatant from wild-type immortalized myoblast cells, supernatant for anti-CTLA4-expressing myoblasts. Time windows for peaks integration were highlighted in purple, red, and blue. Analytical conditions are described in the materials and methods.
Figure 6 Novel immortalized myoblasts can be used for the continuous delivery of complex therapeutic macromolecules with preserved functionality (A) Human anti-CD20-expressing myoblasts were encapsulated and kept in culture for up to 40 weeks. Repeated quantification of anti-CD20 levels was performed by ELISA during the course of the experiment. Each point represents the mean of two technical replicates. The line represents a linear regression with a slope not different from zero, p = 0.7246. (B) The specific binding between human anti-CD20 produced by myoblasts and human CD20 was evaluated by a flow cytometry competition assay. Human PBMCs were pre-incubated with different concentrations of either the myoblast-produced anti-CD20 IgG or commercial rituximab and then incubated with a fluorescent-tagged anti-CD20 antibody. The percentage of cells expressing CD20 was then assessed. (C) The functionality of human anti-CD20 produced by myoblasts was evaluated by an antibody-dependent cellular cytotoxicity (ADCC) assay. A mantle cell lymphoma (MCL) cell line expressing CD20 (JeKo-1) pre-exposed to either rituximab or myoblast-produced anti-CD20 were co-cultured with PBMCs for 4 h. The upregulation of the degranulation marker CD107a expression was evaluated on NK cells (CD56+ CD3−, CD14− CD19−) by flow cytometry. (D) The anti-CD20-secreting myoblast cells were encapsulated, implanted into Rag2/IL2rg−/− mice, and kept for 5 months in the mice. Human anti-CD20 was quantified in the mouse serum over the course of the experiment. N = 5. (E) Human anti-CTLA-4-expressing myoblasts were encapsulated and kept in culture for 15 weeks. Repeated quantification of anti-CTLA-4 levels was performed by ELISA during the course of the experiment. Each point represents the mean of six technical replicates. The line represents linear regression with a slope not different from zero, p = 0.8791. (F) The CTLA-4 blockade assay was performed using myoblast-produced supernatant containing anti-CTLA-4. The blockade capacity was directly correlated with the EC50 and determined with an eight-point titration curve. Each point represents the mean ± SD of two technical replicates. (G) RPLC-FL chromatograms of intact commercial ipilimumab and reduced ipilimumab (inset), as well as culture medium, supernatant from wild-type immortalized myoblast cells, supernatant for anti-CTLA4-expressing myoblasts. Time windows for peaks integration were highlighted in purple, red, and blue. Analytical conditions are described in the materials and methods.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 3 references

Research works printed but not linked: 70

  1. Calafiore, 2006, Standard technical procedures for microencapsulation of human islets for graft into nonimmunosuppressed patients with type 1 diabetes mellitus, Transplant. Proc., 38, 1156, 10.1016/j.transproceed.2006.03.014 · DOI
  2. Basta, 2011, Long-term metabolic and immunological follow-up of nonimmunosuppressed patients with type 1 diabetes treated with microencapsulated islet allografts: four cases, Diabetes Care, 34, 2406, 10.2337/dc11-0731 · DOI
  3. Tuch, 2009, Safety and viability of microencapsulated human islets transplanted into diabetic humans, Diabetes Care, 32, 1887, 10.2337/dc09-0744 · DOI
  4. Read, 2001, Intravital microscopy reveals novel antivascular and antitumor effects of endostatin delivered locally by alginate-encapsulated cells, Cancer. Res., 61, 6830
  5. Hortelano, 1996, Delivery of human factor IX in mice by encapsulated recombinant myoblasts: a novel approach towards allogeneic gene therapy of hemophilia B, Blood, 87, 5095, 10.1182/blood.V87.12.5095.bloodjournal87125095 · DOI
  6. Antequera, 2012, Encapsulated VEGF-secreting cells enhance proliferation of neuronal progenitors in the hippocampus of AbetaPP/Ps1 mice, J. Alzheimers Dis., 29, 187, 10.3233/JAD-2011-111646 · DOI
  7. Joki, 2001, Continuous release of endostatin from microencapsulated engineered cells for tumor therapy, Nat. Biotechnol., 19, 35, 10.1038/83481 · DOI
  8. Kauer, 2011, Encapsulated therapeutic stem cells implanted in the tumor resection cavity induce cell death in gliomas, Nat. Neurosci., 15, 197, 10.1038/nn.3019 · DOI
  9. Löhr, 2001, Microencapsulated cell-mediated treatment of inoperable pancreatic carcinoma, Lancet, 357, 1591, 10.1016/S0140-6736(00)04749-8 · DOI
  10. Visted, 2001, Cell encapsulation technology as a therapeutic strategy for CNS malignancies, Neuro Oncol., 3, 201, 10.1093/neuonc/3.3.201 · DOI
  11. Prakash, 1996, Microencapsulated genetically engineered live E. coli DH5 cells administered orally to maintain normal plasma urea level in uremic rats, Nat. Med., 2, 883, 10.1038/nm0896-883 · DOI
  12. Zhang, 2011, Ciliary neurotrophic factor delivered by encapsulated cell intraocular implants for treatment of geographic atrophy in age-related macular degeneration, Proc. Natl. Acad. Sci. USA, 108, 6241, 10.1073/pnas.1018987108 · DOI
  13. Eyjolfsdottir, 2016, Targeted delivery of nerve growth factor to the cholinergic basal forebrain of Alzheimer's disease patients: application of a second-generation encapsulated cell biodelivery device, Alzheimers Res. Ther., 8, 30, 10.1186/s13195-016-0195-9 · DOI
  14. Aebischer, 1996, Intrathecal delivery of CNTF using encapsulated genetically modified xenogeneic cells in amyotrophic lateral sclerosis patients, Nat. Med., 2, 696, 10.1038/nm0696-696 · DOI
  15. Bloch, 2004, Neuroprotective gene therapy for Huntington's disease, using polymer-encapsulated cells engineered to secrete human ciliary neurotrophic factor: results of a phase I study, Hum. Gene. Ther., 15, 968, 10.1089/hum.2004.15.968 · DOI
  16. Lathuilière, 2015, Encapsulated cellular implants for recombinant protein delivery and therapeutic modulation of the immune system, Int. J. Mol. Sci., 16, 10578, 10.3390/ijms160510578 · DOI
  17. Santos-Vizcaino, 2020, Clinical applications of cell encapsulation technology, Methods. Mol. Biol., 2100, 473, 10.1007/978-1-0716-0215-7_32 · DOI
  18. Broadhead, 2002, Hollow fiber membrane diffusive permeability regulates encapsulated cell line biomass, proliferation, and small molecule release, Biomaterials, 23, 4689, 10.1016/S0142-9612(02)00212-0 · DOI
  19. Déglon, 1996, Central nervous system delivery of recombinant ciliary neurotrophic factor by polymer encapsulated differentiated C2C12 myoblasts, Hum. Gene. Ther., 7, 2135, 10.1089/hum.1996.7.17-2135 · DOI
  20. Lacy, 1991, Maintenance of normoglycemia in diabetic mice by subcutaneous xenografts of encapsulated islets, Science, 254, 1782, 10.1126/science.1763328 · DOI
  21. Loudovaris, 1992, Destruction of xenografts but not allografts within cell impermeable membranes, Transplant. Proc., 24, 2291
  22. Weber, 1990, The role of CD4+ helper T cells in the destruction of microencapsulated islet xenografts in nod mice, Transplantation, 49, 396, 10.1097/00007890-199002000-00034 · DOI
  23. Peduto, 2000, Long-term host unresponsiveness to encapsulated xenogeneic myoblasts after transient immunosuppression, Transplantation, 70, 78
  24. Loudovaris, 1996, CD4+ T cell mediated destruction of xenografts within cell-impermeable membranes in the absence of CD8+ T cells and B cells, Transplantation, 61, 1678, 10.1097/00007890-199606270-00003 · DOI
  25. Gray, 2001, An overview of the immune system with specific reference to membrane encapsulation and islet transplantation, Ann. N. Y. Acad. Sci., 944, 226, 10.1111/j.1749-6632.2001.tb03835.x · DOI
  26. Gray, 1997, Encapsulated islet cells: the role of direct and indirect presentation and the relevance to xenotransplantation and autoimmune recurrence, Br. Med. Bull., 53, 777, 10.1093/oxfordjournals.bmb.a011647 · DOI
  27. Gill, 2001, Use of small animal models for screening immunoisolation approaches to cellular transplantation, Ann. N. Y. Acad. Sci., 944, 35, 10.1111/j.1749-6632.2001.tb03821.x · DOI
  28. Lathuilière, 2016, A subcutaneous cellular implant for passive immunization against amyloid-beta reduces brain amyloid and tau pathologies, Brain, 139, 1587, 10.1093/brain/aww036 · DOI
  29. Régulier, 1998, Continuous delivery of human and mouse erythropoietin in mice by genetically engineered polymer encapsulated myoblasts, Gene. Ther., 5, 1014, 10.1038/sj.gt.3300687 · DOI
  30. Li, 2000, Encapsulation matrices for neurotrophic factor-secreting myoblast cells, Tissue. Eng., 6, 151, 10.1089/107632700320775 · DOI
  31. Liu, 2012, Hypoxia promotes satellite cell self-renewal and enhances the efficiency of myoblast transplantation, Development, 139, 2857, 10.1242/dev.079665 · DOI
  32. Schneider, 2003, Prevention of the initial host immuno-inflammatory response determines the long-term survival of encapsulated myoblasts genetically engineered for erythropoietin delivery, Mol. Ther., 7, 506, 10.1016/S1525-0016(03)00055-8 · DOI
  33. Rinsch, 2002, Delivery of erythropoietin by encapsulated myoblasts in a genetic model of severe anemia, Kidney. Int., 62, 1395, 10.1111/j.1523-1755.2002.kid574.x · DOI
  34. Lathuilière, 2014, A high-capacity cell macroencapsulation system supporting the long-term survival of genetically engineered allogeneic cells, Biomaterials, 35, 779, 10.1016/j.biomaterials.2013.09.071 · DOI
  35. Rinsch, 2001, Delivery of FGF-2 but not VEGF by encapsulated genetically engineered myoblasts improves survival and vascularization in a model of acute skin flap ischemia, Gene. Ther., 8, 523, 10.1038/sj.gt.3301436 · DOI
  36. Consiglio, 2007, Metabolic correction in oligodendrocytes derived from metachromatic leukodystrophy mouse model by using encapsulated recombinant myoblasts, J. Neurol. Sci., 255, 7, 10.1016/j.jns.2007.01.010 · DOI
  37. Scharp, 1994, Protection of encapsulated human islets implanted without immunosuppression in patients with type I or type II diabetes and in nondiabetic control subjects, Diabetes, 43, 1167, 10.2337/diab.43.9.1167 · DOI
  38. Agulnick, 2015, Insulin-Producing endocrine cells differentiated in vitro from human embryonic stem cells function in macroencapsulation devices in vivo, Stem Cells Transl. Med., 4, 1214, 10.5966/sctm.2015-0079 · DOI · Paper page
  39. Wright, 2012, Encapsulated glucagon-like peptide-1-producing mesenchymal stem cells have a beneficial effect on failing pig hearts, Stem Cells Transl. Med., 1, 759, 10.5966/sctm.2012-0064 · DOI
  40. Ashimova, 2019, Cell encapsulation within alginate microcapsules: immunological challenges and outlook, Front. Bioeng. Biotechnol., 7, 380, 10.3389/fbioe.2019.00380 · DOI
  41. Di Donna, 2003, Telomerase can extend the proliferative capacity of human myoblasts, but does not lead to their immortalization, Mol. Cancer Res., 1, 643
  42. Mamchaoui, 2011, Immortalized pathological human myoblasts: towards a universal tool for the study of neuromuscular disorders, Skelet. Muscle, 1, 34, 10.1186/2044-5040-1-34 · DOI
  43. Thorley, 2016, Skeletal muscle characteristics are preserved in hTERT/cdk4 human myogenic cell lines, Skelet. Muscle, 6, 43, 10.1186/s13395-016-0115-5 · DOI
  44. Firth, 1994, Oxygen-regulated control elements in the phosphoglycerate kinase 1 and lactate dehydrogenase A genes: similarities with the erythropoietin 3' enhancer, Proc. Natl. Acad. Sci. USA, 91, 6496, 10.1073/pnas.91.14.6496 · DOI
  45. Zhu, 2007, Cellular senescence in human myoblasts is overcome by human telomerase reverse transcriptase and cyclin-dependent kinase 4: consequences in aging muscle and therapeutic strategies for muscular dystrophies, Aging Cell, 6, 515, 10.1111/j.1474-9726.2007.00306.x · DOI
  46. Gossett, 1989, A new myocyte-specific enhancer-binding factor that recognizes a conserved element associated with multiple muscle-specific genes, Mol. Cell. Biol., 9, 5022
  47. Osmond, 2010, Development of cell-based assays for cytokine receptor signaling, using an AlphaScreen SureFire assay format, Anal. Biochem., 403, 94, 10.1016/j.ab.2010.04.007 · DOI
  48. Lathuilière, 2014, Genetic engineering of cell lines using lentiviral vectors to achieve antibody secretion following encapsulated implantation, Biomaterials, 35, 792, 10.1016/j.biomaterials.2013.10.026 · DOI
  49. Fransen, 2013, Controlled local delivery of CTLA-4 blocking antibody induces CD8+ T-cell-dependent tumor eradication and decreases risk of toxic side effects, Clin. Cancer. Res., 19, 5381, 10.1158/1078-0432.CCR-12-0781 · DOI
  50. Wrapp, 2020, Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation, Science, 367, 1260, 10.1126/science.abb2507 · DOI · Paper page
  51. Marchetti, 2020, AI334, AQ806 and RB596 antibodies recognize the spike S protein from SARS-CoV-2 by immunofluorescence, Antib. Rep., 3, e219, 10.24450/journals/abrep.2020.e219 · DOI
  52. De Vos, 1999, Why do microencapsulated islet grafts fail in the absence of fibrotic overgrowth?, Diabetes, 48, 1381, 10.2337/diabetes.48.7.1381 · DOI
  53. Orive, 2015, Cell encapsulation: technical and clinical advances, Trends. Pharmacol. Sci., 36, 537, 10.1016/j.tips.2015.05.003 · DOI
  54. Chew, 2019, Effect of ciliary neurotrophic factor on retinal neurodegeneration in patients with macular telangiectasia type 2: a randomized clinical trial, Ophthalmology, 126, 540, 10.1016/j.ophtha.2018.09.041 · DOI
  55. Wahlberg, 2012, Targeted delivery of nerve growth factor via encapsulated cell biodelivery in Alzheimer disease: a technology platform for restorative neurosurgery, J. Neurosurg., 117, 340, 10.3171/2012.2.JNS11714 · DOI
  56. Wahlberg, 2020, Long-term, stable, targeted biodelivery and efficacy of GDNF from encapsulated cells in the rat and Goettingen miniature pig brain, Curr. Res. Pharmacol. Drug Discov., 1, 19, 10.1016/j.crphar.2020.04.001 · DOI
  57. Fjord-Larsen, 2010, Long-term delivery of nerve growth factor by encapsulated cell biodelivery in the Gottingen minipig basal forebrain, Mol. Ther., 18, 2164, 10.1038/mt.2010.154 · DOI
  58. Fjord-Larsen, 2012, Increased encapsulated cell biodelivery of nerve growth factor in the brain by transposon-mediated gene transfer, Gene. Ther., 19, 1010, 10.1038/gt.2011.178 · DOI
  59. Mach, 2000, Differences in dendritic cells stimulated in vivo by tumors engineered to secrete granulocyte-macrophage colony-stimulating factor or Flt3-ligand, Cancer. Res., 60, 3239
  60. Parmiani, 2007, Opposite immune functions of GM-CSF administered as vaccine adjuvant in cancer patients, Ann. Oncol., 18, 226, 10.1093/annonc/mdl158 · DOI
  61. Schwenter, 2011, Cell encapsulation technology as a novel strategy for human anti-tumor immunotherapy, Cancer. Gene. Ther., 18, 553, 10.1038/cgt.2011.22 · DOI
  62. Burgess, 1977, Serum half-life and organ distribution of radiolabeled colony stimulating factor in mice, Exp. Hematol., 5, 456
  63. Kindler, 2021, Human myoblasts differentiate in various mesenchymal lineages and inhibit allogeneic T cell proliferation through an indolamine 2, 3 dioxygenase dependent pathway, Exp. Cell. Res., 403, 10.1016/j.yexcr.2021.112586 · DOI
  64. Vargas, 2016, Retroviral vectors and transposons for stable gene therapy: advances, current challenges and perspectives, J. Transl. Med., 14, 288, 10.1186/s12967-016-1047-x · DOI
  65. Bulcha, 2021, Viral vector platforms within the gene therapy landscape, Signal Transduct. Target. Ther., 6, 53, 10.1038/s41392-021-00487-6 · DOI · Paper page
  66. Andersson, 1979, K562--a human erythroleukemic cell line, Int. J. Cancer., 23, 143, 10.1002/ijc.2910230202 · DOI
  67. Soiffer, 2021, Whole tumor cell vaccines engineered to secrete GM-CSF (GVAX), ImmunoMedicine, 1, e1025, 10.1002/imed.1025 · DOI
  68. Giry-Laterrière, 2011, Lentiviral vectors, Methods. Mol. Biol., 737, 183, 10.1007/978-1-61779-095-9_8 · DOI
  69. Barde, 2010, Production and titration of lentiviral vectors, Curr. Protoc. Neurosci., 10.1002/0471142301.ns0421s53 · DOI
  70. Zhang, 1999, A simple statistical parameter for use in evaluation and validation of high throughput screening assays, J. Biomol. Screen., 4, 67, 10.1177/108705719900400206 · DOI · Paper page

Cited by

Metadata

Authors
Lathuiliere, A., Vernet, R., Charrier, E., Urwyler, M., Von Rohr, O., Belkouch, M.-C., Saingier, V., Bouvarel, T., Guillarme, D., Engel, A., Salmon, P., Laumonier, T., Grogg, J., & Mach, N.
ORCID
Lathuiliere, Aurelien
Venue
Molecular Therapy - Methods & Clinical Development
Publisher
Elsevier BV
Published
2022-09
Volume
26
Pages
441-458
ISSN
2329-0501
DOI
10.1016/j.omtm.2022.07.017
PMC
PMC9418741
Cited by
14
References
3
Language
en
Update notices
erratum (2023-12-14)
Licence

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review