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Genistein induces degradation of mutant huntingtin in fibroblasts from Huntington’s disease patients

Pierzynowska, Karolina, Gaffke, Lidia, Cyske, Zuzanna, Węgrzyn, Grzegorz·2019·Metabolic Brain Disease

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Fig 1 Genistein reduces the number of mHTT aggregates in human fibroblasts. Cultures of fibroblasts derived from four patients suffering from Huntington’s disease (HD) and four healthy persons (WT) were treated with either DMSO (control) or 30, 60 and 100 μM genistein, for 48 h. Cells were immuno-stained with anti-huntingtin antibody, secondary antibody conjugated with Alexa Fluor 488, and analyzed by fluorescent microscopy at 1000 x magnification. The number of aggregates per 100 μm2 were counted in 100 cells per culture. The experiments were performed in triplicates. Panel A demonstrates representative cells from each group. Panel B shows quantitative analysis of the number of aggregates, where bars represent mean values ± SD, and asterisks indicate statistically significant differences (p < 0.05) between WT and HD groups. Panel C demonstrates association of mHTT with cytoskeletal fibers in fibroblasts derived from HD patient. In panels A and C, white scale bars indicate 10 μm
Fig 1 Genistein reduces the number of mHTT aggregates in human fibroblasts. Cultures of fibroblasts derived from four patients suffering from Huntington’s disease (HD) and four healthy persons (WT) were treated with either DMSO (control) or 30, 60 and 100 μM genistein, for 48 h. Cells were immuno-stained with anti-huntingtin antibody, secondary antibody conjugated with Alexa Fluor 488, and analyzed by fluorescent microscopy at 1000 x magnification. The number of aggregates per 100 μm2 were counted in 100 cells per culture. The experiments were performed in triplicates. Panel A demonstrates representative cells from each group. Panel B shows quantitative analysis of the number of aggregates, where bars represent mean values ± SD, and asterisks indicate statistically significant differences (p < 0.05) between WT and HD groups. Panel C demonstrates association of mHTT with cytoskeletal fibers in fibroblasts derived from HD patient. In panels A and C, white scale bars indicate 10 μmCC BY · PubMed Central
Fig 2 Genistein normalizes levels of HTT in HD fibroblasts. Cultures of fibroblasts derived from four HD patients (HD) and four healthy persons (WT) were treated with either DMSO (control) or 30, 60 and 100 μM genistein, for 48 h. Cellular proteins were separated and detected using the WES system. Four HD and four WT cell lines were used, and the analyses were performed in triplicates. Representative blots are shown in the upper panel, and quantitative analysis is presented in the lower panel. Bars represent mean values ± SD from three independent experiments. Asterisks indicate statistically significant differences (p < 0.05) between WT control and HD groups
Fig 2 Genistein normalizes levels of HTT in HD fibroblasts. Cultures of fibroblasts derived from four HD patients (HD) and four healthy persons (WT) were treated with either DMSO (control) or 30, 60 and 100 μM genistein, for 48 h. Cellular proteins were separated and detected using the WES system. Four HD and four WT cell lines were used, and the analyses were performed in triplicates. Representative blots are shown in the upper panel, and quantitative analysis is presented in the lower panel. Bars represent mean values ± SD from three independent experiments. Asterisks indicate statistically significant differences (p < 0.05) between WT control and HD groupsCC BY · PubMed Central

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Research works printed but not linked: 22

  1. Aguzzi A, O’Connor T (2010) Protein aggregation diseases: pathogenicity and therapeutic perspectives. Nat Rev Drug Discov 9:237–248 · DOI
  2. Guo F, Liu X, Cai H, Le W (2018) Autophagy in neurodegenerative diseases: pathogenesis and therapy. Brain Pathol 28:3–13 · DOI
  3. Huntington Study Group (1996) Unified Huntington’s disease rating scale: reliability and consistency. Mov Disord 11:136–142 · DOI
  4. Jędrak P, Krygier M, Tońska K et al (2017a) Mitochondrial DNA levels in Huntington disease leukocytes and dermal fibroblasts. Metab Brain Dis 32:1237–1247 · DOI
  5. Jędrak P, Sowa N, Barańska S, Węgrzyn G (2017b) Characterization of conditions and determination of practical tips for mtDNA level estimation in various human cells. Acta Biochim Pol 64:699–704 · DOI
  6. Jędrak P, Mozolewski P, Węgrzyn G, Więckowski MR (2018) Mitochondrial alterations accompanied by oxidative stress conditions in skin fibroblasts of Huntington's disease patients. Metab Brain Dis 33:2005–2017 · DOI
  7. Kegel KB, Meloni AR, Yi Y et al (2002) Huntingtin is present in the nucleus, interacts with the transcriptional corepressor C-terminal binding protein, and represses transcription. J Biol Chem 277:7466–7476 · DOI
  8. Kim KH, Dodsworth C, Paras A, Burton BK (2013) High dose genistein aglycone therapy is safe in patients with mucopolysaccharidoses involving the central nervous system. Mol Genet Metab 109:382–385 · DOI
  9. Malinowska M, Wilkinson FL, Bennett W, Langford-Smith KJ, O'Leary HA, Jakobkiewicz-Banecka J, Wynn R, Wraith JE, Wegrzyn G, Bigger BW (2009) Genistein reduces lysosomal storage in peripheral tissues of mucopolysaccharide IIIB mice. Mol Genet Metab 98:235–242 · DOI
  10. Malinowska M, Wilkinson FL, Langford-Smith KJ, Langford-Smith A, Brown JR, Crawford BE, Vanier MT, Grynkiewicz G, Wynn RF, Wraith JE, Wegrzyn G, Bigger BW (2010) Genistein improves neuropathology and corrects behaviour in a mouse model of neurodegenerative metabolic disease. PLoS One 5:e14192 · DOI
  11. Marchina E, Misasi S, Bozzato A et al (2014) Gene expression profile in fibroblasts of Huntington’s disease patients and controls. J Neurol Sci 337:42–46 · DOI
  12. Morreale MK (2015) Huntington's disease: looking beyond the movement disorder. Adv Psychosom Med 34:135–142 · DOI
  13. Moskot M, Montefusco S, Jakóbkiewicz-Banecka J, Mozolewski P, Węgrzyn A, Di Bernardo D, Węgrzyn G, Medina DL, Ballabio A, Gabig-Cimińska M (2014) The phytoestrogen genistein modulates lysosomal metabolism and transcription factor EB (TFEB) activation. J Biol Chem 289:17054–17069 · DOI
  14. Petersen MH, Budtz-Jørgensen E, Sørensen SA et al (2014) Reduction in mitochondrial DNA copy number in peripheral leukocytes after onset of Huntington’s disease. Mitochondrion 17:14–21 · DOI
  15. Pierzynowska K, Gaffke L, Cyske Z, Puchalski M, Rintz E, Bartkowski M, Osiadły M, Pierzynowski M, Mantej J, Piotrowska E, Węgrzyn G (2018a) Autophagy stimulation as a promising approach in treatment of neurodegenerative diseases. Metab Brain Dis 33:989–1008 · DOI
  16. Pierzynowska K, Gaffke L, Hać A, Mantej J, Niedziałek N, Brokowska J, Węgrzyn G (2018b) Correction of Huntington's disease phenotype by genistein-induced autophagy in the cellular model. NeuroMolecular Med 20:112–123 · DOI
  17. Pierzynowska K, Podlacha M, Gaffke L, Majkutewicz I, Mantej J, Wegrzyn A, Osiadły M, Myslinska D, Wegrzyn G (2019) Autophagy-dependent mechanism of genistein-mediated elimination of behavioral and biochemical defects in the rat model of sporadic Alzheimer's disease. Neuropharmacology 148:332–346 · DOI
  18. Shannon KM, Fraint A (2015) Therapeutic advances in Huntington's disease. Mov Disord 30:1539–1546 · DOI
  19. Sharp AH, Loev SJ, Schilling G et al (1995) Widespread expression of Huntington’s disease gene (IT15) protein product. Neuron 14:1065–1074 · DOI
  20. Tousley A, Iuliano M, Weisman E, Sapp E, Richardson H, Vodicka P, Alexander J, Aronin N, DiFiglia M, Kegel-Gleason KB (2019) Huntingtin associates with the actin cytoskeleton and α-actinin isoforms to influence stimulus dependent morphology changes. PLoS One 14:e0212337 · DOI
  21. Wu HC, Hu QL, Zhang SJ, Wang YM, Jin ZK, Lv LF, Zhang S, Liu ZL, Wu HL, Cheng OM (2018) Neuroprotective effects of genistein on SH-SY5Y cells overexpressing A53T mutant α-synuclein. Neural Regen Res 13:1375–1383 · DOI
  22. Yang YP, Hu LF, Zheng HF, Mao CJ, Hu WD, Xiong KP, Wang F, Liu CF (2013) Application and interpretation of current autophagy inhibitors and activators. Acta Pharmacol Sin 34:625–635 · DOI

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Metadata

Authors
Pierzynowska, K., Gaffke, L., Cyske, Z., & Węgrzyn, G.
Venue
Metabolic Brain Disease
Published
2019-03-09
Volume
34
Issue
3
Pages
715-720
ISSN
  • 0885-7490
  • 1573-7365
Cited by
32
References
1
Language
en
Funders
Narodowym Centrum Nauki (2017/25/N/NZ2/00812)

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CoChat. (2026). Citation check: Genistein induces degradation of mutant huntingtin in fibroblasts from Huntington’s disease patients. https://app.cochat.ai/papers/10.1007/s11011-019-00405-4
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Pierzynowska, K., Gaffke, L., Cyske, Z., & Węgrzyn, G. (2019). Genistein induces degradation of mutant huntingtin in fibroblasts from Huntington’s disease patients. Metabolic Brain Disease. https://doi.org/10.1007/s11011-019-00405-4