Cited by 74

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Maternal inhalation of carbon black nanoparticles induces neurodevelopmental changes in mouse offspring

Umezawa, Masakazu, Onoda, Atsuto, Korshunova, Irina, Jensen, Alexander C. Ø., Koponen, Ismo K., Jensen, Keld A., Khodosevich, Konstantin, Vogel, Ulla, Hougaard, Karin S.·2018·Particle and Fibre Toxicology

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 · 10.1186/s12989-018-0272-2

Cites

16 of 16 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1 Average particle size distributions measured by the ELPI+ for the low and high exposure groups (sham exposure level for control animals not shown)
Fig. 1 Average particle size distributions measured by the ELPI+ for the low and high exposure groups (sham exposure level for control animals not shown)CC BY · PubMed Central
Fig. 2 Relative Saa3 mRNA levels in lungs from time-mated mice exposed to Printex 90 by inhalation, at PND 9 and PND 26–27 (corresponding to 11 and 28–29 days after termination of exposure). Expression of mRNA was normalized to 18S rRNA
Fig. 2 Relative Saa3 mRNA levels in lungs from time-mated mice exposed to Printex 90 by inhalation, at PND 9 and PND 26–27 (corresponding to 11 and 28–29 days after termination of exposure). Expression of mRNA was normalized to 18S rRNACC BY · PubMed Central
Fig. 3 Maternal exposure to Printex 90 carbon nanoparticles affects astrocytes and perivascular macrophages (PVMs) in the offspring cerebral cortex (n = 4–6). a-b show representative light micrographs of glial fibrillary acidic protein (GFAP)-positive astrocytes and PVMs in the cerebral cortices of 6 week old male offspring in the control (a-c, j), low exposure (d-f), and high exposure groups (g-i, k, l). a, d and g gives an overview of the cerebral cortex, with b, e, and h providing enlarged views hereof, respectively, which is further enlarged in c, f, and i, respectively. These enlarged panels were taken from the same location in all brains. c, f, and i show that the expression levels of GFAP around blood vessels are dose-dependently increased by maternal exposure to carbon black nanoparticles. j and k show representative light micrographs of granules in PVMs of 6 week old male offspring in the control and high exposure groups, respectively. l is an enlarged view of panel k. White arrows indicate normal granules and black arrow indicates enlarged granules of PVMs. l shows that the granules in PVMs next to GFAP positive astrocytes are enlarged. Enlarged granules represent a typical histopathological finding following denaturation of PVMs
Fig. 3 Maternal exposure to Printex 90 carbon nanoparticles affects astrocytes and perivascular macrophages (PVMs) in the offspring cerebral cortex (n = 4–6). a-b show representative light micrographs of glial fibrillary acidic protein (GFAP)-positive astrocytes and PVMs in the cerebral cortices of 6 week old male offspring in the control (a-c, j), low exposure (d-f), and high exposure groups (g-i, k, l). a, d and g gives an overview of the cerebral cortex, with b, e, and h providing enlarged views hereof, respectively, which is further enlarged in c, f, and i, respectively. These enlarged panels were taken from the same location in all brains. c, f, and i show that the expression levels of GFAP around blood vessels are dose-dependently increased by maternal exposure to carbon black nanoparticles. j and k show representative light micrographs of granules in PVMs of 6 week old male offspring in the control and high exposure groups, respectively. l is an enlarged view of panel k. White arrows indicate normal granules and black arrow indicates enlarged granules of PVMs. l shows that the granules in PVMs next to GFAP positive astrocytes are enlarged. Enlarged granules represent a typical histopathological finding following denaturation of PVMsCC BY · PubMed Central
Fig. 4 Maternal exposure to Printex 90 carbon nanoparticles dose-dependently increases expression levels of glial fibrillary acidic protein (GFAP) in astrocytes in the offspring cerebral cortex. a, b, d, e, g and h show representative fluorescent micrographs of GFAP-positive astrocytes in the cerebral cortices of 6 week old male offspring in the control (a, b), low exposure (d, e), and high exposure groups (g, h). a, d and g gives an overview of the cerebral cortex, with b, e, and h providing enlarged views hereof, respectively. c, f, and i are grayscale views of b, e, and h, respectively, for quantification of the GFAP expression. j indicates averages of the expression area of GFAP-positive astrocytes in the cerebral cortices of offspring based on the grayscale views provided in [Additional files 3, 4 and 5], and shows that the maternal exposure to the nanoparticles significantly increases expression levels of GFAP in astrocytes in offspring cerebral cortices. N is the number of brains analysed, mean ± SEM
Fig. 4 Maternal exposure to Printex 90 carbon nanoparticles dose-dependently increases expression levels of glial fibrillary acidic protein (GFAP) in astrocytes in the offspring cerebral cortex. a, b, d, e, g and h show representative fluorescent micrographs of GFAP-positive astrocytes in the cerebral cortices of 6 week old male offspring in the control (a, b), low exposure (d, e), and high exposure groups (g, h). a, d and g gives an overview of the cerebral cortex, with b, e, and h providing enlarged views hereof, respectively. c, f, and i are grayscale views of b, e, and h, respectively, for quantification of the GFAP expression. j indicates averages of the expression area of GFAP-positive astrocytes in the cerebral cortices of offspring based on the grayscale views provided in [Additional files 3, 4 and 5], and shows that the maternal exposure to the nanoparticles significantly increases expression levels of GFAP in astrocytes in offspring cerebral cortices. N is the number of brains analysed, mean ± SEMCC BY · PubMed Central
Fig. 5 Maternal exposure to Printex 90 carbon nanoparticles dose-dependently increases expression levels of glial fibrillary acidic protein (GFAP) in astrocytes in the offspring hippocampus. a, b, d, e, g and h show representative fluorescent micrographs of GFAP-positive astrocytes in the hippocampi of 6 week old male offspring in the control (a, b), low exposure (d, e), and high exposure group (g, h). a, d and g gives an overview of the hippocampus, with b, e, and h providing enlarged views of panels a, d, and g, respectively. c, f, and i are grayscale views of b, e, and h, respectively, for quantification of GFAP expression. j indicates averages of the expression area of GFAP-positive astrocytes in the hippocampus of offspring based on grayscale views provided in [Additional files 6, 7 and 8], and shows that maternal exposure to the nanoparticles significantly increases expression levels of GFAP of astrocytes in the hippocampus. N is the number of brains analysed, mean ± SEM
Fig. 5 Maternal exposure to Printex 90 carbon nanoparticles dose-dependently increases expression levels of glial fibrillary acidic protein (GFAP) in astrocytes in the offspring hippocampus. a, b, d, e, g and h show representative fluorescent micrographs of GFAP-positive astrocytes in the hippocampi of 6 week old male offspring in the control (a, b), low exposure (d, e), and high exposure group (g, h). a, d and g gives an overview of the hippocampus, with b, e, and h providing enlarged views of panels a, d, and g, respectively. c, f, and i are grayscale views of b, e, and h, respectively, for quantification of GFAP expression. j indicates averages of the expression area of GFAP-positive astrocytes in the hippocampus of offspring based on grayscale views provided in [Additional files 6, 7 and 8], and shows that maternal exposure to the nanoparticles significantly increases expression levels of GFAP of astrocytes in the hippocampus. N is the number of brains analysed, mean ± SEMCC BY · PubMed Central
Fig. 6 Maternal exposure to Printex 90 carbon nanoparticles affects parvalbumin (PV) expressing interneurons in the cortex. a-f: The density of PV interneurons is changed in the prefrontal (PFC) and motor (MT) cortices of the offspring following maternal exposure to carbon black (only control (CO) and high (HI) exposure groups investigated). a and b show an overview of the PFC and MT regions, respectively, which have been used for quantifications of PV interneurons. In both panels, the dashed line indicates separation of the upper (up; L1-L3) and lower (low; L4–6) cortical layers. c and d show that the density of PV interneurons in the PFC is decreased in both PND 25 and PND 120 offspring, respectively. The upper and lower layers of the PFC are similarly affected. e and f: The density of PV interneurons in the MT is affected by the maternal exposure. At PND 25 (e), there is an increase in the density of PV interneurons in the upper layers and a trend towards decrease (p = 0.078) in the lower layers at the highest maternal exposure level. At PND 120 (f) both upper and lower layers exhibit similar decreases in the density of PV interneurons. In all quantifications, the density of PV interneurons in control mice was normalized to 1 and the exposure group was normalized to the corresponding controls. N is the number of brains analysed. Mean ± SD. g-h: Expression of PV is decreased in the MT of maternally particle exposed offspring. g shows representative images of PV interneurons that were acquired without saturating the fluorescence signal. h shows that in prenatally exposed offspring PV interneurons have a dramatically decreased expression of PV both at PND 25 and PND 120. N denotes the number of cells measured
Fig. 6 Maternal exposure to Printex 90 carbon nanoparticles affects parvalbumin (PV) expressing interneurons in the cortex. a-f: The density of PV interneurons is changed in the prefrontal (PFC) and motor (MT) cortices of the offspring following maternal exposure to carbon black (only control (CO) and high (HI) exposure groups investigated). a and b show an overview of the PFC and MT regions, respectively, which have been used for quantifications of PV interneurons. In both panels, the dashed line indicates separation of the upper (up; L1-L3) and lower (low; L4–6) cortical layers. c and d show that the density of PV interneurons in the PFC is decreased in both PND 25 and PND 120 offspring, respectively. The upper and lower layers of the PFC are similarly affected. e and f: The density of PV interneurons in the MT is affected by the maternal exposure. At PND 25 (e), there is an increase in the density of PV interneurons in the upper layers and a trend towards decrease (p = 0.078) in the lower layers at the highest maternal exposure level. At PND 120 (f) both upper and lower layers exhibit similar decreases in the density of PV interneurons. In all quantifications, the density of PV interneurons in control mice was normalized to 1 and the exposure group was normalized to the corresponding controls. N is the number of brains analysed. Mean ± SD. g-h: Expression of PV is decreased in the MT of maternally particle exposed offspring. g shows representative images of PV interneurons that were acquired without saturating the fluorescence signal. h shows that in prenatally exposed offspring PV interneurons have a dramatically decreased expression of PV both at PND 25 and PND 120. N denotes the number of cells measuredCC BY · PubMed Central
Fig. 7 Maternal exposure to carbon black nanoparticles affects behaviour in the open field test during a 3 min observation period in male and female offspring. a shows the total ambulation during the 3 min test period where, overall, exposed offspring moved a longer distance than control offspring. b shows time spent in the central zone of field, where prenatally exposed offspring overall spent significantly longer time than exposed offspring. c shows the number of visits to the central zone, showing that prenatally exposed offspring visited the central zone more frequently than frequently than control offspring. d gives the velocity of ambulation. Mean ± SEM, n = 9–13
Fig. 7 Maternal exposure to carbon black nanoparticles affects behaviour in the open field test during a 3 min observation period in male and female offspring. a shows the total ambulation during the 3 min test period where, overall, exposed offspring moved a longer distance than control offspring. b shows time spent in the central zone of field, where prenatally exposed offspring overall spent significantly longer time than exposed offspring. c shows the number of visits to the central zone, showing that prenatally exposed offspring visited the central zone more frequently than frequently than control offspring. d gives the velocity of ambulation. Mean ± SEM, n = 9–13CC 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

Research works printed but not linked: 75

  1. Bakand S, Hayes A. Toxicological considerations, toxicity assessment, and risk Management of Inhaled Nanoparticles. Int J Mol Sci. 2016;17 · DOI
  2. Takeda K, Shinkai Y, Suzuki K, Yanagita S, Umezawa M, Yokota S, et al. Health effects of nanomaterials on next generation. Yakugaku Zasshi-Journal of the Pharmaceutical Society of Japan. 2011;131:229–36. · DOI
  3. Hougaard KS, Campagnolo L, Chavatte-Palmer P, Tarrade A, Rousseau-Ralliard D, Valentino S, et al. A perspective on the developmental toxicity of inhaled nanoparticles. Reprod Toxicol. 2015;56:118–40. · DOI · Paper page
  4. Umezawa M, Onoda A, Takeda K. Developmental toxicity of nanoparticles on the brain. Yakugaku Zasshi. 2017;137:73–8. · DOI
  5. Stone V, Miller MR, Clift MJD, Elder A, Mills NL, Moller P, et al. Nanomaterials versus ambient ultrafine particles: an opportunity to exchange toxicology knowledge. Environ Health Perspect. 2017;125:106002. · DOI · Paper page
  6. Oberdörster G, Oberdörster E, Oberdörster J. Nanotoxicology: an emerging discipline evolving from studies of ultrafine particles. Environ Health Perspect. 2005;113:823–39. · DOI · Paper page
  7. Choi M, Cho M, Han BS, Hong J, Jeong J, Park S, et al. Chitosan nanoparticles show rapid extrapulmonary tissue distribution and excretion with mild pulmonary inflammation to mice. Toxicol Lett. 2010;199:144–52. · DOI
  8. Kreyling WG, Holzwarth U, Haberl N, Kozempel J, Wenk A, Hirn S, et al. Quantitative biokinetics of titanium dioxide nanoparticles after intratracheal instillation in rats: part 3. Nanotoxicology. 2017;11:454–64. · DOI
  9. Semmler-Behnke M, Lipka J, Wenk A, Hirn S, Schaffler M, Tian F, et al. Size dependent translocation and fetal accumulation of gold nanoparticles from maternal blood in the rat. Part Fibre Toxicol. 2014;11:33. · DOI · Paper page
  10. Modrzynska J, Berthing T, Ravn-Haren G, Jacobsen NR, Weydahl IK, Loeschner K, et al. Primary genotoxicity in the liver following pulmonary exposure to carbon black nanoparticles in mice. Part Fibre Toxicol. 2018;15:2. · DOI
  11. Takeda K, Suzuki K, Ishihara A, Kubo-Irie M, Fujimoto R, Tabata M, et al. Nanoparticles transferred from pregnant mice to their offspring can damage the genital and cranial nerve systems. J Health Sci. 2009;55:95–102. · DOI · Paper page
  12. Pietroiusti A, Campagnolo L, Fadeel B. Interactions of engineered nanoparticles with organs protected by internal biological barriers. Small. 2012; · DOI
  13. Moller P, Jacobsen NR, Folkmann JK, Danielsen PH, Mikkelsen L, Hemmingsen JG, et al. Role of oxidative damage in toxicity of particulates. Free Radic Res. 2010;44:1–46. · DOI
  14. Jacobsen NR, Pojana G, White P, Moller P, Cohn CA, Korsholm KS, et al. Genotoxicity, cytotoxicity, and reactive oxygen species induced by single-walled carbon nanotubes and C(60) fullerenes in the FE1-Mutatrade markMouse lung epithelial cells. Environ Mol Mutagen. 2008;49:476–87. · DOI
  15. Jacobsen NR, Saber AT, White P, Moller P, Pojana G, Vogel U, et al. Increased mutant frequency by carbon black, but not quartz, in the lacZ and cII transgenes of muta mouse lung epithelial cells. Environ Mol Mutagen. 2007;48:451–61. · DOI
  16. Wang Y, Xiong L, Tang M. Toxicity of inhaled particulate matter on the central nervous system: neuroinflammation, neuropsychological effects and neurodegenerative disease. J Appl Toxicol. 2017;37:644–67. · DOI
  17. Ema M, Hougaard KS, Kishimoto A, Honda K. Reproductive and developmental toxicity of carbon-based nanomaterials: a literature review. Nanotoxicology. 2016;10:391–412. · DOI
  18. Meyer U. Developmental neuroinflammation and schizophrenia. Prog Neuro-Psychopharmacol Biol Psychiatry. 2013;42:20–34. · DOI
  19. Graciarena M, Depino AM, Pitossi FJ. Prenatal inflammation impairs adult neurogenesis and memory related behavior through persistent hippocampal TGF beta(1) downregulation. Brain Behavior and Immunity. 2010;24:1301–9. · DOI
  20. Meyer U. Prenatal poly(I:C) exposure and other developmental immune activation models in rodent systems. Biol Psychiatry. 2014;75:307–15. · DOI · Paper page
  21. Reisinger S, Khan D, Kong E, Berger A, Pollak A, Pollak DD. The poly(I:C)-induced maternal immune activation model in preclinical neuropsychiatric drug discovery. Pharmacol Ther. 2015;149:213–26. · DOI
  22. Brown AS. Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism. Dev Neurobiol. 2012;72(10):1272–6. · DOI
  23. Boksa P, Zhang Y, Nouel D, Wong A, Wong TP. Early development of Parvalbumin-, somatostatin-, and cholecystokinin-expressing neurons in rat brain following prenatal immune activation and maternal Iron deficiency. Dev Neurosci. 2016;38:342–53. · DOI
  24. Meyer U, Nyffeler M, Yee BK, Knuesel I, Feldon J. Adult brain and behavioral pathological markers of prenatal immune challenge during early/middle and late fetal development in mice. Brain Behavior and Immunity. 2008;22:469–86. · DOI · Paper page
  25. Heusinkveld HJ, Wahle T, Campbell A, Westerink RHS, Tran L, Johnston H, et al. Neurodegenerative and neurological disorders by small inhaled particles. Neurotoxicology. 2016;56:94–106. · DOI · Paper page
  26. Jacobsen NR, White PA, Gingerich J, Moller P, Saber AT, Douglas GR, et al. Mutation spectrum in FE1-MUTA(TM) mouse lung epithelial cells exposed to nanoparticulate carbon black. Environ Mol Mutagen. 2011;52:331–7. · DOI
  27. Jackson P, Hougaard KS, Vogel U, Wu D, Casavant L, Williams A, et al. Exposure of pregnant mice to carbon black by intratracheal instillation: Toxicogenomic effects in dams and offspring. Mutat Res. 2012;745:73–83. · DOI · Paper page
  28. Bourdon JA, Halappanavar S, Saber AT, Jacobsen NR, Williams A, Wallin H, et al. Hepatic and pulmonary toxicogenomic profiles in mice intratracheally instilled with carbon black nanoparticles reveal pulmonary inflammation, acute phase response and alterations in lipid homeostasis. Toxicol Sci. 2012;127:474–84. · DOI
  29. Kyjovska ZO, Jacobsen NR, Saber AT, Bengtson S, Jackson P, Wallin H, et al. DNA strand breaks, acute phase response and inflammation following pulmonary exposure by instillation to the diesel exhaust particle NIST1650b in mice. Mutagenesis. 2015;30:499–507. · DOI
  30. El-Sayed YS, Shimizu R, Onoda A, Takeda K, Umezawa M. Carbon black nanoparticle exposure during middle and late fetal development induces immune activation in male offspring mice. Toxicology. 2015;327:53–61. · DOI · Paper page
  31. Onoda A, Umezawa M, Takeda K, Ihara T, Sugamata M. Effects of maternal exposure to ultrafine carbon black on brain perivascular macrophages and surrounding astrocytes in offspring mice. PLoS One. 2014;9:e94336. · DOI · Paper page
  32. Onoda A, Takeda K, Umezawa M. Dose-dependent induction of astrocyte activation and reactive astrogliosis in mouse brain following maternal exposure to carbon black nanoparticle. Part Fibre Toxicol. 2017;14:4. · DOI · Paper page
  33. Molofsky AV, Krenick R, Ullian E, Tsai HH, Deneen B, Richardson WD, et al. Astrocytes and disease: a neurodevelopmental perspective. Genes Dev. 2012;26:891–907. · DOI · Paper page
  34. Jackson P, Vogel U, Wallin H, Hougaard KS. Prenatal exposure to carbon black (Printex 90): effects on sexual development and Neurofunction. Basic Clin Pharmacol Toxicol. 2011;109:434–7. · DOI · Paper page
  35. Jackson P, Hougaard KS, Boisen AM, Jacobsen NR, Jensen KA, Moller P, et al. Pulmonary exposure to carbon black by inhalation or instillation in pregnant mice: effects on liver DNA strand breaks in dams and offspring. Nanotoxicology. 2012;6:484–500. · DOI
  36. Jackson P, Kling K, Jensen KA, Clausen PA, Madsen AM, Wallin H, et al. Characterization of genotoxic response to 15 multiwalled carbon nanotubes with variable physicochemical properties including surface functionalizations in the FE1-Muta(TM) mouse lung epithelial cell line. Environ Mol Mutagen. 2015;56:183–203. · DOI
  37. Hougaard KS, Jackson P, Jensen KA, Sloth JJ, Loschner K, Larsen EH, et al. Effects of prenatal exposure to surface-coated nanosized titanium dioxide (UV-Titan). A study in mice. Part Fibre Toxicol. 2010;7:16:16. · DOI · Paper page
  38. Wallin H, Kyjovska ZO, Poulsen SS, Jacobsen NR, Saber AT, Bengtson S, et al. Surface modification does not influence the genotoxic and inflammatory effects of TiO2 nanoparticles after pulmonary exposure by instillation in mice. Mutagenesis. 2017;32:47–57. · DOI
  39. Saber AT, Halappanavar S, Folkmann JK, Bornholdt J, Boisen AM, Moller P, et al. Lack of acute phase response in the livers of mice exposed to diesel exhaust particles or carbon black by inhalation. Part Fibre Toxicol. 2009;6:12:12. · DOI
  40. Millan MJ, Andrieux A, Bartzokis G, Cadenhead K, Dazzan P, Fusar-Poli P, et al. Altering the course of schizophrenia: progress and perspectives. Nat Rev Drug Discov. 2016;15:485–515. · DOI · Paper page
  41. Caballero A, Tseng KY. GABAergic function as a limiting factor for prefrontal maturation during adolescence. Trends Neurosci. 2016;39:441–8. · DOI
  42. Rubenstein JLR, Merzenich MM. Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes Brain and Behavior. 2003;2:255–67. · DOI · Paper page
  43. Khodosevich K, Zuccotti A, Kreuzberg MM, Le MC, Frank M, Willecke K, et al. Connexin45 modulates the proliferation of transit-amplifying precursor cells in the mouse subventricular zone. Proc Natl Acad Sci U S A. 2012;109:20107–12. · DOI
  44. Garcia-Gonzalez D, Khodosevich K, Watanabe Y, Rollenhagen A, Lubke JHR, Monyer H. Serotonergic projections govern postnatal neuroblast migration. Neuron. 2017;94:534–49. · DOI
  45. Schindelin J, Rganda-Carreras I, Frise E, Kaynig V, Longair M, Pietzsch T, et al. Fiji: an open-source platform for biological-image analysis. Nat Methods. 2012;9:676–82. · DOI · Paper page
  46. Husain M, Kyjovska ZO, Bourdon-Lacombe J, Saber AT, Jensen KA, Jacobsen NR, et al. Carbon black nanoparticles induce biphasic gene expression changes associated with inflammatory responses in the lungs of C57BL/6 mice following a single intratracheal instillation. Toxicol Appl Pharmacol. 2015;289:573–88. · DOI
  47. Driscoll KE, Carter JM, Howard BW, Hassenbein DG, Pepelko W, Baggs RB, et al. Pulmonary inflammatory, chemokine, and mutagenic responses in rats after subchronic inhalation of carbon black. Toxicol Appl Pharmacol. 1996;136:372–80. · DOI
  48. Saber AT, Bornholdt J, Dybdahl M, Sharma AK, Loft S, Vogel U, et al. Tumor necrosis factor is not required for particle-induced genotoxicity and pulmonary inflammation. Arch Toxicol. 2005;79:177–82. · DOI
  49. Halappanavar S, Jackson P, Williams A, Jensen KA, Hougaard KS, Vogel U, et al. Pulmonary response to surface-coated nanotitanium dioxide particles includes induction of acute phase response genes, inflammatory cascades, and changes in microRNAs: a toxicogenomic study. Environ Mol Mutagen. 2011;52:425–39. · DOI
  50. Saber AT, Lamson JS, Jacobsen NR, Ravn-Haren G, Hougaard KS, Nyendi AN, et al. Particle-induced pulmonary acute phase response correlates with neutrophil influx linking inhaled particles and cardiovascular risk. PLoS One. 2013;8:e69020. · DOI
  51. Saber AT, Jacobsen NR, Jackson P, Poulsen SS, Kyjovska ZO, Halappanavar S, et al. Particle-induced pulmonary acute phase response may be the causal link between particle inhalation and cardiovascular disease. Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2014;6:517–31. · DOI
  52. Rodriguez JJ, Olabarria M, Chvatal A, Verkhratsky A. Astroglia in dementia and Alzheimer's disease. Cell Death Differ. 2009;16:378–85. · DOI
  53. Butt AM, Hamilton N, Hubbard P, Pugh M, Ibrahim M. Synantocytes: the fifth element. J Anat. 2005;207:695–706. · DOI
  54. Pekny M, Wilhelmsson U, Bogestal YR, Pekna M. The role of astrocytes and complement system in neural plasticity. Neuroinflammation in Neuronal Death and Repair. 2007;82:95–111. · DOI
  55. Calderon-Garciduenas L, Reed W, Maronpot RR, Henriquez-Roldan C, Delgado-Chavez R, Calderon-Garciduenas A, et al. Brain inflammation and Alzheimer's-like pathology in individuals exposed to severe air pollution. Toxicol Pathol. 2004;32:650–8. · DOI
  56. Kohama SG, Goss JR, Finch CE, McNeill TH. Increases of glial fibrillary acidic protein in the aging female mouse brain. Neurobiol Aging. 1995;16:59–67. · DOI
  57. Nichols NR, Day JR, Laping NJ, Johnson SA, Finch CE. GFAP mRNA increases with age in rat and human brain. Neurobiol Aging. 1993;14:421–9. · DOI · Paper page
  58. Chen JC, Wang X, Wellenius GA, Serre ML, Driscoll I, Casanova R, et al. Ambient air pollution and neurotoxicity on brain structure: evidence from women's health initiative memory study. Ann Neurol. 2015;78:466–76. · DOI
  59. de Souza DF, Wartchow KM, Lunardi PS, Brolese G, Tortorelli LS, Batassini C, et al. Changes in Astroglial markers in a maternal immune activation model of schizophrenia in Wistar rats are dependent on sex. Front Cell Neurosci. 2015;9 · DOI
  60. Hawkes CA, Gentleman SM, Nicoll JAR, Carare RO. Prenatal high-fat diet alters the cerebrovasculature and clearance of beta-amyloid in adult offspring. J Pathol. 2015;235:619–31. · DOI
  61. Kim DW, Glendining KA, Grattan DR, Jasoni CL. Maternal obesity leads to increased proliferation and numbers of astrocytes in the developing fetal and neonatal mouse hypothalamus. Int J Devl Neurosci. 2016;53:18–25. · DOI · Paper page
  62. Woiciechowsky C, Schoning B, Stoltenburg-Didinger G, Stockhammer F, Volk HD. Brain-IL-1 beta triggers astrogliosis through induction of IL-6: inhibition by propranolol and IL-10. Med Sci Monit. 2004;10:BR325–30.
  63. Alshammari TK, Alshammari MA, Nenov MN, Hoxha E, Cambiaghi M, Marcinno A, et al. Genetic deletion of fibroblast growth factor 14 recapitulates phenotypic alterations underlying cognitive impairment associated with schizophrenia. Transl Psychiatry. 2016;6 · DOI
  64. Mauney SA, Athanas KM, Pantazopoulos H, Shaskan N, Passeri E, Berretta S, et al. Developmental pattern of Perineuronal nets in the human prefrontal cortex and their deficit in schizophrenia. Biol Psychiatry. 2013;74:427–35. · DOI · Paper page
  65. Gruol DL, Nelson TE. Physiological and pathological roles of interleukin-6 in the central nervous system. Mol Neurobiol. 1997;15:307–39. · DOI
  66. Kern JK, Geier DA, Homme KG, King PG, Bjorklund G, Chirumbolo S, et al. Developmental neurotoxicants and the vulnerable male brain: a systematic review of suspected neurotoxicants that disproportionally affect males. Acta Neurobiol Exp (Wars). 2017;77(4):269–96. · DOI
  67. Williams CL, Meck WH. The organizational effects of gonadal steroids on sexually dimorphic spatial ability. Psychoneuroendocrinology. 1991;16:155–76. · DOI
  68. Hougaard KS, Hass U, Lund SP, Simonsen L. Effects of prenatal exposure to toluene on postnatal development and behavior in rats. Neurotoxicol Teratol. 1999;21:241–50. · DOI
  69. Hougaard KS, Jackson P, Kyjovska ZO, Birkedal RK, De Temmerman PJ, Brunelli A, et al. Effects of lung exposure to carbon nanotubes on female fertility and pregnancy. A study in mice. Reprod Toxicol. 2013;41:86–97. · DOI
  70. Meyer U, Feldon J, Schedlowski M, Yee BK. Towards an immuno-precipitated neurodevelopmental animal model of schizophrenia. Neurosci Biobehav Rev. 2005;29:913–47. · DOI · Paper page
  71. Murray AJ, Woloszynowska-Fraser MU, Ansel-Bollepalli L, Cole KL, Foggetti A, Crouch B, et al. Parvalbumin-positive interneurons of the prefrontal cortex support working memory and cognitive flexibility. Sci Rep. 2015;5:16778. · DOI
  72. Kafri T, Ariel M, Brandeis M, Shemer R, Urven L, Mccarrey J, et al. Developmental pattern of gene-specific Dna methylation in the mouse embryo and germ line. Genes Dev. 1992;6:705–14. · DOI
  73. Marcho C, Cui W, Mager J. Epigenetic dynamics during preimplantation development. Reproduction. 2015;150:R109–20. · DOI
  74. Prinz M, Erny D, Hagemeyer N. Ontogeny and homeostasis of CNS myeloid cells. Nat Immunol. 2017;18:385–92. · DOI
  75. Goldmann T, Wieghofer P, Jordao MJ, Prutek F, Hagemeyer N, Frenzel K, et al. Origin, fate and dynamics of macrophages at central nervous system interfaces. Nat Immunol. 2016;17:797–805. · DOI · Paper page

Cited by

Sorted by citations

See all 74

Metadata

Authors
Umezawa, M., Onoda, A., Korshunova, I., Jensen, A. C. Ø., Koponen, I. K., Jensen, K. A., Khodosevich, K., Vogel, U., & Hougaard, K. S.
Venue
Particle and Fibre Toxicology
Published
2018-09-10
Volume
15
Issue
1
ISSN
1743-8977
Cited by
74
References
16
Language
en
Funders
  • Strategic Research Foundation at Private Universities (S1101015)
  • Working Environment Research Fund (20110092173 3)
  • Japanese Society for the Promotion of Science (JSPS) Research Fellow (15J05718)
  • Hallas Moeller Investigator Grant (NNF16OC0019920)
  • Agnes og Poul Friis Fond (1208011)

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