Parental Folate Deficiency Inhibits Proliferation and Increases Apoptosis of Neural Stem Cells in Rat Offspring: Aggravating Telomere Attrition as a Potential Mechanism.

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  • Additional Information
    • Source:
      Publisher: MDPI Publishing Country of Publication: Switzerland NLM ID: 101521595 Publication Model: Electronic Cited Medium: Internet ISSN: 2072-6643 (Electronic) Linking ISSN: 20726643 NLM ISO Abbreviation: Nutrients Subsets: MEDLINE
    • Publication Information:
      Original Publication: Basel, Switzerland : MDPI Publishing
    • Subject Terms:
    • Abstract:
      The effect of maternal folate status on the fetal central nervous system (CNS) is well recognized, while evidence is emerging that such an association also exists between fathers and offspring. The biological functions of telomeres and telomerase are also related to neural cell proliferation and apoptosis. The study aimed to investigate the effect of parental folate deficiency on the proliferation and apoptosis of neural stem cells (NSCs) in neonatal offspring and the role of telomeres in this effect. In this study, rats were divided into four groups: maternal folate-deficient and paternal folate-deficient diet (D-D) group; maternal folate-deficient and paternal folate-normal diet (D-N) group; maternal folate-normal and paternal folate-deficient diet (N-D) group; and the maternal folate-normal and paternal folate-normal diet (N-N) group. The offspring were sacrificed at postnatal day 0 (PND0), and NSCs were cultured from the hippocampus and striatum tissues of offspring for future assay. The results revealed that parental folate deficiency decreased folate levels, increased homocysteine (Hcy) levels of the offspring's brain tissue, inhibited proliferation, increased apoptosis, shortened telomere length, and aggravated telomere attrition of offspring NSCs in vivo and in vitro. In vitro experiments further showed that offspring NSCs telomerase activity was inhibited due to parental folate deficiency. In conclusion, parental folate deficiency inhibited the proliferation and increased apoptosis of offspring NSCs, maternal folate deficiency had more adverse effects than paternal, and the mechanisms may involve the telomere attrition of NSCs.
    • References:
      Oxid Med Cell Longev. 2019 Dec 14;2019:4569614. (PMID: 31949878)
      Fluids Barriers CNS. 2022 Nov 23;19(1):92. (PMID: 36419095)
      Eur J Nutr. 2020 Jun;59(4):1345-1356. (PMID: 31098661)
      Methods Mol Biol. 2008;438:185-96. (PMID: 18369758)
      Br J Nutr. 2019 Sep;122(s1):S1-S9. (PMID: 31638501)
      Int J Mol Sci. 2022 Jan 25;23(3):. (PMID: 35163253)
      J Nutr. 2004 Jan;134(1):162-6. (PMID: 14704311)
      Nutr Rev. 2021 Jan 9;79(2):148-159. (PMID: 32968801)
      Development. 2004 Aug;131(16):4059-70. (PMID: 15269166)
      Hum Reprod Update. 2007 May-Jun;13(3):225-38. (PMID: 17307774)
      Am J Pathol. 2007 Feb;170(2):667-79. (PMID: 17255334)
      Nat Rev Genet. 2019 May;20(5):299-309. (PMID: 30760854)
      EMBO Mol Med. 2012 Aug;4(8):691-704. (PMID: 22585399)
      Int J Dev Neurosci. 2019 Feb;72:6-12. (PMID: 30447272)
      Cell Mol Life Sci. 2020 Jan;77(1):61-79. (PMID: 31728577)
      Nutrients. 2021 Aug 17;13(8):. (PMID: 34444978)
      Development. 2019 Feb 18;146(4):. (PMID: 30777863)
      Mol Neurobiol. 2022 Jan;59(1):590-602. (PMID: 34741234)
      J Neurosci. 2009 Nov 18;29(46):14394-407. (PMID: 19923274)
      Biomark Med. 2017 Sep;11(9):799-810. (PMID: 30669856)
      J Frailty Aging. 2021;10(1):2-9. (PMID: 33331615)
      Adv Clin Chem. 2019;90:81-132. (PMID: 31122612)
      Nutrients. 2022 Jan 15;14(2):. (PMID: 35057545)
      Cereb Cortex. 2019 Jul 22;29(8):3390-3397. (PMID: 30137237)
      Mol Nutr Food Res. 2013 Apr;57(4):671-6. (PMID: 23229416)
      Neuroscience. 2015 Aug 6;300:1-9. (PMID: 25956258)
      J Nutr. 2009 Jul;139(7):1273-8. (PMID: 19458030)
      Mol Nutr Food Res. 2020 May;64(9):e1900696. (PMID: 32032459)
      Clin Nutr. 2021 Feb;40(2):476-487. (PMID: 32571678)
      J Biomed Res. 2012 Sep;26(5):381-8. (PMID: 23554775)
      Front Mol Neurosci. 2018 May 16;11:160. (PMID: 29867352)
      Cell Discov. 2022 Feb 22;8(1):18. (PMID: 35190523)
      J Nutr Biochem. 2021 Nov;97:108796. (PMID: 34102282)
      BMC Med. 2019 Oct 31;17(1):196. (PMID: 31672132)
      Clin Nutr. 2021 May;40(5):3391-3400. (PMID: 33279309)
      Cell Death Dis. 2020 Oct 24;11(10):910. (PMID: 33099583)
      Mol Psychiatry. 2018 May;23(5):1345-1355. (PMID: 28373690)
      Int J Biol Macromol. 2020 Nov 15;163:1060-1078. (PMID: 32673712)
      FASEB J. 2012 Oct;26(10):3980-92. (PMID: 22713523)
      Nutr Res Pract. 2011 Apr;5(2):112-6. (PMID: 21556224)
      Biosci Rep. 2018 Jul 6;38(4):. (PMID: 29945927)
      Cell. 2021 Feb 4;184(3):709-722.e13. (PMID: 33482084)
      Public Health Nutr. 2016 Jan;19(1):176-89. (PMID: 25877429)
      Fertil Steril. 2019 Feb;111(2):270-279. (PMID: 30691629)
      Viruses. 2021 Jul 27;13(8):. (PMID: 34452333)
      Differentiation. 2021 Jan-Feb;117:1-15. (PMID: 33302058)
    • Grant Information:
      82003439 National Natural Science Foundation of China; 2019KJ166 Scientific Research Program of Tianjin Municipal Education Commission; 2022KJ203 Scientific Research Program of Tianjin Municipal Education Commission
    • Contributed Indexing:
      Keywords: apoptosis; folate; neural stem cells; parental; proliferation; telomere attrition
    • Accession Number:
      EC 2.7.7.49 (Telomerase)
      935E97BOY8 (Folic Acid)
    • Publication Date:
      Date Created: 20230714 Date Completed: 20230717 Latest Revision: 20230718
    • Publication Date:
      20240829
    • Accession Number:
      PMC10343379
    • Accession Number:
      10.3390/nu15132843
    • Accession Number:
      37447170