Abstract
Astrocytes are the most widely distributed cells in the brain, and astrocyte apoptosis may play an important role in the pathogenesis of neurodegenerative diseases. Folate is required for the normal development of the nervous system, but its effect on astrocyte apoptosis is unclear. In this study, we hypothesized that folic acid (the therapeutic form of folate) decreases astrocyte apoptosis by preventing oxidative stress-induced telomere attrition. Primary cultures of astrocytes were incubated for 12 days with various concentrations of folic acid (0–40 μmol/L), then cell proliferation, apoptosis, intracellular folate concentration, intracellular homocysteine (Hcy) concentration, intracellular reactive oxygen species (ROS) levels, telomeric DNA oxidative damage, and telomere length were determined. The results showed that folic acid deficiency decreased intracellular folate, cell proliferation, and telomere length, whereas it increased Hcy concentration, ROS levels, telomeric DNA oxidative damage, and apoptosis. In contrast, folic acid dose-dependently increased intracellular folate, cell proliferation, and telomere length but it decreased Hcy concentration, ROS levels, telomeric DNA oxidative damage, and apoptosis. In conclusion, folic acid inhibited apoptosis in astrocytes. The underlying mechanism for this protective effect may be that folic acid decreased oxidative stress and thereby prevented telomeric DNA oxidative damage and telomere attrition.
Highlights
Telomeres are ribonucleoprotein structures capping the end of every linear chromosome [1]
The present study found in astrocytes that folic acid deficiency increased both 8-oxoG in telomeric DNA and telomere attrition, whereas high-dose folic acid decreased these parameters
This study hypothesized a mechanistic link between folate protection against astrocyte apoptosis and reduced telomere attrition and oxidative stress
Summary
Telomeres are ribonucleoprotein structures capping the end of every linear chromosome [1]. Folic acid is the form of folate that is used therapeutically. It stimulates the proliferation of neural stem Icnet.lJl.sMaonl. Whether folic acid can protect against astrocyte apoptosis is unclear This knowFloelidcgaecidgiaspthiesfiomrmpoofrftoalantte btheactaisuusseedasthtreoracpyetuetsicaalrley.tIht setimmuolsattews tihdeeplryoldifiesrtartiiobnuotef dnecueralllsstienmtcheellsbrain and the differentiation of neurons in vitro and in vivo [17,18]. This knowledge gap is important because astrocytes are the most. OTfaken togethfoelirc, tahciedsaet r0e, s1u0,lt2s0 ionrd4i0cμamteodl/Lthwaetrfeo, lriecspaeccitdivedlye,c1r6e.a7s3e±d2.a0p3,o7p.6t4o±si0s.5a3n, d6.5i7n±cr0e.7a6s,e5d.06ce±l0l.9p1r(oFligifuerrea2tbion in a dosaen-dedp).eTnadkeennttogmetahnern, ethr.ese results indicated that folic acid decreased apoptosis and increased cell proliferation in a dose-dependent manner. Faocliicd-AdceifidcDieencrtegarsoedupIn, twrahciellelualahrigHhcydoasnedoRfOfoSlic acid (40 μmol/L) increased intracellular folate compared wAifttherth1e2ndoarymsaolfdionsteerovfefnotliiocna,citdhe(1i0ntμrmacoell/lLu)la(rp f
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