Homocysteine, B vitamins, methylenetetrahydrofolate reductase gene, and risk of primary open-angle glaucoma: a meta-analysis.

BACKGROUND: To evaluate the association between plasma total homocysteine (tHcy) levels, serum folic acid, vitamin B(12) and vitamin B(6) levels, methylenetetrahydrofolate reductase (MTHFR) C677T genotype and risk of primary open-angle glaucoma (POAG). CLINICAL RELEVANCE: There are conflicting reports on the association of Hcy, folic acid, vitamin B(12), vitamin B(6), MTHFR, and risk of POAG. We conducted this meta-analysis to derive a more precise estimation of the association. METHODS: Pertinent articles were identified through a systematic search of the EMBASE and Medline databases. Results were pooled using meta-analytic methods. The main outcome measure included tHcy, folic acid, vitamin B(12) and vitamin B(6) levels, and MTHFR C677T genotype. RESULTS: Twelve studies were eligible for Hcy, 6 studies for folic acid, 6 studies for vitamin B(12), 3 studies for vitamin B(6), and 10 studies for MTHFR. The combined results showed that plasma tHcy levels in POAG were 2.05 µmol/L (95% confidence interval [CI], 0.63-3.47) higher than in controls. There was no difference between serum folic acid, vitamin B(6), and vitamin B(12) levels in POAG and controls. The weighted mean difference with 95% CI were 0.34 µmol/L (-0.37 to 1.05), 2.75 µmol/L (-3.68 to 9.18), and 0.97 µmol/L (-30.45 to 32.40), respectively. The MTHFR 677TT genotype was not associated with the risk of POAG (odds ratio, 1.10; 95% CI, 0.83-1.47). CONCLUSIONS: We found that POAG is associated with elevated plasma tHcy levels, but not serum folic acid, vitamin B(12), vitamin B(6) levels, or MTHFR C677T genotype. FINANCIAL DISCLOSURE(S): The authors have no proprietary or commercial interest in any of the materials discussed in this article.

Alterations in the expression of Hs1-associated protein X-1 in the rat retina after optic nerve crush.

HS-1-associated protein X-1 (Hax-1) has been suggested to be expressed in various rodent and human tissues. Accumulating evidence has demonstrated that Hax­1 exerts an anti­apoptotic effect in neurological diseases. Furthermore, it has also been reported that Hax­1 interacts with various apoptosis­associated proteins, including high temperature-regulated A2 (HtrA2) and caspase­3. Previous studies have indicated that abnormal expression of Hax­1 may be associated with the development of the nervous system and with the pathophysiology of neurological diseases, including traumatic brain injury and cerebral ischemia. The present study reported temporal­spatial patterns of Hax­1 in rat retina following optic nerve crush (ONC). Using western blotting and double­immunofluorescence, significant upregulation of Hax­1 was observed in retinal ganglion cells (RGCs) in the retina following ONC. Increased Hax­1 expression was demonstrated to be accompanied by upregulation of active­caspase­3 and HtrA2 following ONC. In addition, Hax-1 co­localized with active caspase­3 and HtrA2 in RGCs following ONC. Terminal deoxynucleotidyl transferase­mediated biotinylated-dUTP nick­end labeling staining suggested that Hax­1 was involved in RGC apoptosis following ONC. Thus, these results suggested that Hax­1 may participate in regulating RGC apoptosis via interacting with caspase­3 and HtrA2 following ONC.