PMID- 23105606
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121030
LR  - 20240505
IS  - 0970-1915 (Print)
IS  - 0974-0422 (Electronic)
IS  - 0970-1915 (Linking)
VI  - 21
IP  - 2
DP  - 2006 Sep
TI  - Genetic determinants of hyperhomocysteinemia in atherosclerosis.
PG  - 4-11
LID - 10.1007/BF02912904 [doi]
AB  - Hyperhomocysteinemia (Hhcy) is an independent risk factor for the development of 
      atherosclerosis. The mechanisms by which HHcy promotes cardiovascular disease may 
      be due to activation of pro-inflammatory factors, endoplasmic reticulum (ER) 
      stress and oxidative stress. We aimed to study (i) gene mutations that cause 
      HHcy. (ii) Estimation of inflammatory marker like ultrasenitive C-reactive 
      proteins (hs-CRP) and total antioxidant levels (iii) determination of Hcy- 
      dependent gene expression in vivo. 25 HHcy patients and 25 healthy controls were 
      taken for this study. Mutation detection in MTHFR, CBS, MS and eNOS gene was by 
      PCR-based restriction enzyme analysis and subsequently expression study was 
      carried out by Reverse Transcriptase PCR and cloning technique. A significant 
      association of HHcy with MTHFR (C677T) and MS (A2756G) genotype was observed 
      (p<0.05). There was no association of Hhcy and eNOS genotype. The Hhcy patients, 
      showed no expression of the ER stress gene, GRP78 in lymphocytes. Our study 
      showed no effect of Hcy on the CD18 gene (pro-inflammatory pathway) expression, 
      but a significant association of tHcy and hs-CRP levels in HHcy grp (t=2.28, 
      p<0.05). This shows that HHcy induces inflammatory response, which could lead to 
      tissue injury in the pathogenesis of the atherosclerotic process. Our findings 
      show higher mRNA expression of manganese superoxide dismutase (Mn SOD) in HHcy 
      group as compared to the control group. The Total Antioxidant Status (TAS) 
      estimated was found to be significantly lower in the HHcy group as compared to 
      healthy normals (t=4.8, p<0.01). Taken together these findings strongly suggest 
      that the adverse effects of homocysteine are at least partly mediated by 
      oxidative stress. Our study supports the hypothesis that Hcy evokes adverse 
      vascular effects by promoting oxidative damage to endothelial cells.
FAU - Eghlim, Farah F
AU  - Eghlim FF
AD  - Research laboratory, P. D. Hinduja National Hospital & Medical Research Center, 
      400 016 Mumbai, India.
FAU - Ashavaid, Tester F
AU  - Ashavaid TF
FAU - Nair, Kappiareth G
AU  - Nair KG
LA  - eng
PT  - Journal Article
PL  - India
TA  - Indian J Clin Biochem
JT  - Indian journal of clinical biochemistry : IJCB
JID - 8708303
PMC - PMC3454005
OTO - NOTNLM
OT  - Atherosclerosis
OT  - CBS
OT  - Hyperhomocysteinemia
OT  - MS
OT  - MTHFR
OT  - eNOS
EDAT- 2006/09/01 00:00
MHDA- 2006/09/01 00:01
PMCR- 2007/09/01
CRDT- 2012/10/30 06:00
PHST- 2012/10/30 06:00 [entrez]
PHST- 2006/09/01 00:00 [pubmed]
PHST- 2006/09/01 00:01 [medline]
PHST- 2007/09/01 00:00 [pmc-release]
AID - BF02912904 [pii]
AID - 10.1007/BF02912904 [doi]
PST - ppublish
SO  - Indian J Clin Biochem. 2006 Sep;21(2):4-11. doi: 10.1007/BF02912904.