Association between homocysteine and endothelial dysfunction markers in stroke disease

Abdulle, Abdishakur; Yasin, Javed; Moussa, Nagi A.; Gariballa, Salah

doi:10.1179/147683010x12611460763562

Cited by 18 publications

(14 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…found that total plasma homocysteine concentration had an inverse correlation with both vitamin B 12 and folate. [18] In agreement with our study, the results of study conducted in Iranian population showed significant negative correlation between vitamin B12 and homocysteine concentration. [19] It is implied that in our study subjects, deficiency of vitamin B12 may be a cause for the increase in fasting Hcys.…”

Section: Discussionsupporting

confidence: 91%

Hyperhomocysteinemia, low vitamin B12, and low folic acid: Are risk factors of cerebral vascular thrombosis in northwest Iran?

et al. 2016

View full text Add to dashboard Cite

Background:Cerebral vascular thrombosis (CVT) is the thrombosis of intracranial and sinuses. The aim of this is to estimate of risk of low folic acid, low vitamin B12, and hyperhomocysteinemia (hyper-Hcys) for CVT.Materials and Methods:A total of 24 patients with CVT and 36 healthy controls participated in a cross-sectional case-control study. The deficient levels of folic acid and vitamin B12 defined as <10th percentile of folic acid and vitamin B12 level and hyper-Hcys was defined as >90th percentile of homocysteine of control group.Results:Patients had higher levels of total homocysteine (tHcys) than controls (14.7 ± 6.5 vs. 6.4 ± 2.7 μmol/L, P = 0.001). Also, vitamin B12 level in case group was lower compared to control subjects (185.4 ± 58 vs. 299 ± 75 ng/mL, P = 0.001). Hyper-Hcys and low vitamin B12 were significantly more prevalent in CVT patients than controls. Although, significant independent association with risk of CVT was found for hyper-Hcys [adjusted odds ratio (OR) 14.3, 95% confidence interval (CI): 2.6-77.1, P = 0.002] and low vitamin B12 (adjusted OR 24.6, 95% CI: 2.3-262.9, P = 0.008). Association between low folic acid and risk of CVT was not significant. A significant negative correlation was found between the levels of tHcys and vitamin B12 (r = −0.32, P = 0.01).Conclusion:Hyper-Hcys and low vitamin B12 were related with the high risk for CVT.

show abstract

Section: Discussionsupporting

confidence: 91%

Hyperhomocysteinemia, low vitamin B12, and low folic acid: Are risk factors of cerebral vascular thrombosis in northwest Iran?

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Although previous study reported that the inhibition of DDAH activity contributed to homocysteine-induced ADMA accumulation in endothelial cells 15 , it is still unknown whether suppressed DDAH2 expression contributes to the inhibition of DDAH activity and accumulation of endogenous ADMA induced by homocysteine in endothelial cells, because the DDAH2 and DDAH1 expression or transcription were not simultaneously examined in previous studies [2,4,10,[13][14][15]24]. The present study provides the evidence that the suppression of DDAH2 expression is a primary cause for homocysteineinduced impairments of DDAH/ADMA/NOS/NO pathway in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…Endothelial dysfunction, characterized by impairment of endothelium-dependent vasodilatation or endothelium-derived nitric oxide (NO) synthesis, plays a crucial role in pathophysiological process of hyperhomocysteinemia-induced cardiovascular diseases [23,24]. ADMA has emerged as a key factor for homocysteine-associated endothelial dysfunction [2,4,10,[13][14][15].…”

Section: Discussionmentioning

confidence: 99%

Protection of DDAH2 Overexpression Against Homocysteine-Induced Impairments of DDAH/ADMA/NOS/NO Pathway in Endothelial Cells

Liu

Guo

Feng

et al. 2012

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Homocysteine-induced endothelial dysfunction favors the development of cardiovascular diseases through accumulation of endogenous nitric oxide (NO) synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA). Dimethylarginine dimethylaminohydrolase 2 (DDAH2) is the major enzyme for the degradation of ADMA in endothelial cells. The purpose of this study was to determine whether suppressed DDAH2 expression contributed to impairments of DDAH/ADMA/NOS/NO pathway induced by homocysteine in endothelial cells and whether DDAH2 overexpression could prevent endothelial cell dysfunction caused by homocysteine. Methods: Liposome-mediated transfection of endothelial cells was performed to establish the cell line of DDAH2 overexpression. After treatment of cells with 1 mmol/L homocysteine for 24 h, the transcription and expression of DDAH1 and DDAH2, DDAH and NOS activities as well as ADMA and NO concentrations were measured. Results: Treatment of endothelial cells with homocysteine significantly suppressed the transcription and expression of DDAH2 but not DDAH1. This suppression was associated with the declined DDAH activity, increased ADMA accumulation, inhibited NOS activity and decreased NO production in endothelial cells. DDAH2 overexpression not only resisted homocysteine-induced decline of DDAH activity, but also decreased the accumulation of endogenous ADMA, subsequently attenuated the reductions of NOS activity and NO production induced by homocysteine. Conclusions: These results indicate that suppression of DDAH2 expression is a culprit for homocysteine-induced impairments of DDAH/ADMA/NOS/NO pathway in endothelial cells, and therapeutic manipulation of DDAH2 expression may be a promising strategy for preventing endothelial dysfunction and cardiovascular diseases associated with hyperhomocysteinemia.

show abstract

“…Such an interrelationship between these three substances has been shown in multiple studies performed in patients with various conditions including mood disorders [2,16] and has been by some authors regarded as a rationale for supplementation with folic acid or vitamin B 12 for the treatment of depression. However, no direct relationship between improvement of depression and a reduction of HCY level was observed.…”

Section: Discussionmentioning

confidence: 99%

“…Greek researchers found normal values of endothelial function in parkinsonian patients with hyperhomocysteinemia [18]. In another study, an increase in markers of endothelial dysfunction following acute ischemic stroke did not correlate with HCY level [16]. HCY-lowering vitamin treatment in healthy siblings of patients with premature atherosclerotic disease was not associated with a change in these markers [19].…”

Section: Discussionmentioning

confidence: 99%

Hyperhomocysteinemia in Bipolar Depression: Clinical and Biochemical Correlates

Permoda-Osip

Dorszewska²,

Skibińska

et al. 2013

Neuropsychobiology

View full text Add to dashboard Cite

Background: Depression may be associated with elevated homocysteine (HCY) levels. Procedures aiming at its decrease, i.e. supplementation with folic acid or vitamin B₁₂, have antidepressant effect. Both depression and elevated HCY can increase cardiovascular risk. In this study, clinical and biochemical factors, including markers of endothelial function, in relation to hyperhomocysteinemia, in patients with bipolar depression during acute episode were studied. Method: One hundred and twelve patients (24 male, 88 female), aged 20-78 (mean 51 ± 14 years), with depressive episode in the course of bipolar mood disorder have been included. The assays were made of serum concentrations of HCY, vitamin B₁₂, folic acid as well as markers of endothelial function such as E-selectin and intracellular adhesion molecule-1 (ICAM-1). Results: Hyperhomocysteinemia (>15 mM)was found in 50 patients (45%), significantly more frequently in male (67%) than in female subjects (39%). Female patients with hyperhomocysteinemia were significantly older than the remaining ones. A significant inverse correlation between HCY level and concentration of folic acid and vitamin B₁₂ as well as with E-selectin and ICAM-1 was observed. Conclusion: The results point to a significant prevalence of hyperhomocysteinemia in bipolar depressed patients during an acute episode. They also corroborate the correlation between increased concentration of HCY and lower level of vitamin B₁₂ and folic acid. An unexpected finding of negative correlation of HCY level with markers of endothelial functions in such patients is discussed in view of current concepts of the role of HCY in various conditions.

show abstract

Association between homocysteine and endothelial dysfunction markers in stroke disease

Abstract: We found evidence of an increase in markers of endothelial dysfunction following acute ischaemic stroke but this had no relationship with total plasma homocysteine concentrations.

Cited by 18 publications

References 15 publications

Hyperhomocysteinemia, low vitamin B12, and low folic acid: Are risk factors of cerebral vascular thrombosis in northwest Iran?

Hyperhomocysteinemia, low vitamin B12, and low folic acid: Are risk factors of cerebral vascular thrombosis in northwest Iran?

Protection of DDAH2 Overexpression Against Homocysteine-Induced Impairments of DDAH/ADMA/NOS/NO Pathway in Endothelial Cells

Hyperhomocysteinemia in Bipolar Depression: Clinical and Biochemical Correlates

Contact Info

Product

Resources

About