1986
DOI: 10.1172/jci112519
|View full text |Cite
|
Sign up to set email alerts
|

Activation of endogenous factor V by a homocysteine-induced vascular endothelial cell activator.

Abstract: Vascular endothelium possesses multiple procoagulant properties, including synthesis and expression of Factor V. We studied the effects of homocysteine on the regulation of endothelial cell Factor V activity. Elevated levels of homocysteine are associated with the congenital thrombotic disorder homocystinuria. Treatment of cultured endothelial cells with 0.5-10 mM homocysteine had no effect on cell morphology, but did increase Factor V activity and prothrombin activation by Factor Xa. A radioimmunoassay for en… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

7
146
0
11

Year Published

1997
1997
2012
2012

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 372 publications
(164 citation statements)
references
References 46 publications
7
146
0
11
Order By: Relevance
“…28,29) Although the exact mechanisms of homocysteine leading to atherosclerosis have not been fully elucidated, experimental studies have demonstrated that high homocysteine levels lead to endothelial dysfunction and thrombus formation. [30][31][32][33][34][35] These mechanisms of homocysteine may be related to SVG disease after CABG.…”
Section: Discussionmentioning
confidence: 99%
“…28,29) Although the exact mechanisms of homocysteine leading to atherosclerosis have not been fully elucidated, experimental studies have demonstrated that high homocysteine levels lead to endothelial dysfunction and thrombus formation. [30][31][32][33][34][35] These mechanisms of homocysteine may be related to SVG disease after CABG.…”
Section: Discussionmentioning
confidence: 99%
“…49,50 Although the exact mechanism(s) by which hyperhomocysteinaemia causes thrombosis are unknown, it has been shown to be directly toxic to endothelial cells, impair thrombomodulin expression, directly activate factor V and inhibit protein C activation. [51][52][53][54] There are many causes for hyperhomocysteinaemia including vitamin deficiencies (pyridoxine, folic acid, vitamin B12) chronic illnesses (chronic renal failure, diabetes, cancer), drugs (methotrexate, anti-epileptic agents), as well as the rare enzyme deficiencies mentioned above. In 1988 however a mild form of hyperhomocysteinaemia was identified due to a thermolabile variant of MTHFR.…”
Section: Hyperhomocysteinaemiamentioning
confidence: 99%
“…Also, work by several authors suggests that lipid peroxidation, as a result of elevated homocysteine levels, may then cause decreased expression of the enzyme nitric oxide synthase and directly degrade NO (Heinecke et al 1987;Chin et al 1992;Liao et al 1995;Blom et al 1995;Domagala et al 1997) Thrombotic mechanisms Coagulant pathway. Elevated homocysteine levels in vitro have been shown to upset the balance of certain factors within the coagulation pathway, including activation of factors V and X11 (Ratnoff, 1968;Rodgers & Kane, 1986).…”
Section: Atherosclerotic Mechanismsmentioning
confidence: 99%