We have located links that may give you full text access.
ENGLISH ABSTRACT
JOURNAL ARTICLE
REVIEW
[Vascular injury by glucocorticoid; involvement of apoptosis of endothelial cells].
Clinical Calcium 2007 June
Idiopathic osteonecrosis of the femoral head (IONF) is known to be caused by tissue ischemia, which is mainly associated with high-dose glucocorticoid (GC) used for the treatments of systemic autoimmune diseases. However, precise pathological mechanisms of IONF remain unclear. We first found that hypoxia-inducible factor (HIF) -1alpha, a major transcription factor rapidly induced under hypoxic conditions, was highly expressed on endothelial cells of femoral head in patients with IONF. Transfection of HIF-1alpha induced p21-mediated arrest of cell cycle and subsequent apoptosis in endothelial cells. High dose GC also induced cell cycle arrest and apoptosis. Furthermore, there were additional effects between HIF-1alpha and high dose GC for the growth arrests and apoptosis of the cells. However, C-type natriuretic peptide (CNP) inhibited both cell cycle arrest and apoptosis of the endothelial cells in a concentration-dependent manner. There results indicate that hypoxia and high-dose GC play a pivotal role for vascular injury and that CNP could have a potential to protect the vascular injury seen in patients with IONF.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app