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Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model
Published on: August 29, 2012
Soluble endoglin modulates aberrant cerebral vascular remodeling
Yongmei Chen1, Qi Hao, Helen Kim
1Department of Anesthesia and Perioperative Care, Center for Cerebrovascular Research, University of California San Francisco, San Francisco, CA, USA.
Annals of Neurology
|August 12, 2009
Summary
Elevated soluble endoglin (sEng) levels are found in brain arteriovenous malformations (AVMs), suggesting a role in their development. This finding may lead to new therapeutic targets for AVMs.
Area of Science:
- Neuroscience
- Vascular Biology
- Biochemistry
Background:
- Brain arteriovenous malformations (AVMs) are a significant cause of neurological disability in young adults.
- The underlying mechanisms of AVM development are not well understood.
- Soluble endoglin (sEng) is implicated in endothelial dysfunction and preeclampsia.
Purpose of the Study:
- To investigate if sEng is elevated in brain AVM tissues compared to epilepsy tissues.
- To determine if sEng overexpression in the mouse brain induces vascular dysplasia and downstream signaling changes.
Main Methods:
- Western blot and ELISA were used to quantify sEng levels in surgical specimens.
- Immunohistochemistry and gelatin zymography assessed vascular dysplasia, matrix metalloproteinase (MMP) activity, and oxidative stress in mouse models.
Main Results:
- Brain AVMs exhibited significantly higher sEng levels than control tissues (p=0.04).
- sEng gene transfer in mice induced abnormal vascular structures, increased MMP activity (MMP-9 and MMP-2), and elevated oxidants.
- These changes suggest MMPs and oxidative radicals mediate sEng-induced vascular remodeling.
Conclusions:
- Elevated sEng levels may contribute to the pathogenesis of sporadic brain AVMs.
- These findings offer potential new therapeutic targets for brain AVM treatment.
