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Endothelial TMEM16F lipid scramblase regulates angiogenesis
Ke Zoe Shan1, Trieu Le1,2, Pengfei Liang1
1Department of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.
Biorxiv : the Preprint Server for Biology
|August 30, 2023
Summary
Endothelial TMEM16F regulates angiogenesis by impacting VE-cadherin and Src kinase signaling. TMEM16F deficiency impairs blood vessel development in mice and human cells.
Area of Science:
- Cell Biology
- Molecular Biology
- Physiology
Background:
- TMEM16 Ca2+-activated lipid scramblases (CaLSase) are crucial for membrane dynamics.
- TMEM16F's role in endothelial biology and angiogenesis is not well understood.
Approach:
- Investigated TMEM16F function in endothelial cells using in vitro and in vivo models.
- Utilized TMEM16F deficient mice and siRNA knockdown in human umbilical vein endothelial cells.
- Analyzed the impact on angiogenesis, VE-cadherin expression, and Src kinase phosphorylation.
Key Points:
- Endothelial TMEM16F is essential for regulating angiogenesis.
- TMEM16F deficiency impairs retinal angiogenesis in mice.
- TMEM16F knockdown compromises in vitro angiogenesis and affects VE-cadherin and Src kinase signaling.
Conclusions:
- TMEM16F plays a novel role in regulating angiogenesis through intracellular signaling pathways.
- TMEM16F influences angiogenesis by modulating VE-cadherin phosphorylation and expression via Src kinase.
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