Angiotensin II type 1 receptor-associated protein regulates carotid intimal hyperplasia through controlling apoptosis of vascular smooth muscle cells
- Department of Endovascular Surgery, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, 450000 (China)
Highlights: • ATRAP as a negative regulator of AT1 receptor plays an inhibitory role in VSMCs proliferation both in vitro and in vivo. • ATRAP triggers the marked apoptosis of VSMCs in balloon-injuried carotid arteries and depresses neointimal formation. • ATRAP induces VSMCs apoptosis through the influence of the PI3K/Akt signaling pathway. Intimal hyperplasia is the main cause of restenosis after carotid artery injury, and the underlying mechanism involves the proliferation and migration of vascular smooth muscle cells (VSMCs). Angiotensin II Type 1 Receptor-Associated Protein (ATRAP) has been reported to withstand intimal hyperplasia by inhibiting VSMCs proliferation and migration; however, whether the beneficial effect of ATRAP associates with VSMCs apoptosis remains unclarified. We demonstrated that the adenoviral-mediated overexpression of ATRAP induced VSMC apoptosis, alleviating the balloon injury-induced neointima formation in rats. Under the condition of Angiotensin-II stimulation, ATRAP overexpression induced the apoptosis of rat VSMCs by depressing the PI3K-Akt signaling; whereas up-regulation of Akt by PTEN inhibitor abolished the apoptotic death. Thus, ATRAP regulates carotid intimal hyperplasia through controlling the PI3K-Akt signal-mediated VSMCs apoptosis.
- OSTI ID:
- 23134385
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 495, Issue 2; Other Information: Copyright (c) 2017 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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