Abstract:
:Atherosclerotic plaque rupture is the main cause of acute coronary syndrome (ACS). Angiotensin II (Ang II) and macrophage apoptosis are involved in the pathogenesis of atherosclerosis. However, the underlying mechanisms remain unclear. We aimed to address the role of monocyte chemotactic protein-induced protein 1 (MCPIP1) in Ang II-induced macrophage apoptosis and vulnerable plaque formation. In mouse peritoneal macrophages, Ang II promoted endoplasmic reticulum (ER) stress-dependent macrophage apoptosis. Ang II markedly upregulated the expression of MCPIP1 via activating p38 mitogen-activated protein kinase (p38 MAPK). Treatment with MCPIP1 shRNA downregulated ER stress-related proteins and decreased macrophage apoptosis induced by Ang II. Ang II also activated the AMP-activated protein kinase (AMPK) signaling in macrophages. Inhibition of AMPK reduced macrophage apoptosis by inhibiting the p38 MAPK/MCPIP1/ER stress pathway. Furthermore, blocking the Ang II type 1 receptor (AT1R) with losartan effectively inhibited Ang II-induced macrophage apoptosis and AMPK/p38 MAPK/MCPIP1/ER pathway activation. In the atherosclerotic vulnerable plaque model in mice, losartan inhibited the progression of atherosclerosis and transformed vulnerable plaque into a more stable phenotype. Moreover, losartan markedly decreased the number of CD68+TUNEL+, CD68+MCPIP1+, CD68+p-eIF2α+ and CD68+CHOP+ cells in the lesion area. Taken together, Ang II promotes macrophage apoptosis via the AMPK/p38 MAPK/MCPIP1/ER stress pathway in macrophages via its receptor AT1R, which may contribute to vulnerable plaque formation. Our study clarifies a novel regulatory role of MCPIP1 in Ang II-induced macrophage apoptosis and plaque instability, providing a potential therapeutic target for prevention of ACS.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Shu S,Zhang Y,Li W,Wang L,Wu Y,Yuan Z,Zhou Jdoi
10.1016/j.bbrc.2019.05.145subject
Has Abstractpub_date
2019-07-23 00:00:00pages
378-385issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(19)31041-1journal_volume
515pub_type
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