Abstract
This study aimed to explore the effect of angiotensin (1–7) (Ang (1–7)) on palmitate-induced apoptosis in islet endothelial cells and the mechanism of action. MS-1 cells were treated with palmitate in the presence or absence of Ang (1–7). The percentage of apoptotic cells was determined by DNA fragmentation and flow cytometry. Reactive oxygen species (ROS) production was measured using a Reactive Oxygen Species Assay Kit. Expression of AKT, eNOS, C-Jun N-terminal kinase (JNK), and p38 was detected by western blotting. Compared with palmitate treated group, palmitate-induced apoptosis was decreased in MS-1 cells which were preincubated with Ang (1–7) (P < 0.05). Palmitate decreased the phosphorylation of AKT and eNOS, and Ang (1–7) increased the phosphorylation of these kinases (P < 0.05), with a concomitant reduction in MS-1 cells apoptosis. Ang (1–7) also inhibited the palmitate-induced ROS production and attenuated the apoptosis-related signaling molecule JNK and p38 activation (all P < 0.05). PI3K/AKT, eNOS, p38 MAPK, and JNK inhibitors blocked the antilipoapoptosis of Ang (1–7) (all P < 0.05). Our findings suggest that Ang (1–7) reduces palmitate-induced islet endothelial cells apoptosis. AKT/eNOS/NO signaling and JNK and p38 pathway are involved in the Ang (1–7)-mediated modulation of islet endothelial cells lipoapoptosis.
Highlights
Pancreatic islets have a dense capillary network
Western blot results showed that ACE2 protein level decreased significantly after exposing the cell to palmitate for 24 h (P < 0.05)
The ability of ACE2/Ang (1–7)/Mas axis to mediate lipid metabolism has been observed in a number of experimental systems
Summary
Pancreatic islets have a dense capillary network. Intraislet capillaries are lined by fenestrated endothelial cells [1]. Each β-cell is surrounded by at least one islet endothelial cell, which may provide signals for islet cell development [2] and important for adult β-cell proliferation [3]. Endothelial dysfunction was observed in Orientals with insulin resistance and prediabetic population [4], which is a potential contributor to the pathogenesis of diabetes mellitus. Approaches that improve endothelial function, such as treatment with statins, angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARB), or peroxisome proliferator-activated receptor gamma ligands (PPAR-γ), have been shown to prevent diabetes disease [5]. Maintaining survival and function of islet endothelial cells is a major goal of diabetes risk reduction
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