The Pericyte of the Pancreatic Islet Regulates Capillary Diameter and Local Blood Flow

被引:157
作者
Almaca, Joana [1 ]
Weitz, Jonathan [1 ,2 ]
Rodriguez-Diaz, Rayner [1 ]
Pereira, Elizabeth [1 ,3 ]
Caicedo, Alejandro [1 ,3 ,4 ]
机构
[1] Univ Miami, Miller Sch Med, Dept Med, Div Endocrinol Diabet & Metab, Miami, FL 33136 USA
[2] Univ Miami, Miller Sch Med, Mol Cell & Dev Biol Program, Miami, FL 33136 USA
[3] Univ Miami, Miller Sch Med, Dept Physiol & Biophys, Miami, FL 33136 USA
[4] Univ Miami, Miller Sch Med, Program Neurosci, Miami, FL 33136 USA
关键词
DIABETIC GK RATS; PROTEIN-KINASE-I; INSULIN-SECRETION; NITRIC-OXIDE; BETA-CELLS; ENDOCRINE PANCREAS; SIGNALING CASCADE; ANGIOTENSIN-II; GAP-JUNCTIONS; ATP RELEASE;
D O I
10.1016/j.cmet.2018.02.016
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Efficient insulin secretion requires a well-functioning pancreatic islet microvasculature. The dense network of islet capillaries includes the islet pericyte, a cell that has barely been studied. Here we show that islet pericytes help control local blood flow by adjusting islet capillary diameter. Islet pericytes cover 40% of the microvasculature, are contractile, and are innervated by sympathetic axons. Sympathetic adrenergic input increases pericyte activity and reduces capillary diameter and local blood flow. By contrast, activating beta cells by increasing glucose concentration inhibits pericytes, dilates islet capillaries, and increases local blood flow. These effects on pericytes are mediated by endogenous adenosine, which is likely derived from ATP co-released with insulin. Pericyte coverage of islet capillaries drops drastically in type 2 diabetes, suggesting that, under diabetic conditions, islets lose this mechanism to control their own blood supply. This may lead to inadequate insulin release into the circulation, further deteriorating glycemic control.
引用
收藏
页码:630 / +
页数:19
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