二肽基肽酶4的脱落由金属蛋白酶介导，并在人脂肪细胞和平滑肌细胞中由缺氧上调。
Shedding of dipeptidyl peptidase 4 is mediated by metalloproteases and up-regulated by hypoxia in human adipocytes and smooth muscle cells.
作者信息
Röhrborn Diana, Eckel Jürgen, Sell Henrike
机构信息
Paul-Langerhans-Group for Integrative Physiology, German Diabetes Center, Düsseldorf, Germany.
Paul-Langerhans-Group for Integrative Physiology, German Diabetes Center, Düsseldorf, Germany; German Center for Diabetes Research (DZD e.V.), Düsseldorf, Germany.
出版信息
FEBS Lett. 2014 Nov 3;588(21):3870-7. doi: 10.1016/j.febslet.2014.08.029. Epub 2014 Sep 12.
Dipeptidyl peptidase 4 is an important drug target for diabetes and a novel adipokine. However, it is unknown how soluble DPP4 (sDPP4) is cleaved from the cell membrane and released into the circulation. We show here that MMP1, MMP2 and MMP14 are involved in DPP4 shedding from human vascular smooth muscle cells (SMC) and MMP9 from adipocytes. Hypoxia increased DPP4 shedding from SMC which is associated with increased mRNA expression of MMP1. Our data suggest that constitutive as well as hypoxia-induced DPP4 shedding occurs due to a complex interplay between different MMPs in cell type-specific manner.
二肽基肽酶4是糖尿病的重要药物靶点及一种新型脂肪因子。然而，尚不清楚可溶性二肽基肽酶4（sDPP4）是如何从细胞膜上裂解并释放到循环系统中的。我们在此表明，基质金属蛋白酶1（MMP1）、基质金属蛋白酶2（MMP2）和基质金属蛋白酶14（MMP14）参与了人血管平滑肌细胞（SMC）中二肽基肽酶4的脱落过程，而脂肪细胞中的基质金属蛋白酶9（MMP9）参与其中。缺氧增加了SMC中二肽基肽酶4的脱落，这与MMP1的mRNA表达增加有关。我们的数据表明，组成性以及缺氧诱导的二肽基肽酶4脱落是由于不同基质金属蛋白酶之间以细胞类型特异性方式进行复杂相互作用而发生的。
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