Literature DB >> 25217834

Shedding of dipeptidyl peptidase 4 is mediated by metalloproteases and up-regulated by hypoxia in human adipocytes and smooth muscle cells.

Diana Röhrborn1, Jürgen Eckel2, Henrike Sell3.   

Abstract

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.
Copyright © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  CD26/DPP4; Hypoxia; Non-classical secretion; Protease

Mesh:

Substances:

Year:  2014        PMID: 25217834     DOI: 10.1016/j.febslet.2014.08.029

Source DB:  PubMed          Journal:  FEBS Lett        ISSN: 0014-5793            Impact factor:   4.124


  53 in total

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Authors:  Gilberto Vargas-Alarcón; María Del Carmen González-Salazar; Christian Vázquez-Vázquez; Adrián Hernández-Díaz Couder; Fausto Sánchez-Muñoz; Juan Reyes-Barrera; Sergio A Criales-Vera; Marco Sánchez-Guerra; Citlalli Osorio-Yáñez; Rosalinda Posadas-Sánchez
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