| Literature DB >> 33643791 |
Aline Zbinden1,2, Shannon L Layland1,2, Max Urbanczyk1,2, Daniel A Carvajal Berrio1,2,3, Julia Marzi1,2,3,4, Monika Zauner2, Anne Hammerschmidt2, Eva M Brauchle2,3,4, Katrin Sudrow5,6, Simon Fink4, Markus Templin4, Simone Liebscher1,2, Gerd Klein7, Arjun Deb8,9,10,11,12, Garry P Duffy13, Gay M Crooks9,11,14, Johannes A Eble15, Hanna K A Mikkola8,9,10,11, Ali Nsair9,12, Martina Seifert5,6,16, Katja Schenke-Layland1,2,3,4,12.
Abstract
Ischemia impacts multiple organ systems and is the major cause of morbidity and mortality in the developed world. Ischemia disrupts tissue homeostasis, driving cell death, and damages tissue structure integrity. Strategies to heal organs, like the infarcted heart, or to replace cells, as done in pancreatic islet β-cell transplantations, are often hindered by ischemic conditions. Here, it is discovered that the basement membrane glycoprotein nidogen-1 attenuates the apoptotic effect of hypoxia in cardiomyocytes and pancreatic β-cells via the αvβ3 integrin and beneficially modulates immune responses in vitro. It is shown that nidogen-1 significantly increases heart function and angiogenesis, while reducing fibrosis, in a mouse postmyocardial infarction model. These results demonstrate the protective and regenerative potential of nidogen-1 in ischemic conditions.Entities:
Keywords: diabetes; ischemia; myocardial infarction; nidogen‐1; pancreatic β‐cells
Year: 2020 PMID： 33643791 PMCID： PMC7887579 DOI： 10.1002/advs.202002500
Source DB: PubMed Journal: Adv Sci (Weinh) ISSN： 2198-3844 Impact factor: 16.806