TY  - JOUR
A1  - Lu, Shun
A1  - Liu, Shuya
A1  - Wietelmann, Astrid
A1  - Kojonazarov, Baktybek
A1  - Atzberger, Ann
A1  - Tang, Cong
A1  - Schermuly, Ralph Theo
A1  - Gröne, Hermann-Josef
A1  - Offermanns, Stefan
T1  - Developmental vascular remodeling defects and postnatal kidney failure in mice lacking Gpr116 (Adgrf5) and Eltd1 (Adgrl4)
T2  - PLoS one
N2  - GPR116 (ADGRF5) and ELTD1 (ADGRL4) belong to different subfamilies of the adhesion G-protein-coupled receptor group but are both expressed in endothelial cells. We therefore analyzed their functions in mice lacking these receptors. While loss of GPR116 or ELTD1 alone had no obvious effect on cardiovascular or kidney function, mice lacking both, GPR116 and ELTD1, showed malformations of the aortic arch arteries and the cardiac outflow tract leading to perinatal lethality in about 50% of the mutants. In addition to cardiovascular malformations, surviving mice developed renal thrombotic microangiopathy as well as hemolysis and splenomegaly, and their lifespan was significantly reduced. Loss of GPR116 and ELTD1 specifically in endothelial cells or neural crest-derived cells did not recapitulate any of the phenotypes observed in GPR116-ELTD1 double deficient mice, indicating that loss of GPR116 and ELTD1 expressed by other cells accounts for the observed cardiovascular and renal defects.
Y1  - 2017
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/43962
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-439625
SN  - 1932-6203
N1  - Copyright: © 2017 Lu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
VL  - 12
IS  - (8): e0183166
SP  - 1
EP  - 23
PB  - PLoS
CY  - Lawrence, Kan.
ER  -