TY  - JOUR
A1  - Yu, Wei
A1  - Ma, Xueyan
A1  - Xu, Jinjin
A1  - Heumüller, Andreas
A1  - Fei, Zhaoliang
A1  - Feng, Xue
A1  - Wang, Xiaodong
A1  - Liu, Kuo
A1  - Li, Jinhui
A1  - Cui, Guizhong
A1  - Peng, Guangdun
A1  - Ji, Hongbin
A1  - Li, Jinsong
A1  - Jing, Naihe
A1  - Song, Hai
A1  - Lin, Zhiqiang
A1  - Zhao, Yun
A1  - Wang, Zuoyun
A1  - Zhou, Bin
A1  - Zhang, Lei
T1  - VGLL4 plays a critical role in heart valve development and homeostasis
T2  - PLoS Genetics
N2  - Heart valve disease is a major clinical problem worldwide. Cardiac valve development and homeostasis need to be precisely controlled. Hippo signaling is essential for organ development and tissue homeostasis, while its role in valve formation and morphology maintenance remains unknown. VGLL4 is a transcription cofactor in vertebrates and we found it was mainly expressed in valve interstitial cells at the post-EMT stage and was maintained till the adult stage. Tissue specific knockout of VGLL4 in different cell lineages revealed that only loss of VGLL4 in endothelial cell lineage led to valve malformation with expanded expression of YAP targets. We further semi-knockout YAP in VGLL4 ablated hearts, and found hyper proliferation of arterial valve interstitial cells was significantly constrained. These findings suggest that VGLL4 is important for valve development and manipulation of Hippo components would be a potential therapy for preventing the progression of congenital valve disease.
KW  - Heart
KW  - Endothelial cells
KW  - Apoptosis
KW  - Aortic valve
KW  - Alleles
KW  - Homeostasis
KW  - Cell proliferation
KW  - Immunostaining
Y1  - 2019
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/49186
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-491864
SN  - 1553-7404
SN  - 1553-7390
N1  - Copyright: © 2019 Yu 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  - 15
IS  - (2): e1007977
SP  - 1
EP  - 19
PB  - Public Library of Science
CY  - San Francisco, Calif.
ER  -