CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis

Iyer, Swati, Chhabra, Yash, Harvey, Tracey J., Wang, Richard, Chiu, Han Sheng, Smith, A. G., Thomas, Walter G., Pennisi, David J. and Piper, Michael (2017) CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis. Journal of Molecular Histology, 48 1: 53-61. doi:10.1007/s10735-016-9702-3


Author Iyer, Swati
Chhabra, Yash
Harvey, Tracey J.
Wang, Richard
Chiu, Han Sheng
Smith, A. G.
Thomas, Walter G.
Pennisi, David J.
Piper, Michael
Title CRIM1 is necessary for coronary vascular endothelial cell development and homeostasis
Journal name Journal of Molecular Histology   Check publisher's open access policy
ISSN 1567-2379
1567-2387
Publication date 2017-02-01
Year available 2016
Sub-type Article (original research)
DOI 10.1007/s10735-016-9702-3
Open Access Status Not yet assessed
Volume 48
Issue 1
Start page 53
End page 61
Total pages 9
Place of publication Dordrecht, Netherlands
Publisher Springer
Language eng
Subject 2722 Histology
1314 Physiology
1307 Cell Biology
Abstract Endothelial cells form a critical component of the coronary vasculature, yet the factors regulating their development remain poorly defined. Here we reveal a novel role for the transmembrane protein CRIM1 in mediating cardiac endothelial cell development. In the absence of Crim1 in vivo, the coronary vasculature is malformed, the number of endothelial cells reduced, and the canonical BMP pathway dysregulated. Moreover, we reveal that CRIM1 can bind IGFs, and regulate IGF signalling within endothelial cells. Finally, loss of CRIM1 from human cardiac endothelial cells results in misregulation of endothelial genes, predicted by pathway analysis to be involved in an increased inflammatory response and cytolysis, reminiscent of endothelial cell dysfunction in cardiovascular disease pathogenesis. Collectively, these findings implicate CRIM1 in endothelial cell development and homeostasis in the coronary vasculature.
Formatted abstract
Endothelial cells form a critical component of the coronary vasculature, yet the factors regulating their development remain poorly defined. Here we reveal a novel role for the transmembrane protein CRIM1 in mediating cardiac endothelial cell development. In the absence of Crim1 in vivo, the coronary vasculature is malformed, the number of endothelial cells reduced, and the canonical BMP pathway dysregulated. Moreover, we reveal that CRIM1 can bind IGFs, and regulate IGF signalling within endothelial cells. Finally, loss of CRIM1 from human cardiac endothelial cells results in misregulation of endothelial genes, predicted by pathway analysis to be involved in an increased inflammatory response and cytolysis, reminiscent of endothelial cell dysfunction in cardiovascular disease pathogenesis. Collectively, these findings implicate CRIM1 in endothelial cell development and homeostasis in the coronary vasculature.
Keyword Crim 1
Endothelial cells
Heart
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID 1057751
DP160100368
FT120100170
Institutional Status UQ
Additional Notes Published online 1 November 2016

 
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Created: Tue, 08 Nov 2016, 22:19:01 EST by Dr Michael Piper on behalf of School of Biomedical Sciences