Crim1 has cell-autonomous and paracrine roles during embryonic heart development

Iyer, Swati, Chou, Fang Yu, Wang, Richard, Chiu, Han Sheng, Raju, Vinay K. Sundar, Little, Melissa H., Thomas, Walter G., Piper, Michael and Pennisi, David J. (2016) Crim1 has cell-autonomous and paracrine roles during embryonic heart development. Scientific Reports, 6 19832 .1-19832 .15. doi:10.1038/srep19832

Author Iyer, Swati
Chou, Fang Yu
Wang, Richard
Chiu, Han Sheng
Raju, Vinay K. Sundar
Little, Melissa H.
Thomas, Walter G.
Piper, Michael
Pennisi, David J.
Title Crim1 has cell-autonomous and paracrine roles during embryonic heart development
Journal name Scientific Reports   Check publisher's open access policy
ISSN 2045-2322
Publication date 2016-01-29
Sub-type Article (original research)
DOI 10.1038/srep19832
Open Access Status DOI
Volume 6
Start page 19832 .1
End page 19832 .15
Total pages 15
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Collection year 2017
Language eng
Formatted abstract
The epicardium has a critical role during embryonic development, contributing epicardium-derived lineages to the heart, as well as providing regulatory and trophic signals necessary for myocardial development. Crim1 is a unique trans-membrane protein expressed by epicardial and epicardiallyderived cells but its role in cardiogenesis is unknown. Using knockout mouse models, we observe that loss of Crim1 leads to congenital heart defects including epicardial defects and hypoplastic ventricular compact myocardium. Epicardium-restricted deletion of Crim1 results in increased epithelial-tomesenchymal transition and invasion of the myocardium in vivo, and an increased migration of primary epicardial cells. Furthermore, Crim1 appears to be necessary for the proliferation of epicardiumderived cells (EPDCs) and for their subsequent differentiation into cardiac fibroblasts. It is also required for normal levels of cardiomyocyte proliferation and apoptosis, consistent with a role in regulating epicardium-derived trophic factors that act on the myocardium. Mechanistically, Crim1 may also modulate key developmentally expressed growth factors such as TGFβs, as changes in the downstream effectors phospho-SMAD2 and phospho-ERK1/2 are observed in the absence of Crim1. Collectively, our data demonstrates that Crim1 is essential for cell-autonomous and paracrine aspects of heart development.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

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Created: Thu, 04 Feb 2016, 12:26:34 EST by Dr Michael Piper on behalf of School of Biomedical Sciences