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CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42

Cell death & disease, 2021-04, Vol.12 (4), p.355-355, Article 355 [Peer Reviewed Journal]

The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-021-03623-w ;PMID: 33824277

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Title:
CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42
Author: Liu, Dan ; Tian, Xiaoxiang ; Liu, Yanxia ; Song, Haixu ; Cheng, Xiaoli ; Zhang, Xiaolin ; Yan, Chenghui ; Han, Yaling
Subjects: Angiotensin ; Angiotensin II ; Animals ; Cardiac function ; cdc42 GTP-Binding Protein - metabolism ; Cdc42 protein ; Cell division ; Cell migration ; Cells, Cultured ; Collagen ; Disease Models, Animal ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Fibrosis ; Genotype & phenotype ; Heart ; Heart attacks ; Hypoxia ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial infarction ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardium - metabolism ; Myofibroblasts - metabolism ; Phenotype ; Phenotypes ; Proteins ; Repressor Proteins - metabolism
Is Part Of: Cell death & disease, 2021-04, Vol.12 (4), p.355-355, Article 355
Description: Phenotype switching of cardiac fibroblasts into myofibroblasts plays important role in cardiac fibrosis following myocardial infarction (MI). Cellular repressor of E1A-stimulated genes (CREG) protects against vascular and cardiac remodeling induced by angiotensin-II. However, the effects and mechanisms of CREG on phenotype switching of cardiac fibroblasts after MI are unknown. This study aimed to investigate the role of CREG on the phenotype switching of cardiac fibroblasts following MI and its mechanism. Our findings demonstrated that, compared with littermate control mice, cardiac function was deteriorated in CREG mice on day 14 post-MI. Fibrosis size, αSMA, and collagen-1 expressions were increased in the border regions of CREG mice on day 14 post-MI. Conversely, exogenous CREG protein significantly improved cardiac function, inhibited fibrosis, and reduced the expressions of αSMA and collagen-1 in the border regions of C57BL/6J mice on day 14. In vitro, CREG recombinant protein inhibited αSMA and collagen-1 expression and blocked the hypoxia-induced proliferation and migration of cardiac fibroblasts, which was mediated through the inhibition of cell division control protein 42 (CDC42) expression. Our findings could help in establishing new strategies based on the clarification of the role of the key molecule CREG in phenotype switching of cardiac fibroblasts following MI.
Publisher: England: Springer Nature B.V
Language: English
Identifier: ISSN: 2041-4889
EISSN: 2041-4889
DOI: 10.1038/s41419-021-03623-w
PMID: 33824277
Source: Nature Open Access
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PubMed Central
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ProQuest Central
DOAJ Directory of Open Access Journals

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CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42

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