NDLI: Cardiomyocyte-derived CXCL12 is not involved in cardiogenesis but plays a crucial role in myocardial infarction

Content Provider	Springer Nature Link
Author	Mühlstedt, Silke Ghadge, Santhosh K. Duchene, Johan Qadri, Fatimunnisa Järve, Anne Viliavich, Larisa Popova, Elena Pohlmann, Andreas Niendorf, Thoralf Boyé, Philipp Özcelik, Cemil Bader, Michael
Copyright Year	2016
Abstract	The chemokine CXCL12/SDF-1 is crucial for heart development and affects cardiac repair processes due to its ability to attract leukocytes and stem cells to injured myocardium. However, there is a great controversy whether CXCL12 is beneficial or detrimental after myocardial infarction (MI). The divergence in the reported CXCL12 actions may be due to the cellular source and time of release of the chemokine after MI. This study was designed to evaluate the role of cardiomyocyte-derived CXCL12 for cardiogenesis and heart repair after MI. We generated two rodent models each targeting CXCL12 in only one cardiac cell type: cardiomyocyte-specific CXCL12-overexpressing transgenic (Tg) rats and CXCL12 conditional knockout (cKO) mice. Animals of both models did not show any signs of cardiac abnormalities under baseline conditions. After induction of MI, cKO mice displayed preserved cardiac function and remodeling. Moreover, fibrosis was less pronounced in the hearts of cKO mice after MI. Accordingly, CXCL12 Tg rats revealed impaired cardiac function post-MI accompanied by enhanced fibrosis. Furthermore, we observed decreased numbers of infiltrating Th1 cells in the hearts of cKO mice. Collectively, our findings demonstrate that cardiomyocyte-derived CXCL12 is not involved in cardiac development but has adverse effects on the heart after injury via promotion of inflammation and fibrosis.• CXCL12 in cardiomyocytes is not involved in cardiac development.• CXCL12 deficiency in cardiomyocytes improves outcome of myocardial infarction.• CXCL12 overexpression in cardiomyocytes worsens outcome of myocardial infarction.• CXCL12 increases fibrosis and invasion of Th1 cells in the heart after infarction.
Starting Page	1005
Ending Page	1014
Page Count	10
File Format	PDF
ISSN	09462716
Journal	Journal of Molecular Medicine
Volume Number	94
Issue Number	9
e-ISSN	14321440
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2016-06-01
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	CXCL12 Hypertrophy Myocardial infarction Fibrosis Inflammation Molecular Medicine Human Genetics Internal Medicine
Content Type	Text
Resource Type	Article
Subject	Drug Discovery Molecular Medicine Genetics (clinical)

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