NDLI: Early fibroblast progenitor cell migration to the AngII-exposed myocardium is not CXCL12 or CCL2 dependent as previously thought.

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Early fibroblast progenitor cell migration to the AngII-exposed myocardium is not CXCL12 or CCL2 dependent as previously thought.

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Early fibroblast progenitor cell migration to the AngII-exposed myocardium is not CXCL12 or CCL2 dependent as previously thought.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Falkenham, Alec Sopel, Mryanda Rosin, Nicole Lee, Tim D. G. Issekutz, Thomas Légaré, Jean-Francois
Description	Country affiliation: Canada Author Affiliation: Falkenham A ( Department of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada.)
Abstract	Fibroblast progenitor cells (fibrocytes) are important to the development of myocardial fibrosis and are suggested to migrate to the heart via CXCL12 and chemokine ligand (CCL) 2. We hypothesized that if these chemokines are recruiting fibrocytes, disrupting their signaling will reduce early (3-day) fibrocyte infiltration and, consequently, fibrosis in the myocardium. C57/Bl6 and CCR2(-/-) mice were infused with saline or angiotensin (Ang) II, with or without CXC receptor 4 blockade (AMD3100). Hearts were assessed for chemokine up-regulation, immunofluorescence, and histological features. AngII caused early myocardial up-regulation of CXCL12 and CCL2, which corresponded to significant myocardial infiltration and fibrosis compared with controls. Animals receiving AMD3100 and/or with the genotype CCR2(-/-) failed to demonstrate reductions in infiltrate or fibrosis after 3 days of AngII, and AngII + AMD3100 animals showed exacerbated fibrocyte infiltration and fibrosis compared with AngII alone. CCR2(-/-) mice demonstrated significant reductions in myocardial fibrosis relative to wild type, but this was after 28 days of AngII infusion and was the result of reduced infiltrating cell proliferation. An alternative CCR2 ligand, CCL12, was found to be increasing infiltrating cell proliferation in the heart after AngII infusion, which we confirmed in vitro. In conclusion, early fibrocyte recruitment cannot be inhibited through modulating CXCL12 or CCL2, as previously thought. Ablating CCR2 signaling did confer myocardial fibrosis reductions, but these benefits were not observed until much later and were likely the result of modulated proliferation through ablating the CCL12-CCR2 interaction.
File Format	HTM / HTML
ISSN	00029440
Issue Number	2
Volume Number	183
e-ISSN	15252191
Journal	The American Journal of Pathology
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2013-08-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Research Support, Non-u.s. Gov't Cell Proliferation Male Antagonists & Inhibitors Journal Article Stem Cells Chemokine Cxcl12 Fibroblasts Physiology Receptors, Cxcr4 Mice, Inbred C57bl Heterocyclic Compounds Discipline Pathology Pharmacology Metabolism Drug Effects Pathology Animals Vasoconstrictor Agents Fibrosis Up-regulation Myocardium Mice Chemokine Ccl2 Angiotensin Ii Cell Movement
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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