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Connective tissue growth factor expression and Smad signaling during mouse heart development and myocardial infarction
Author(s) -
Chuva De Sousa Lopes Susana M.,
Feijen Alie,
Korving Jeroen,
Korchynskyi Olexander,
Larsson Jonas,
Karlsson Stefan,
Ten Dijke Peter,
Lyons Karen M.,
Goldschmeding Roel,
Doevendans Pieter,
Mummery Christine L.
Publication year - 2004
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20162
Subject(s) - ctgf , biology , connective tissue , growth factor , smad , heart development , transforming growth factor , angiogenesis , medicine , microbiology and biotechnology , myocardial infarction , endocrinology , bone morphogenetic protein , cancer research , receptor , gene , genetics , embryonic stem cell
Connective tissue growth factor (CTGF) is reported to be a target gene of transforming growth factor β (TGFβ) and bone morphogenetic protein (BMP) in vitro. Its physiological role in angiogenesis and skeletogenesis during mouse development has been described recently. Here, we have mapped expression of CTGF mRNA during mouse heart development, postnatal adult life, and after experimental myocardial infarction. Furthermore, we investigated the relationship between CTGF and the BMP/TGFβ signaling pathway in particular during heart development in mutant mice. Postnatally, CTGF expression in the heart became restricted to the atrium. Strikingly, 1 week after myocardial infarction, when myocytes have disappeared from the infarct zone, CTGF and TGFβ expression as well as activated forms of TGFβ but not BMP, Smad effector proteins are colocalized exclusively in the fibroblasts of the scar tissue, suggesting possible cooperation between CTGF and TGFβ during the pathological fibrotic response. Developmental Dynamics 231:542–550, 2004. © 2004 Wiley‐Liss, Inc.