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Connective tissue growth factor expression and Smad signaling during mouse heart development and myocardial

Susana M Chuva de Sousa Lopes1, Alie Feijen, Jeroen Korving

  • 1Hubrecht Laboratory, Netherlands Institute of Developmental Biology, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|September 18, 2004
PubMed

Insights

Connective tissue growth factor (CTGF) is expressed in the adult mouse heart and its expression increases after myocardial infarction. CTGF and transforming growth factor beta (TGFbeta) cooperate in fibroblasts during the fibrotic response.

Area of Science:

  • Cardiovascular biology
  • Developmental biology
  • Molecular signaling

Background:

  • Connective tissue growth factor (CTGF) is a downstream target of transforming growth factor beta (TGFbeta) and bone morphogenetic protein (BMP) signaling in vitro.
  • Recent studies have elucidated CTGF's roles in angiogenesis and skeletogenesis during mouse development.

Purpose of the Study:

  • To map CTGF mRNA expression during mouse heart development, adulthood, and post-myocardial infarction.
  • To investigate the relationship between CTGF and the BMP/TGFbeta signaling pathway, particularly during heart development in mutant mice.

Main Methods:

  • In situ hybridization to detect CTGF mRNA expression.
  • Analysis of mutant mice to study signaling pathways.
  • Immunohistochemistry to examine protein localization and activation states.

Main Results:

  • Postnatally, CTGF expression in the heart localized to the atrium.
  • Following myocardial infarction, CTGF and TGFbeta, along with activated TGFbeta, were found exclusively in fibroblasts within the scar tissue.
  • Bone morphogenetic protein (BMP) and Smad effector proteins were not co-localized in the infarct zone fibroblasts.

Conclusions:

  • CTGF plays a role in the adult mouse heart, with altered expression patterns post-myocardial infarction.
  • CTGF and TGFbeta signaling likely cooperate in cardiac fibroblasts during the pathological fibrotic response to injury.

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