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TGFbeta2 activation status during cardiac morphogenesis.

K M McCormick1

  • 1Department of Physical Therapy, Exercise and Nutrition Sciences, University at Buffalo, State University of New York, Buffalo, New York 14214, USA. kmmccorm@buffalo.edu

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|August 17, 2001
PubMed
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Transforming growth factor beta 2 (TGFbeta2) in embryonic chicken hearts is mostly latent, with active TGFbeta2 levels decreasing during development. This suggests TGFbeta2 activation is a regulated process crucial for cardiac morphogenesis.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Transforming growth factor beta (TGFbeta) is secreted in an inactive form, but its in vivo activation status is poorly understood.
  • Investigating TGFbeta activation is crucial for understanding its biological roles in development and disease.

Purpose of the Study:

  • To examine the in vivo expression and activation status of TGFbeta2 during embryonic chicken heart development.
  • To determine how active and total TGFbeta2 levels change throughout cardiac morphogenesis.

Main Methods:

  • Enzyme-linked immunoassay to quantify active and total TGFbeta2 in embryonic chicken hearts (stages 10-24).
  • Immunostaining for active TGFbeta2 distribution in heart sections before and after acid treatment.

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Main Results:

  • Total TGFbeta2 increased significantly (16-fold) during development, while active TGFbeta2 remained relatively constant.
  • The proportion of active TGFbeta2 decreased from 70% to 7% from early to late embryonic stages.
  • Active TGFbeta2 was detected in specific heart tissues, with increased staining after acid treatment indicating latent TGFbeta2.

Conclusions:

  • A significant portion of TGFbeta2 exists in a latent form in the embryonic chicken heart.
  • TGFbeta2 activation is a developmentally regulated process in the chick heart.
  • TGFbeta2 activation is critical for regulating its function during cardiac morphogenesis.