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Regulation of IGFBP secretion and modulation of cell growth in MDBK cells

W S Cohick1, D R Clemmons

  • 1University of North Carolina School of Medicine, Division of Endocrinology, Chapel Hill 27599-7170.

Growth Regulation
|March 1, 1993
PubMed

Insights

Insulin-like growth factor binding proteins (IGFBPs) influence epithelial cell growth. IGFBP-3 expression in Madin-Darby bovine kidney cells altered morphology and IGF-I responsiveness, suggesting a role in cell function.

Area of Science:

  • Cell Biology
  • Endocrinology
  • Molecular Biology

Background:

  • Insulin-like growth factor binding proteins (IGFBPs) are crucial regulators of insulin-like growth factor (IGF) action.
  • Epithelial cells respond to IGFs, but the role of specific IGFBPs in modulating this response is not fully understood.

Purpose of the Study:

  • To investigate how IGF binding proteins (IGFBPs) affect the growth and IGF-I responsiveness of Madin-Darby bovine kidney (MDBK) cells.
  • To characterize the changes in IGFBP expression in response to stimuli and their impact on cell behavior.

Main Methods:

  • MDBK cells were cultured and treated with forskolin to alter IGFBP expression.
  • Cells were exposed to varying concentrations of IGF-I alone or in combination with exogenous IGFBP-3.
  • Transfection with IGFBP-3 cDNA was used to induce endogenous IGFBP-3 secretion and assess its effects on cell morphology and growth.

Main Results:

  • Forskolin treatment decreased IGFBP-2 and increased IGFBP-3 and IGFBP-4 abundance in MDBK cell conditioned media, correlating with mRNA changes.
  • IGF-I stimulated MDBK cell growth in a dose-dependent manner.
  • Overexpression of IGFBP-3 led to altered cell morphology and increased IGF-I responsiveness in serum-free media, despite slower growth in serum.

Conclusions:

  • IGFBP-2, -3, and -4 levels are dynamically regulated in MDBK cells by agents like forskolin.
  • IGFBP-3 can potentiate IGF-I-mediated growth and influence epithelial cell characteristics.
  • Further research is needed to elucidate the precise mechanisms by which IGFBP-3 mediates these effects.

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