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Growth hormone stimulation of the mitogen-activated protein kinase pathway is cell type specific

D W Love1, A J Whatmore, P E Clayton

  • 1Department of Internal Medicine, University of Virginia, Charlottesville 22908, USA.

Endocrinology
|April 7, 1998
PubMed

Insights

Growth hormone (GH) activates the mitogen-activated protein kinase (MAPK) pathway in mouse preadipocytes but not in human lymphocytes. This differential signaling highlights cell-specific responses to GH.

Area of Science:

  • Cellular signaling pathways
  • Hormone receptor interactions
  • Molecular endocrinology

Background:

  • The growth hormone (GH) receptor belongs to the cytokine receptor superfamily.
  • GH signaling involves Janus kinase (JAK2), signal transducers and activators of transcription (STATs), and mitogen-activated protein kinase (MAPK).
  • Previous studies showed GH activates JAK2 and STAT5 in human IM-9 lymphocytes, but not STAT1 or STAT3.

Purpose of the Study:

  • To investigate the activation of the MAPK pathway by GH in human IM-9 lymphocytes.
  • To compare GH-induced MAPK signaling in IM-9 lymphocytes with that in 3T3-F442A mouse preadipocytes.
  • To elucidate the differential signaling mechanisms of GH in distinct cell types.

Main Methods:

  • Western blotting using antiphosphotyrosine, anti-MAPK, and anti-phospho-MAPK antibodies.
  • In vitro kinase assays with a synthetic peptide substrate.
  • Immunoprecipitation assays to identify signaling intermediates like c-Raf-1 and Shc adapter proteins.

Main Results:

  • GH activated MAPK in 3T3-F442A cells but not in IM-9 lymphocytes within 5-60 minutes.
  • Phorbol 12-myristate 13-acetate (PMA) activated MAPK in IM-9 cells via c-Raf-1.
  • GH treatment did not induce tyrosine phosphorylation of 52- and 46-kDa Shc forms in IM-9 cells, unlike the 52- and 66-kDa forms in 3T3-F442A cells.

Conclusions:

  • GH does not activate the MAPK pathway in human IM-9 lymphocytes.
  • The MAPK pathway activation by GH differs significantly between mouse preadipocytes and human lymphocytes.
  • These findings underscore cell-type-specific differences in GH receptor downstream signaling.

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