Growth arrest of a murine mesangial cell line by transforming growth factor β1 is associated with inhibition of mitogen-induced Ca2+ mobilization

Gyorgy Baffy, Kumar Sharma, Wenyao Shi, Fuad N. Ziyadeh, John R. Williamson

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Transforming growth factor-β (TGFβ) is a multifunctional cytokine showing growth effects on many cell types. In the present study effects of TGFβ1 on mitogen-induced Ca2+ responses were investigated in an immortalized murine mesangial cell line where TGFβ1 effects on growth are inhibitory. TGFβ1 was found to inhibit intracellular Ca2+ mobilization induced by platelet-derived growth factor (PDGF). This effect was completely reversed by previous addition of the non-specific serine/threonine kinase inhibitor H-7, but was unaffected by GF 109203X, a specific inhibitor of protein kinase C (PKC). These findings suggest that inhibition of mitogen-induced Ca2+ mobilization by TGFβ1 appears not to involve prior activation of PKC, but may participate in the mechanisms whereby mesangial cell growth is inhibited by TGFβ1.

Original languageEnglish (US)
Pages (from-to)378-383
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume210
Issue number2
DOIs
StatePublished - Jan 1 1995
Externally publishedYes

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Mesangial Cells
Transforming Growth Factors
Mitogens
Protein Kinase C
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Cell Line
Protein-Serine-Threonine Kinases
Platelet-Derived Growth Factor
Cell growth
Growth
Chemical activation
Cytokines
bisindolylmaleimide I

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Growth arrest of a murine mesangial cell line by transforming growth factor β1 is associated with inhibition of mitogen-induced Ca2+ mobilization. / Baffy, Gyorgy; Sharma, Kumar; Shi, Wenyao; Ziyadeh, Fuad N.; Williamson, John R.

In: Biochemical and Biophysical Research Communications, Vol. 210, No. 2, 01.01.1995, p. 378-383.

Research output: Contribution to journalArticle

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