Vasopressin stimulates the induction of heat shock protein 27 and alphaB-crystallin via protein kinase C activation in vascular smooth muscle cells

Exp Cell Res. 1999 Feb 1;246(2):327-37. doi: 10.1006/excr.1998.4277.

Abstract

In the present study, we examined the effect of vasopressin on the induction of the low-molecular-weight heat shock proteins heat shock protein 27 (HSP27) and alphaB-crystallin in an aortic smooth muscle cell line, A10 cells. Vasopressin induced a time-dependent accumulation of HSP27 and alphaB-crystallin. The stimulatory effects of vasopressin were dose-dependent over the range 0.1 nmol/L to 0.1 micromol/L. The EC50 values for vasopressin were 2 (HSP27) and 4 nmol/L (alphaB-crystallin). Vasopressin induced increases in the levels of the mRNAs for HSP27 and alphaB-crystallin. 12-O-Tetradecanoylphorbol 13-acetate (TPA), a protein kinase C (PKC)-activating phorbol ester, induced an accumulation of HSP27 (EC50, 20 nmol/L) and alphaB-crystallin (EC50, 2 nmol/L). In contrast, 4alpha-phorbol 12,13-didecanoate, a non-PKC-activating phorbol ester, had no such effect. Staurosporine and calphostin C, inhibitors of PKC, significantly reduced the vasopressin-induced accumulation of HSP27 and alphaB-crystallin as well as that induced by TPA. BAPTA/AM and TMB-8, inhibitors of intracellular Ca2+ mobilization, significantly reduced the vasopressin-induced accumulation of HSP27 and alphaB-crystallin. These results strongly suggest that vasopressin stimulates the induction of HSP27 and alphaB-crystallin via PKC activation in vascular smooth muscle cells and that this effect of vasopressin is dependent on intracellular Ca2+ mobilization.

MeSH terms

  • Animals
  • Blotting, Northern
  • Calcium Channel Blockers / pharmacology
  • Cell Line
  • Choline / biosynthesis
  • Crystallins / biosynthesis*
  • Crystallins / genetics
  • Egtazic Acid / analogs & derivatives
  • Egtazic Acid / pharmacology
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Gallic Acid / analogs & derivatives
  • Gallic Acid / pharmacology
  • Heating
  • Inositol Phosphates / biosynthesis
  • Intracellular Signaling Peptides and Proteins
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / enzymology
  • Muscle, Smooth, Vascular / metabolism*
  • Neomycin / pharmacology
  • Phosphatidate Phosphatase / antagonists & inhibitors
  • Propranolol / pharmacology
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism*
  • Protein Serine-Threonine Kinases / biosynthesis*
  • Protein Serine-Threonine Kinases / genetics
  • Rats
  • Tetradecanoylphorbol Acetate / pharmacology
  • Type C Phospholipases / antagonists & inhibitors
  • Vasoconstrictor Agents / pharmacology*
  • Vasopressins / pharmacology*

Substances

  • Calcium Channel Blockers
  • Crystallins
  • Enzyme Inhibitors
  • Inositol Phosphates
  • Intracellular Signaling Peptides and Proteins
  • Vasoconstrictor Agents
  • Vasopressins
  • Egtazic Acid
  • 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate
  • Gallic Acid
  • Propranolol
  • MAP-kinase-activated kinase 2
  • Protein Serine-Threonine Kinases
  • Protein Kinase C
  • Phosphatidate Phosphatase
  • Type C Phospholipases
  • Neomycin
  • 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
  • Choline
  • Tetradecanoylphorbol Acetate