Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose

Am J Physiol Heart Circ Physiol. 2008 Jul;295(1):H69-76. doi: 10.1152/ajpheart.00341.2008. Epub 2008 May 2.

Abstract

This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. Isolated MRA were subjected to a pressure-passive-diameter relationship. To delineate cell types and mechanisms, cultured VSMC were prepared from MRA and stimulated with ANG II (100 nM) and high glucose (HG, 22 mM). Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. This pathway could be a potential target for overcoming small artery complications in diabetes and hypertension.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetates / pharmacology
  • Angiotensin II
  • Animals
  • Antibodies
  • Benzodiazepinones / pharmacology
  • Blood Glucose / metabolism
  • Blood Pressure
  • Cells, Cultured
  • Collagen Type I / metabolism*
  • Diabetes Mellitus, Experimental / metabolism*
  • Diabetes Mellitus, Experimental / pathology
  • Elasticity
  • Fibrosis
  • Hypertension / chemically induced
  • Hypertension / metabolism*
  • Hypertension / pathology
  • Hypertension / physiopathology
  • Integrin alphaVbeta3 / antagonists & inhibitors
  • Integrin alphaVbeta3 / immunology
  • Integrin alphaVbeta3 / metabolism*
  • Mesenteric Arteries / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Microcirculation / metabolism
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / enzymology
  • Muscle, Smooth, Vascular / metabolism*
  • Muscle, Smooth, Vascular / pathology
  • Myocytes, Smooth Muscle / metabolism
  • Phosphorylation
  • RNA Interference
  • Signal Transduction
  • Smad2 Protein / metabolism
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / immunology
  • Transforming Growth Factor beta1 / metabolism*

Substances

  • Acetates
  • Antibodies
  • Benzodiazepinones
  • Blood Glucose
  • Collagen Type I
  • Integrin alphaVbeta3
  • SB 223245
  • Smad2 Protein
  • Smad2 protein, mouse
  • Transforming Growth Factor beta1
  • Angiotensin II
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3