Regulation of fibrillar collagen types I and III and basement membrane type IV collagen gene expression in pressure overloaded rat myocardium

D. Chapman, Karl Weber, M. Eghbali

Research output: Contribution to journalArticle

200 Citations (Scopus)

Abstract

Left ventricular hypertrophy is based on cardiac myocyte growth. The hypertrophic process can be considered heterogeneous based on whether it also includes a remodeling and accumulation of fibrillar types I and III collagens that are responsible for impaired myocardial stiffness. In the heart, the messenger RNA (mRNA) for fibrillar collagen types I and III has been detected only in cardiac fibroblasts, whereas mRNA for basement membrane collagen type IV is present in both fibroblasts and myocytes. We studied the early and long-term expression of these collagenous proteins in rat myocardium after abdominal aortic banding with renal ischemia. Complementary DNA probes for rat pro-α2(I), mouse type III and mouse type IV collagens, and chicken β-actin were used. Northern and dot blot analysis on total RNA extracted from left ventricular tissue indicated a sixfold increase in steady-state levels of mRNA for collagen type I on day 3 of abdominal aortic banding, which had declined to control levels by day 7 where it remained rather constant at 4 and 8 weeks. Type III collagen showed a similar pattern of gene expression after banding. mRNA levels for type IV collagen, on the other hand, were elevated on day 1 after banding returning to control at day 7 and remaining constant. Actin mRNA levels also increased on day 1 of banding, followed by a rapid return to control levels. Monospecific antibody to types I and III collagens and immunofluorescent light microscopy on frozen sections of the myocardium revealed that at 1 week after banding, the distribution and density of these collagens were similar to those of control animals. At 8 weeks, the density of collagen type I fibers was greater than controls, and a perivascular fibrosis involving intramyocardial coronary arteries also as present. The distribution and density of collagen types III and IV, however, remained unchanged at these intervals. Thus, fibrillar collagen gene regulation and subsequent myocardial fibrosis are integral components of renovascular hypertension. The cellular origins of the fibrillar and nonfibrillar collagen mRNAs and their temporally disparate regulation suggest that separate regulatory mechanisms, involving myocytes and fibroblasts, may be responsible for the remodeling of the myocardium.

Original languageEnglish (US)
Pages (from-to)787-794
Number of pages8
JournalCirculation Research
Volume67
Issue number4
DOIs
StatePublished - Jan 1 1990
Externally publishedYes

Fingerprint

Fibrillar Collagens
Collagen Type III
Collagen Type IV
Collagen Type I
Myocardium
Gene Expression
Pressure
Messenger RNA
Fibroblasts
Muscle Cells
Non-Fibrillar Collagens
Actins
Fibrosis
Renovascular Hypertension
DNA Probes
Frozen Sections
Left Ventricular Hypertrophy
Cardiac Myocytes
Northern Blotting
Microscopy

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Regulation of fibrillar collagen types I and III and basement membrane type IV collagen gene expression in pressure overloaded rat myocardium. / Chapman, D.; Weber, Karl; Eghbali, M.

In: Circulation Research, Vol. 67, No. 4, 01.01.1990, p. 787-794.

Research output: Contribution to journalArticle

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