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Elastolytic cathepsin induction/activation system exists in myocardium and is upregulated in hypertensive heart

Xian Wu Cheng1, Koji Obata, Masafumi Kuzuya

  • 1Department of Cardiovascular Genome Science, Nagoya University School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan. xianwu@med.nagoya-u.ac.jp

Hypertension (Dallas, Tex. : 1979)
|September 20, 2006
PubMed

Insights

Cathepsin S expression increases in heart failure, contributing to cardiac remodeling and elastin breakdown. Targeting this protease may offer new therapies for heart failure.

Area of Science:

  • Cardiovascular Biology
  • Protease Biochemistry
  • Pathology

Background:

  • Cathepsins are proteases involved in tissue remodeling.
  • Their role in myocardial remodeling, particularly in heart failure, is not well understood.

Purpose of the Study:

  • To investigate the expression and role of cathepsins, specifically cathepsin S, in the left ventricular (LV) myocardium during hypertension-induced cardiac hypertrophy and heart failure (HF).

Main Methods:

  • Real-time PCR and immunoblot analysis of LV tissues from rats and humans.
  • Immunostaining for cathepsin S localization.
  • Assessment of elastic lamina fragmentation and elastolytic activity.
  • Measurement of elastin and interleukin-1beta mRNA.
  • In vitro studies using cultured neonatal cardiomyocytes.

Main Results:

  • Cathepsin S mRNA and protein levels were significantly elevated in the LV myocardium of HF patients and rats compared to hypertrophy and control groups.
  • Cathepsin S was localized to cardiac myocytes, vascular smooth muscle cells, and macrophages.
  • Increased elastic lamina fragmentation and elastolytic activity, primarily driven by cathepsin S, were observed in HF rat aortas.
  • Interleukin-1beta expression was upregulated in HF rat myocardium and enhanced cathepsin S expression and activity in cultured cardiomyocytes.

Conclusions:

  • Cathepsin S plays a significant role in the pathological cardiac remodeling associated with hypertension-induced heart failure.
  • The protease contributes to elastin degradation in the myocardium.
  • Cathepsin S represents a potential therapeutic target for preventing or reversing cardiac remodeling in heart failure.

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