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Characteristics of inflammation-induced hypertrophy of rat intestinal smooth muscle cell

M G Blennerhassett1, F M Bovell, S Lourenssen

  • 1Gastrointestinal Diseases Research Unit, Queens University, Hotel Dieu Hospital, Kingston, Ontario, Canada.

Digestive Diseases and Sciences
|September 18, 1999
PubMed

Insights

Trichinella spiralis infection causes intestinal smooth muscle cell (ISMC) hyperplasia and increased smooth muscle actin protein. This highlights the plasticity of intestinal smooth muscle during inflammation.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Immunology

Background:

  • Intestinal inflammation can lead to smooth muscle layer thickening.
  • Studies in rats infected with Trichinella spiralis (Tsp) indicate intestinal smooth muscle cell (ISMC) hyperplasia.

Purpose of the Study:

  • To investigate the changes in protein content and expression of smooth muscle-specific actins in ISMC during Tsp-induced intestinal inflammation.
  • To assess the impact of inflammation on ISMC hypertrophy and actin density.

Main Methods:

  • Quantification of total protein per ISMC in control and Tsp-infected rats.
  • Measurement of alpha-smooth muscle (SM) actin protein levels and proportion.
  • Analysis of gamma-SM actin messenger RNA (mRNA) and protein content postinfection (PI).

Main Results:

  • Tsp-induced inflammation caused a fivefold increase in total protein per ISMC.
  • ISMC from noninflamed distal ileum showed a threefold protein increase.
  • Alpha-SM actin per ISMC increased nearly 500% by day 6 PI.
  • The proportion of alpha-SM actin in total cellular protein doubled by day 6 PI.
  • Gamma-SM actin mRNA and protein levels increased significantly.

Conclusions:

  • Tsp infection induces significant ISMC hypertrophy and hyperplasia.
  • Increased smooth muscle-specific actin content suggests altered force production capacity.
  • These findings demonstrate the remarkable plasticity of intestinal smooth muscle in response to inflammation.

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