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Different response of satellite cells in the kinetics of myogenic regulatory factors and ultrastructural pathology after Trichinella spiralis and T. pseudospiralis infection

Published online by Cambridge University Press:  23 July 2001

Z. WU
Affiliation:
Department of Parasitology, Gifu University School of Medicine, Tsukasa 40, Gifu 500-8705, Japan
A. MATSUO
Affiliation:
Department of Parasitology, Gifu University School of Medicine, Tsukasa 40, Gifu 500-8705, Japan
T. NAKADA
Affiliation:
Department of Parasitology, Gifu University School of Medicine, Tsukasa 40, Gifu 500-8705, Japan
I. NAGANO
Affiliation:
Department of Parasitology, Gifu University School of Medicine, Tsukasa 40, Gifu 500-8705, Japan
Y. TAKAHASHI
Affiliation:
Department of Parasitology, Gifu University School of Medicine, Tsukasa 40, Gifu 500-8705, Japan

Abstract

Infection of an intracellular parasitic nematode, Trichinella spiralis, resulted in severe damage in muscle cells which was followed by activation and proliferation of satellite cells. The repairing process, shortly after the damage, histopathologically resembled those seen after mechanical injury. Resemblance was also true for kinetics of expression of myogenic regulatory factors (MyoD, myogenin and MRF4). The difference resided in the next step where the muscle cell infected with T. spiralis transformed to a unique cell which is parasitologically known as the nurse cell, and the proliferated satellite cells did not differentiate to the muscle cell but to the nurse cell (misdifferentiation). Thus the nurse cell was a fusion of the transformed infected muscle cell and misdifferentiated satellite cells. Infection with another species of Trichinella, T. pseudospiralis, also caused cell damage, but more extensively involving the entire length of the infected muscle cells because no septum was formed to minimize the affected area. Therefore, a large number of satellite cells were activated and proliferated. The myogenic regulatory factors such as MyoD and myogenin were activated for a longer period than in the case with T. spiralis infection. The infected muscle cell transformed to the nurse cell, whose cytoplasm was characterized by extensive smooth endoplasmic reticulum. Satellite cells misdifferentiated to the nurse cell, whose cytoplasm was amorphous, void of distinct cell organelles. The two kinds of cytoplasm did not fuse as examined thus far. Thus infection with T. spiralis and T. pseudospiralis caused misdifferentiation of satellite cells, but in a different way.

Type
Research Article
Copyright
© 2001 Cambridge University Press

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