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Cell elongation induces laminin alpha2 chain expression in mouse embryonic mesenchymal cells: role in visceral myogenesis.

Relan NK, Yang Y, Beqaj S, Miner JH, Schuger L - J. Cell Biol. (1999)

Bottom Line: In comparison, the expression of LM beta1 and gamma1 remains unchanged.These deficiencies were completely corrected by exogenous LM-2.The intestine, however, showed compensatory hyperplasia, perhaps related to its higher contractile activity.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

ABSTRACT
Bronchial smooth muscle (SM) mesenchymal cell precursors change their shape from round to spread/elongated while undergoing differentiation. Here we show that this change in cell shape induces the expression of laminin (LM) alpha2 chain not present in round mesenchymal cells. LM alpha2 expression is reversible and switched on and off by altering the cell's shape in culture. In comparison, the expression of LM beta1 and gamma1 remains unchanged. Functional studies showed that mesenchymal cell spreading and further differentiation into SM are inhibited by an antibody against LM alpha2. Dy/dy mice express very low levels of LM alpha2 and exhibit congenital muscular dystrophy. Lung SM cells isolated from adult dy/dy mice spread defectively and synthesized less SM alpha-actin, desmin, and SM-myosin than controls. These deficiencies were completely corrected by exogenous LM-2. On histological examination, dy/dy mouse airways and gastrointestinal tract had shorter SM cells, and lungs from dy/dy mice contained less SM-specific protein. The intestine, however, showed compensatory hyperplasia, perhaps related to its higher contractile activity. This study therefore demonstrated a novel role for the LM alpha2 chain in SM myogenesis and showed that its decrease in dy/dy mice results in abnormal SM.

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Related in: MedlinePlus

SM cell size in circular layer of intestinal muscularis propria of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.03). (B) Immunoblots demonstrating slightly higher levels of SM proteins in dy/dy intestine compared with controls, consistent with the hyperplasia described in Results.
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Figure 10: SM cell size in circular layer of intestinal muscularis propria of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.03). (B) Immunoblots demonstrating slightly higher levels of SM proteins in dy/dy intestine compared with controls, consistent with the hyperplasia described in Results.

Mentions: The SMs of stomach and intestine were also studied. Histological examination and morphometric studies of the stomach revealed no alterations in dy/dy mice when compared with controls. The intestine, however, exhibited shorter SM cells, similar to what was seen in the lung (Fig. 10 A). Unlike the trachea and bronchi, the SM cells in the intestinal wall were arranged in more layers (hyperplasia) resulting in a thicker muscularis wall. In the thinnest areas, the muscular circular layer was 2 ± 1-SM cell–thick in dy/dy mouse intestine and 1 ± 1-SM cell–thick in control animals. In the thickest sites, the circular layer was 15 ± 3-cell-thick in dydy intestine and 12 ± 2-cell-thick in controls. Reflecting this hyperplasia, immunoblotting showed a slight increase in SM-specific proteins in the intestine of dy/dy mice compared with controls (Fig. 10 B).


Cell elongation induces laminin alpha2 chain expression in mouse embryonic mesenchymal cells: role in visceral myogenesis.

Relan NK, Yang Y, Beqaj S, Miner JH, Schuger L - J. Cell Biol. (1999)

SM cell size in circular layer of intestinal muscularis propria of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.03). (B) Immunoblots demonstrating slightly higher levels of SM proteins in dy/dy intestine compared with controls, consistent with the hyperplasia described in Results.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2168094&req=5

Figure 10: SM cell size in circular layer of intestinal muscularis propria of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.03). (B) Immunoblots demonstrating slightly higher levels of SM proteins in dy/dy intestine compared with controls, consistent with the hyperplasia described in Results.
Mentions: The SMs of stomach and intestine were also studied. Histological examination and morphometric studies of the stomach revealed no alterations in dy/dy mice when compared with controls. The intestine, however, exhibited shorter SM cells, similar to what was seen in the lung (Fig. 10 A). Unlike the trachea and bronchi, the SM cells in the intestinal wall were arranged in more layers (hyperplasia) resulting in a thicker muscularis wall. In the thinnest areas, the muscular circular layer was 2 ± 1-SM cell–thick in dy/dy mouse intestine and 1 ± 1-SM cell–thick in control animals. In the thickest sites, the circular layer was 15 ± 3-cell-thick in dydy intestine and 12 ± 2-cell-thick in controls. Reflecting this hyperplasia, immunoblotting showed a slight increase in SM-specific proteins in the intestine of dy/dy mice compared with controls (Fig. 10 B).

Bottom Line: In comparison, the expression of LM beta1 and gamma1 remains unchanged.These deficiencies were completely corrected by exogenous LM-2.The intestine, however, showed compensatory hyperplasia, perhaps related to its higher contractile activity.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

ABSTRACT
Bronchial smooth muscle (SM) mesenchymal cell precursors change their shape from round to spread/elongated while undergoing differentiation. Here we show that this change in cell shape induces the expression of laminin (LM) alpha2 chain not present in round mesenchymal cells. LM alpha2 expression is reversible and switched on and off by altering the cell's shape in culture. In comparison, the expression of LM beta1 and gamma1 remains unchanged. Functional studies showed that mesenchymal cell spreading and further differentiation into SM are inhibited by an antibody against LM alpha2. Dy/dy mice express very low levels of LM alpha2 and exhibit congenital muscular dystrophy. Lung SM cells isolated from adult dy/dy mice spread defectively and synthesized less SM alpha-actin, desmin, and SM-myosin than controls. These deficiencies were completely corrected by exogenous LM-2. On histological examination, dy/dy mouse airways and gastrointestinal tract had shorter SM cells, and lungs from dy/dy mice contained less SM-specific protein. The intestine, however, showed compensatory hyperplasia, perhaps related to its higher contractile activity. This study therefore demonstrated a novel role for the LM alpha2 chain in SM myogenesis and showed that its decrease in dy/dy mice results in abnormal SM.

Show MeSH
Related in: MedlinePlus