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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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SM cell size in intraparenchymal bronchi of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections of lungs (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.05). (B) Immunoblots demonstrating lower levels of SM proteins in dy/dy lungs compared with controls.
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Figure 8: SM cell size in intraparenchymal bronchi of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections of lungs (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.05). (B) Immunoblots demonstrating lower levels of SM proteins in dy/dy lungs compared with controls.

Mentions: Dy/dy mice have SM abnormalities in vivo, including shorter cells and deficiencies in SM-specific protein production. Cell morphometry studies showed that bronchial SM cells in dy/dy mice were shorter than in control animals in a statistically significant manner (Fig. 8 A). No differences in size were found, however, in lung vascular SM cells or bronchial columnar epithelial cells (not shown). Immunoblots demonstrated that adult dy/dy mouse lungs contained less SM-specific proteins, including SM α-actin, desmin, and myosin (Fig. 8 B). On histological examination, the most abnormal SM was that of the trachea and main bronchi. In those sites, the visceral SM cells were shorter and underdeveloped (Fig. 9B and Fig. D). For comparison, A and C show tracheal and bronchial SM in normal animals of the same strain. Unlike the extraparenchymal airway, the changes in the intraparenchymal bronchial SM were subtle and detected mainly by cell morphometry (shorter cells) and immunoblotting as already shown in Fig. 8. On immunohistochemistry using an anti-SM α-actin antibody, the large and medium sized bronchial muscle exhibited slightly, but clear thinning and more discontinuity than the normal counterparts (Fig. 9E and Fig. F).


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 intraparenchymal bronchi of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections of lungs (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.05). (B) Immunoblots demonstrating lower levels of SM proteins in dy/dy lungs compared with controls.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2168094&req=5

Figure 8: SM cell size in intraparenchymal bronchi of dy/dy mice and controls. (A) Histogram showing maximal nuclear diameter as an indicator of cell size in hematoxylin eosin-stained histological sections of lungs (cell boundaries are not seen in organs). Dy/dy mice showed shorter nuclei compared with controls (P < 0.05). (B) Immunoblots demonstrating lower levels of SM proteins in dy/dy lungs compared with controls.
Mentions: Dy/dy mice have SM abnormalities in vivo, including shorter cells and deficiencies in SM-specific protein production. Cell morphometry studies showed that bronchial SM cells in dy/dy mice were shorter than in control animals in a statistically significant manner (Fig. 8 A). No differences in size were found, however, in lung vascular SM cells or bronchial columnar epithelial cells (not shown). Immunoblots demonstrated that adult dy/dy mouse lungs contained less SM-specific proteins, including SM α-actin, desmin, and myosin (Fig. 8 B). On histological examination, the most abnormal SM was that of the trachea and main bronchi. In those sites, the visceral SM cells were shorter and underdeveloped (Fig. 9B and Fig. D). For comparison, A and C show tracheal and bronchial SM in normal animals of the same strain. Unlike the extraparenchymal airway, the changes in the intraparenchymal bronchial SM were subtle and detected mainly by cell morphometry (shorter cells) and immunoblotting as already shown in Fig. 8. On immunohistochemistry using an anti-SM α-actin antibody, the large and medium sized bronchial muscle exhibited slightly, but clear thinning and more discontinuity than the normal counterparts (Fig. 9E and Fig. F).

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