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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

Proposed role of LM-1 and LM-2 in bronchial myogenesis. e, Epithelial cells (gray); m, mesenchymal cells (yellow); SM, smooth muscle cells (from pink to red); BM, basement membrane. The asterisk tags the relative position adopted by an epithelial cell from the moment it is born and establishes a new contact with the mesenchyme.
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Figure 11: Proposed role of LM-1 and LM-2 in bronchial myogenesis. e, Epithelial cells (gray); m, mesenchymal cells (yellow); SM, smooth muscle cells (from pink to red); BM, basement membrane. The asterisk tags the relative position adopted by an epithelial cell from the moment it is born and establishes a new contact with the mesenchyme.

Mentions: Fig. 11 depicts the proposed roles of LM α1 and α2 chains in bronchial myogenesis. Our studies suggest that the development of new epithelial-mesenchymal contacts during lung organogenesis results in the induction of LM α1 chain expression and deposition of LM-1 at the epithelial/mesenchymal interface (Schuger et al. 1997). LM-1 molecules polymerize, contributing to the formation of a basement membrane (Schuger et al. 1995, Schuger et al. 1998). The mesenchymal cells apposed to the newly formed basement membrane utilize this meshwork to spread/elongate through binding to LM α1 (Schuger et al. 1997). This change in cell shape induces them to synthesize LM α2 chain and concomitantly to differentiate into SM. Once secreted as part of LM-2, LM α2 chain stimulates spreading and SM differentiation of nearby mesenchymal cells, eventually leading to the establishment of a multilayered visceral muscle. The process of myogenesis could stop when LM α2 chain expression drops dramatically at the end of the pseudo glandular period (Virtanen et al. 1996) whereby preventing excessive SM formation.


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)

Proposed role of LM-1 and LM-2 in bronchial myogenesis. e, Epithelial cells (gray); m, mesenchymal cells (yellow); SM, smooth muscle cells (from pink to red); BM, basement membrane. The asterisk tags the relative position adopted by an epithelial cell from the moment it is born and establishes a new contact with the mesenchyme.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 11: Proposed role of LM-1 and LM-2 in bronchial myogenesis. e, Epithelial cells (gray); m, mesenchymal cells (yellow); SM, smooth muscle cells (from pink to red); BM, basement membrane. The asterisk tags the relative position adopted by an epithelial cell from the moment it is born and establishes a new contact with the mesenchyme.
Mentions: Fig. 11 depicts the proposed roles of LM α1 and α2 chains in bronchial myogenesis. Our studies suggest that the development of new epithelial-mesenchymal contacts during lung organogenesis results in the induction of LM α1 chain expression and deposition of LM-1 at the epithelial/mesenchymal interface (Schuger et al. 1997). LM-1 molecules polymerize, contributing to the formation of a basement membrane (Schuger et al. 1995, Schuger et al. 1998). The mesenchymal cells apposed to the newly formed basement membrane utilize this meshwork to spread/elongate through binding to LM α1 (Schuger et al. 1997). This change in cell shape induces them to synthesize LM α2 chain and concomitantly to differentiate into SM. Once secreted as part of LM-2, LM α2 chain stimulates spreading and SM differentiation of nearby mesenchymal cells, eventually leading to the establishment of a multilayered visceral muscle. The process of myogenesis could stop when LM α2 chain expression drops dramatically at the end of the pseudo glandular period (Virtanen et al. 1996) whereby preventing excessive SM formation.

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