Laminin variants and integrin laminin receptors in developing and adult human smooth muscle.
Distribution of laminin variant chains and of laminin-binding beta 1-associated alpha integrin subunits was studied in human arterial and visceral smooth muscle during development using the immunofluorescence method. In aortic media of 10-week-old fetuses (early fetal stage of development), B1, B2, and A chains were found, and at 27 weeks of gestation (late fetal step), in addition, the S chain was revealed. In the major part of adult aortic media, staining for the B1 chain was substituted by staining for the S chain. A reasonable explanation for this is that the basement membrane of arterial SMCs contains the A-B1-B2 laminin trimer at the early fetal stage of development, a mixture of A-B1-B2 and A-S-B2 variants during the late fetal period, and the A-S-B2 form in adult media. In the intimal thickening of adult arteries, staining for A and S chains was decreased, and the B1 chain was detected, thus suggesting coexistence of A-B1-B2 and A-S-B2 variants similar to the fetal aorta. These data led us to propose that maturation of arterial SMCs is accompanied by a switch from expression of A-B1-B2 to A-S-B2 laminin, the only protein variant associated with the differentiated SMC phenotype. The M chain was not detected in fetal and adult arterial smooth muscle. In differentiated visceral SMCs from adult colon, in contrast to arterial medial SMCs, B1, S, B2, and A chains, i.e., both B1 chain- and S chain-containing laminin molecules, were present. Similar to vascular smooth muscle, the expression of A and S laminin chains in SMCs of the intestine was developmentally regulated. Of the four beta 1-associated alpha integrin subunits that have been shown to recognize laminin ( alpha 1, alpha 2, alpha 3, and alpha 6), only alpha 1 was revealed during the early fetal stage of development in smooth muscle of the arteries and digestive tract. alpha 3 appeared in aortic media only during the late fetal period. In adult arterial media and smooth muscle of the colon, alpha 1 and alpha 3 were the major potential laminin-binding integrins. The spatial-temporal distribution of laminin variants in developing and adult smooth muscle suggests that a variant laminin (possibly A-S-B2) interacting with its receptor ( alpha 1 beta 1 or alpha 3 beta 1) may be important for maintenance of the differentiated SMC phenotype in vivo.[1]References
- Laminin variants and integrin laminin receptors in developing and adult human smooth muscle. Glukhova, M., Koteliansky, V., Fondacci, C., Marotte, F., Rappaport, L. Dev. Biol. (1993) [Pubmed]
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