Myosin isoforms and cell heterogeneity in vascular smooth muscle

The Future of Cell Therapy and Tissue Engineering in Cardiovascular Disease: The New Era of Biological Therapeutics

“…These tendencies depend, however, on cellular density, serum concentration, and substrate for attachment. Myosin gene expression can be regulated during early development (effect on the differentiation phase of the SMC lineage program) or in adulthood (alteration of the stability of the fully differentiated SMC phenotype) (Zanellato AMC 1990;Somlyo AP 1993). High levels of SM--actin and basic calponin in particular were observed in the present study, with lower levels of SM myosin and h-caldesmon-expressing cells.…”

“…These tendencies depend, however, on cellular density, serum concentration, and substrate for attachment. Myosin gene expression can be regulated during early development (effect on the differentiation phase of the SMC lineage program) or in adulthood (alteration of the stability of the fully differentiated SMC phenotype) (Zanellato AMC 1990;Somlyo AP 1993). The general feature of cultured SMCs is the downregulation of SM myosin expression, particularly of SM2 concomitant with upregulation of non-muscle myosin variants MyHC-A pla1, MyHC-A, and MyHC-B (Somlyo AP 1993).…”

Smooth Muscle Myosin Heavy Chain Isoforms Are Developmentally Regulated in Male Fetal and Neonatal Sheep

“…MHC-A was initially identified in human platelets (4,13). Subsequently it was observed in aortic smooth muscle from neonatal rats (14) and the bovine fetus (15) and was reported to decrease with increasing age. Its presence, however, in fetal rabbit aorta is questionable (3,16).…”

Calponin Developmental isoforms and a low molecular weight variant

“…The appearance of phenotypicallyspecific proteins during the differentiation of smooth muscle is not synchronized, but temporally separated [19]. Whereas a-smooth muscle actin and smooth muscle specific myosin isoforms belong to the early differentiation markers [3,4], h-caldesmon and metavinculin appear comparatively late in fetal development [19]. The increase in number of calponin isoforms, up to at least 4 in the human adult, occurs gradually throughout fetal development, but I-calponin has been detected only showing the dependence of calponin isoform expression on seeding density.…”

“…[l-5]). Antibodies against one or another actin or myosin isoform are already proving useful as markers of smooth muscle cells [3,4,6], but since these isoforms may be differentially expressed in different smooth muscle populations [1,4] and in cells other than smooth muscle [3,7,8] more markers of the smooth muscle phenotype are called for. Studies along the latter lines have already pinpointed metavinculin [9] and the heavy isoform of caldesmon [lo] as alternative and complementary markers of the smooth muscle phenotype, The present study was undertaken to establish the possible existence of other smooth muscle specific proteins, emphasis being placed on analysis of the pattern of human basic proteins separated by two-dimensional gel electrophoresis under non-equilibrium conditions.…”