Phenotypic changes of human smooth muscle cells during development: Late expression of heavy caldesmon and calponin

Frid, Maria G.; Shekhonin, B. V.; Koteliansky, Victor; Glukhova, Marina A.

doi:10.1016/0012-1606(92)90104-o

Cited by 252 publications

(152 citation statements)

References 32 publications

Supporting

Mentioning

144

Contrasting

Order By: Relevance

“…These include myofibroblasts of the healing wounds and tumor stroma, bone marrow stroma cells, and glandular myoepithelium (Sappino et al, 1988; Galmiche et al, 1993; Gugliotta In this study we have analyzed expression of the smooth muscle markers in developing rat myoepithelial cells. Expression of these proteins in vascular and visceral smooth muscles is developmentally regulated (Glukhova et al, 1990;Frid et al, 1992). a-SM-actin and SM-MHC appear in smooth muscle cells quite early, while calponin and PGM start to be expressed later during vascular smooth muscle cell maturation.…”

Section: Developmental Changes Of the Myoepithelial Cellsmentioning

confidence: 99%

“…Vinculin is strongly enriched in developing and adult smooth muscles as compared to other tissues. Metavinculin, a muscle-specific variant of the protein that appears as a result of alternative splicing of a single vinculin gene transcript (Price et al, 1989;Koteliansky et al, 1992), is a late marker of vascular smooth muscle. Meta-vinculin co-localizes with vinculin in dense plaques, the cell-extracellular matrix adherens junctions of smooth muscle cells (Belkin et al, 1988).…”

Section: Developmental Changes Of the Myoepithelial Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Myoepithelial cell diffeentiation in the developing mammary gland: Progressive acquisition of smooth muscle phenotype

Deugnier

Moiseyeva

Thiery

et al. 1995

Developmental Dynamics

View full text Add to dashboard Cite

The most important portion of the mammary gland development occurs postnatally, with distinct periods of intensive morphogenesis taking place between birth and puberty and during pregnancy and lactation. To characterize the differentiation process of mammary myoepithelial cells, we have studied the expression patterns of several smooth muscle phenotypic markers, including contractile proteins, a-smooth muscle-actin (a-SM-actin), smooth muscle myosin heavy chains (SM-MHC), and calponin; components of cell-extracellular matrix adherens junctions, phosphoglucomutase-related protein (PGM), vinculin variants, integrin subunits; and laminin variant chains in the developing rat mammary gland using immunofluorescence microscopy. a-SM-actin-and SM-MHC-positive cells were found first in newborn animals, while calponin, PGM and a1 integrin subunit began to be expressed in prepubertal animals (1.5 weeks). Vinculin, p1 and a3 integrin subunits were largely confined to the basal cell layer at all developmental stages examined with greater staining starting at 1.5 weeks. Meta-vinculin was identified only in myoepithelial cells of the lactating gland. yl laminin chain was present in the mammary gland basement membrane throughout development, while the p2 chain was revealed in 3-week-old animals and accumulated later in postpubertal animals (7 weeks). Similarly, p2 laminin chain was absent from the forming alveoli basement membrane in pregnant rats and started to accumulate in the lactating gland. In addition to temporal changes, we have observed spatial differences in the distribution of the phenotypic markers. Both in pre-and in postpubertal animals, a-SM-actinand SM-MHC-positive cells of the growing ductal ends contained low amounts if any of calponin, PGM, and p2 laminin chain. We conclude that during postnatal development, mammary myoepithelial cells progressively acquire a differentiated phenotype as revealed by the expression of various smooth muscle markers. Maturation of the myoepithelial cells is accompanied by upregulation of the smooth muscle integrin expression followed by accumulation of P2-containing laminin variant. Thus, changes in adhesion system parallel with the myoepithelial cell differentiation.D 1995 Wiley-Liss, Inc.

show abstract

Section: Developmental Changes Of the Myoepithelial Cellsmentioning

confidence: 99%

Section: Developmental Changes Of the Myoepithelial Cellsmentioning

confidence: 99%

Myoepithelial cell diffeentiation in the developing mammary gland: Progressive acquisition of smooth muscle phenotype

Deugnier

Moiseyeva

Thiery

et al. 1995

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…PM, although bidirectional, in the present study refers to the process of transition from differentiated phenotype to dedifferentiated phenotype [1]. The differentiated SMC show a high level of expression of a unique repertoire of marker genes that includes smooth muscle α-actin (SMA) [2], smooth muscle myosin heavy chain (SMMHC) [3], calponin (CN) [4], SM-22α (SM22) [4,5], and h-caldesmon (CALD1) [6]. They also exhibit an extremely low rate of proliferation and synthetic activity.…”

Section: Introductionmentioning

confidence: 99%

“…Here, we examined cultured VSMC [42] and thoracic aortic rings of mice cultured in serumfree medium for 1,3,6,12,24,48, and 72 h. The expression of VSMC-specific marker genes was determined by quantitative RT-PCR (QPCR) and Western blot analysis. We found that early PM which manifested in significant downregulation of the expression of these VSMC-specific marker genes as early as 3 h was followed by substantial decrease in protein levels by 12 h. Finally, we determined whether loss of mechanical force is the cause of early PM.…”

Section: Introductionmentioning

confidence: 99%

The early- and late stages in phenotypic modulation of vascular smooth muscle cells: Differential roles for lysophosphatidic acid

Guo

Makarova

Cheng

et al. 2008

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

View full text Add to dashboard Cite

Lysophosphatidic acid (LPA) has been implicated as causative in phenotypic modulation (PM) of cultured vascular smooth muscle cells (VSMC) in their transition to the dedifferentiated phenotype. We evaluated the contribution of the three major LPA receptors, LPA 1 and LPA 2 GPCR and PPARγ, on PM of VSMC. Expression of differentiated VSMC-specific marker genes, including smooth muscle α-actin, smooth muscle myosin heavy chain, calponin, SM-22α, and hcaldesmon, was measured by quantitative real-time PCR in VSMC cultures and aortic rings kept in serum-free chemically defined medium or serum-or LPA-containing medium using wild-type C57BL/6, LPA 1 , LPA 2 , and LPA 1&2 receptor knockout mice. Within hours after cells were deprived of physiological cues, the expression of VSMC marker genes, regardless of genotype, rapidly decreased. This early PM was neither prevented by IGF-I, inhibitors of p38, ERK1/2, or PPARγ nor significantly accelerated by LPA or serum. To elucidate the mechanism of PM in vivo, carotid artery ligation with/without replacement of blood with Krebs solution was used to evaluate contributions of blood flow and pressure. Early PM in the common carotid was induced by depressurization regardless of the presence/absence of blood, but eliminating blood flow while maintaining blood pressure or after sham surgery elicited no early PM. The present results indicate that LPA, serum, dissociation of VSMC, IGF-I, p38, ERK1/2, LPA 1 , and LPA 2 are not causative factors of early PM of VSMC. Tensile stress generated by blood pressure may be the fundamental signal maintaining the fully differentiated phenotype of VSMC.

show abstract

“…Mesodermal lineage cells were identified as follows: 24 Skeletal muscle was identified as mononucleated myoblasts staining with OP137 (Calbiochem, San Diego, CA) for MyoD , F5D (DSHB) for myogenin , and DEU-10 (Sigma) for desmin , and as multinucleated spontaneously contracting structures staining with MF-20 (DSHB) for sarcomeric myosin , MY-32 (Sigma) for skeletal muscle fast myosin (Naumann and Pette, 1994), ALD-58 (DSHB) for myosin heavy chain , and A4.74 (DSHB) for myosin fast chain . 25 Smooth muscle was identified as mononucleated cells staining with antibodies IA4 (Sigma) for smooth muscle alpha-actin and Calp (Sigma) for calponin (Frid et al, 1992;Lazard et al, 1993). 26 Cardiac muscle was identified as binucleated cells co-staining with MF-20 (DSHB) ϩ IA4 (Sigma) for sarcomeric myosin and smooth muscle alpha actin (Eisenberg and Markwald, 1997;, MAB3252 (Chemicon) for cardiotin (Schaart et al, 1997) and MAB1548 for cardiac muscle (Chemicon).…”

Section: Phenotypic Bioassay Of Scl-40␤mentioning

confidence: 99%

Clonogenic analysis reveals reserve stem cells in postnatal mammals. II. Pluripotent epiblastic‐like stem cells

et al. 2004

View full text Add to dashboard Cite

Undifferentiated cells have been identified in the prenatal blastocyst, inner cell mass, and gonadal ridges of rodents and primates, including humans. After isolation these cells express molecular and immunological markers for embryonic cells, capabilities for extended self‐renewal, and telomerase activity. When allowed to differentiate, embryonic stem cells express phenotypic markers for tissues of ectodermal, mesodermal, and endodermal origin. When implanted in vivo, undifferentiated noninduced embryonic stem cells formed teratomas. In this report we describe a cell clone isolated from postnatal rat skeletal muscle and derived by repetitive single‐cell clonogenic analysis. In the undifferentiated state it consists of very small cells having a high ratio of nucleus to cytoplasm. The clone expresses molecular and immunological markers for embryonic stem cells. It exhibits telomerase activity, which is consistent with its extended capability for self‐renewal. When induced to differentiate, it expressed phenotypic markers for tissues of ectodermal, mesodermal, and endodermal origin. The clone was designated as a postnatal pluripotent epiblastic‐like stem cell (PPELSC). The undifferentiated clone was transfected with a genomic marker and assayed for alterations in stem cell characteristics. No alterations were noted. The labeled clone, when implanted into heart after injury, incorporated into myocardial tissues undergoing repair. The labeled clone was subjected to directed lineage induction in vitro, resulting in the formation of islet‐like structures (ILSs) that secreted insulin in response to a glucose challenge. This study suggests that embryonic‐like stem cells are retained within postnatal mammals and have the potential for use in gene therapy and tissue engineering. Anat Rec Part A 277A:178–203, 2004. © 2004 Wiley‐Liss, Inc.

show abstract

Phenotypic changes of human smooth muscle cells during development: Late expression of heavy caldesmon and calponin

Cited by 252 publications

References 32 publications

Myoepithelial cell diffeentiation in the developing mammary gland: Progressive acquisition of smooth muscle phenotype

Myoepithelial cell diffeentiation in the developing mammary gland: Progressive acquisition of smooth muscle phenotype

The early- and late stages in phenotypic modulation of vascular smooth muscle cells: Differential roles for lysophosphatidic acid

Clonogenic analysis reveals reserve stem cells in postnatal mammals. II. Pluripotent epiblastic‐like stem cells

Contact Info

Product

Resources

About