Embryonic mesenchymal cells share the potential for smooth muscle differentiation: myogenesis is controlled by the cell's shape

Development ◽  
1999 ◽  
Vol 126 (13) ◽  
pp. 3027-3033 ◽  
Author(s):  
Y. Yang ◽  
N.K. Relan ◽  
D.A. Przywara ◽  
L. Schuger
Keyword(s):  
Smooth Muscle ◽  
Mesenchymal Cell ◽  
Muscle Differentiation ◽  
Mesenchymal Cells ◽  
Membrane Potentials ◽  
Main Role ◽  
Visceral Muscle ◽  
Smooth Muscle Differentiation

Undifferentiated embryonic mesenchymal cells are round/cuboidal in shape. During development, visceral myogenesis is shortly preceded by mesenchymal cell elongation. To determine the role of the cell's shape on smooth muscle development, undifferentiated embryonic mesenchymal cells from intestine (abundant visceral muscle), lung (some visceral muscle) or kidney (no visceral muscle) were plated under conditions that maintained cell rounding or promoted elongation. Regardless of their fate in vivo, all the cells differentiated into smooth muscle upon elongation as indicated by the expression of smooth muscle-specific proteins and the development of membrane potentials of −60 mV and voltage-dependent Ca2+ currents, characteristic of excitable cells. Smooth muscle differentiation occurred within 24 hours and was independent of cell proliferation. Regardless of their fate in vivo, all the round cells remained negative for smooth muscle markers, had membrane potentials of −30 mV and showed no voltage-activated current. These cells, however, differentiated into smooth muscle upon elongation. The role of the cell's shape in controlling smooth muscle differentiation was not overcome by treatment with retinoic acid, TGF-beta1, PDGF BB or epithelial-conditioned medium (all modulators of smooth muscle differentiation). These studies suggest that the mesenchymal cell shape plays a main role in visceral myogenesis.

Role of laminin polymerization at the epithelial mesenchymal interface in bronchial myogenesis

Development ◽  
1998 ◽  
Vol 125 (14) ◽  
pp. 2621-2629 ◽  
Author(s):  
Y. Yang ◽  
K.C. Palmer ◽  
N. Relan ◽  
C. Diglio ◽  
L. Schuger
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Basement Membrane ◽  
Mesenchymal Cell ◽  
Cell Types ◽  
Mesenchymal Cells ◽  
Cell Contact ◽  
Alpha Actin ◽  
Muscle Myosin

Undifferentiated mesenchymal cells were isolated from mouse embryonic lungs and plated at subconfluent and confluent densities. During the first 5 hours in culture, all the cells were negative for smooth muscle markers. After 24 hours in culture, the mesenchymal cells that spread synthesized smooth muscle alpha-actin, muscle myosin, desmin and SM22 in levels comparable to those of mature smooth muscle. The cells that did not spread remained negative for smooth muscle markers. SM differentiation was independent of cell-cell contact or proliferation. In additional studies, undifferentiated lung mesenchymal cells were cocultured with lung embryonic epithelial cells at high density. The epithelial cells aggregated into cysts surrounded by mesenchymal cells and a basement membrane was formed between the two cell types. In these cocultures, the mesenchymal cells in contact with the basement membrane spread and differentiated into smooth muscle. The rest of the mesenchymal cells remained round and negative for smooth muscle markers. Inhibition of laminin polymerization by an antibody to the globular regions of laminin beta1/gamma1 chains blocked basement membrane assembly, mesenchymal cell spreading and smooth muscle differentiation. These studies indicated that lung embryonic mesenchymal cells have the potential to differentiate into smooth muscle and the process is triggered by their spreading along the airway basement membrane.

Transforming growth factor-beta dynamically regulates vascular smooth muscle differentiation in vivo

1998 ◽  
Vol 111 (19) ◽  
pp. 2977-2988 ◽  
Author(s):  
D.J. Grainger ◽  
J.C. Metcalfe ◽  
A.A. Grace ◽  
D.E. Mosedale
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Muscle Differentiation ◽  
Tgf Beta ◽  
Differentiation Markers ◽  
Smooth Muscle Tissue ◽  
Smooth Muscle Differentiation

Variations in the levels of smooth muscle-specific isoforms of contractile proteins have been reported to occur in many different vascular diseases. However, although much work has been done in vitro to investigate the regulation of smooth muscle cell differentiation, the molecular mechanisms which regulate the differentiation of vascular smooth muscle tissue in vivo are unknown. Using quantitative immunofluorescence, we show that in rat arteries levels of smooth muscle differentiation markers correlate with the levels of the cytokine TGF-beta. In young mice with one allele of the TGF-beta1 gene deleted, the levels of both TGF-beta1 and smooth muscle differentiation markers are reduced compared to wild-type controls. This regulation of smooth muscle differentiation by TGF-beta during post-natal development also occurs dynamically in the adult animal. Following various pharmacological or surgical interventions, including treatment of mice with tamoxifen and balloon injury of rat carotid arteries, there is a strong correlation between the changes in the levels of TGF-beta and changes in the levels of smooth muscle differentiation markers (r=0. 9, P<0.0001 for n=26 experiments). We conclude that TGF-beta dynamically regulates smooth muscle differentiation in rodent arteries in vivo.

cFKBP/SMAP; a novel molecule involved in the regulation of smooth muscle differentiation

Development ◽  
1998 ◽  
Vol 125 (18) ◽  
pp. 3535-3542 ◽  
Author(s):  
K. Fukuda ◽  
Y. Tanigawa ◽  
G. Fujii ◽  
S. Yasugi ◽  
S. Hirohashi
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscles ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Muscle Differentiation ◽  
Mesenchymal Cells ◽  
Fk506 Binding Protein ◽  
Smooth Muscle Differentiation ◽  
Muscle Precursor Cells

During embryogenesis, smooth muscle cells of the gut differentiate from mesenchymal cells derived from splanchnic mesoderm. We have isolated a gene involved in the differentiation of smooth muscle cells in the gut using differential display between the chicken proventriculus in which the smooth muscle layer develops poorly and the gizzard in which smooth muscles develop abundantly. The protein encoded by this gene showed highest similarity to mouse FK506 binding protein, FKBP65, and from the function of this protein it was designated chicken FKBP/smooth muscle activating protein (cFKBP/SMAP). cFKBP/SMAP was first expressed in smooth muscle precursor cells of the gut and, after smooth muscles differentiate, expression was restricted to smooth muscle cells. In organ culture of the gizzard, the differentiation of smooth muscle cells was inhibited by the addition of FK506, the inhibitor of FKBPs. Moreover, overexpression of cFKBP/SMAP in lung and gizzard mesenchymal cells induced smooth muscle differentiation. In addition, cFKBP/SMAP-induced smooth muscle differentiation was inhibited by FK506. We postulate therefore that cFKBP/SMAP plays a crucial role in smooth muscle differentiation in the gut and provides a powerful tool to study smooth muscle differentiation mechanisms, which have been poorly analyzed so far.

scholarly journals STUDIES IN THE DYNAMICS OF HISTOGENESIS

1920 ◽  
Vol 2 (4) ◽  
pp. 357-372 ◽  
Author(s):  
Eben J. Carey
Keyword(s):  
Smooth Muscle ◽  
Cross Section ◽  
Rapid Growth ◽  
Muscle Differentiation ◽  
Mesenchymal Cells ◽  
Circular Smooth Muscle ◽  
Epithelial Tube ◽  
Smooth Muscle Differentiation ◽  
Mitotic Figures ◽  
Muscle Coat

1. The region of most active mitosis per mm. of cross-section in the intestine is the entodermal epithelial tube. The mitotic figures primarily follow the path of a right-handed helix. In one of the twenty embryos the mitotic figures describe the path of a right-handed helix. 2. The region of least active or relatively passive growth per mm. of cross-section is the mesenchyme, derived from the splanchnic mesoderm surrounding the epithelial tube. 3. The rapid expansion, due to epithelial growth in a rotating spiral manner, of the intestinal lumen is greater than the activity manifest in the surrounding mesenchyme. This causes a pressure in the latter resulting in a flattening and elongation of the mesenchymal cells. The successive changes in shape of these cells through the spherical, ellipsoidal, and spindle cellular phases are seen. The mesenchymal wall decreases in thickness, due to tension caused by epithelial tubular dilation. 4. The rotating spiral growth of the epithelial cells causes the formation of a series of mesenchymal cellular and fibrillar concentric rings due to the centripetal force of the former. 5. The circular, smooth muscle cells are differentiated in the outer, more condensed margins of the ring. At these points the developing tensional stresses are greater than within the ring. 6. The inner circular smooth muscle coat is the first one differentiated and is incident to the rapid growth of the epithelial tube in diameter. The former soon tends to restrict the growth of the epithelial tube in diameter. The tube, pursuing the lines of least resistance, grows in length. During the period of rapid growth in length the outer longitudinal muscle coat is in the process of formation. 7. The tensional stresses to which the elongated strained mesenchymal cells are subjected appear to be a dynamic stimulus to smooth muscle differentiation. 8. From this study of a closely graded and progressive series of sections of intestinal development, the conclusion is drawn that muscle tissue is not self-differentiating, in the strict sense of the term, but that the tension of differential growth acts as the stimulus to smooth muscle differentiation.

scholarly journals Stromal cells from human long-term marrow cultures are mesenchymal cells that differentiate following a vascular smooth muscle differentiation pathway

Blood ◽  
1993 ◽  
Vol 82 (1) ◽  
pp. 66-76 ◽  
Author(s):  
MC Galmiche ◽  
VE Koteliansky ◽  
J Briere ◽  
P Herve ◽  
P Charbord
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Stromal Cells ◽  
Muscle Cells ◽  
Mesenchymal Cells ◽  
Myoid Cells ◽  
Marrow Cultures

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.

scholarly journals Malignant Melanoma with Probable Smooth Muscle Differentiation

2014 ◽  
Vol 6 (1) ◽  
pp. 16-19 ◽  
Author(s):  
Aya Morimoto ◽  
Jun Asai ◽  
Yusuke Wakabayashi ◽  
Satoshi Komori ◽  
Keiji Hanada ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Malignant Melanoma ◽  
Muscle Differentiation ◽  
Smooth Muscle Differentiation
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