Apoptotic death of smooth muscle cells in human endometriosis, a light and electron microscopic analysis

2002 ◽  
Vol 9 (3) ◽  
pp. S72-S73
Author(s):  
M Nakakuma
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Microscopic Analysis ◽  
Muscle Cells ◽  
Electron Microscopic Analysis ◽  
Electron Microscopic ◽  
Apoptotic Death

Abstract WMP31: Dedifferentiation of Smooth Muscle Cells and its Potential Contribution to Pathogenesis of Intracranial Aneurysms

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Mieko Oka ◽  
Nobuhiko Ohno ◽  
Takakazu Kawamata ◽  
Tomohiro Aoki
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Inflammatory Responses ◽  
Muscle Cells ◽  
Inflammatory Factors ◽  
Potential Contribution ◽  
Electron Microscopic

Introduction: Intracranial aneurysm (IA) affects 1 to 5 % in general public and becomes the primary cause of subarachnoid hemorrhage, the most severe form of stroke. However, currently, no drug therapy is available for IAs to prevent progression and rupture of lesions. Elucidation of mechanisms underlying the disease is thus mandatory. Considering the important role of vascular smooth muscle cells (SMCs) in the maintenance of stiffness of arterial walls and also in the pathogenesis of atherosclerosis via mediating inflammatory responses, we in the present study analyzed morphological or phenotypical changes of SMCs during the disease development in the lesions. Methods: We subjected rats to an IA model in which lesions are induced by increase of hemodynamic force loading on intracranial arterial bifurcations and performed histopathological analyses of induced lesions including the electron microscopic examination. We then immunostained specimens from induced lesions to explore factors responsible for dedifferentiation or migration of SMCs. In vitro study was also done to examine effect of some candidate factors on dedifferentiation or migration of cultured SMCs. Results: We first found the accumulation of SMCs underneath the endothelial cell layer mainly at the neck portion of the lesion. These cells was positive for the embryonic form of myosin heavy chain, a marker for the dedifferentiated SMCs, and the expression of pro-inflammatory factors like TNF-α. In immunostaining to explore the potential factor regulating the dedifferentiation of SMCs, we found that Platelet-derived growth factor-BB (PDGF-BB) was expressed in endothelial cells at the neck portion of IA walls. Consistently, recombinant PDGF-BB could promote the dedifferentiate of SMCs and chemo-attracted them in in vitro. Finally, in the stenosis model of the carotid artery, PDGF-BB expression was induced in endothelial cells in which high wall shear stress was loaded and the dedifferentiation of SMCs occurred there. Conclusions: The findings from the present study imply the role of dedifferentiated SMCs partially recruited by PDGF-BB from endothelial cells in the formation of inflammatory microenvironment at the neck portion of IA walls, leading to the progression of the disease.

scholarly journals CENTRIOLES AND THE FORMATION OF RUDIMENTARY CILIA BY FIBROBLASTS AND SMOOTH MUSCLE CELLS

1962 ◽  
Vol 15 (2) ◽  
pp. 363-377 ◽  
Author(s):  
Sergei Sorokin
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Sensory Function ◽  
Second Phase ◽  
Electron Microscopic ◽  
Internal Development ◽  
Whole Process ◽  
Third Phase ◽  
Mammalian Tissues

Cells from a variety of sources, principally differentiating fibroblasts and smooth muscle cells from neonatal chicken and mammalian tissues and from organ cultures of chicken duodenum, were used as materials for an electron microscopic study on the formation of rudimentary cilia. Among the differentiating tissues many cells possessed a short, solitary cilium, which projected from one of the cell's pair of centrioles. Many stages evidently intermediate in the fashioning of cilium from centriole were encountered and furnished the evidence from which a reconstruction of ciliogenesis was attempted. The whole process may be divided into three phases. At first a solitary vesicle appears at one end of a centriole. The ciliary bud grows out from the same end of the centriole and invaginates the sac, which then becomes the temporary ciliary sheath. During the second phase the bud lengthens into a shaft, while the sheath enlarges to contain it. Enlargement of the sheath is effected by the repeated appearance of secondary vesicles nearby and their fusion with the sheath. Shaft and sheath reach the surface of the cell, where the sheath fuses with the plasma membrane during the third phase. Up to this point, formation of cilia follows the classical descriptions in outline. Subsequently, internal development of the shaft makes the rudimentary cilia of the investigated material more like certain non-motile centriolar derivatives than motile cilia. The pertinent literature is examined, and the cilia are tentatively assigned a non-motile status and a sensory function.

Fas/Fas ligand-mediated death pathway is involved in oxLDL-induced apoptosis in vascular smooth muscle cells

2001 ◽  
Vol 280 (3) ◽  
pp. C709-C718 ◽  
Author(s):  
Tzong-Shyuan Lee ◽  
Lee-Young Chau
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Fas Ligand ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Potent Inducer ◽  
Apoptotic Death

Oxidized low-density lipoprotein (oxLDL) is a potent inducer of apoptosis for vascular cells. In the present study, we demonstrate that the expression of death mediators, including p53, Fas, and Fas ligand (FasL) was substantially upregulated by oxLDL in cultured vascular smooth muscle cells (SMCs). The induction of these death mediators was time dependent and was accompanied by an increase in apoptotic death of SMCs following oxLDL treatment. Two oxysterols, 7β-hydroxycholesterol and 25-hydroxycholesterol, were also effective to induce the expression of death mediators and apoptosis. α-Tocopherol and deferoxamine significantly attenuated the induction of death mediators and cell death induced by oxLDL and oxysterols, suggesting that reactive oxygen species are involved in triggering the apoptotic event. Incubation of cells with FasL-neutralizing antibody inhibited the oxLDL-induced cell death up to 50%. Furthermore, caspase 8 and caspase 3 activities were induced time dependently in SMCs following oxLDL treatment. Collectively, these data suggest that the Fas/FasL death pathway is activated and responsible for, at least in part, the apoptotic death in vascular SMCs upon exposure to oxLDL.

scholarly journals Myocardin is differentially required for the development of smooth muscle cells and cardiomyocytes

2011 ◽  
Vol 300 (5) ◽  
pp. H1707-H1721 ◽  
Author(s):  
Mark H. Hoofnagle ◽  
Ronald L. Neppl ◽  
Erica L. Berzin ◽  
G. C. Teg Pipes ◽  
Eric N. Olson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ventricular Myocytes ◽  
Embryoid Body ◽  
Embryonic Stem ◽  
Muscle Cells ◽  
Atrial Myocytes ◽  
Electron Microscopic ◽  
Virtual Absence ◽  
Vascular Smcs

Myocardin is a serum response factor (SRF) coactivator exclusively expressed in cardiomyocytes and smooth muscle cells (SMCs). However, there is highly controversial evidence as to whether myocardin is essential for normal differentiation of these cell types, and there are no data showing whether cardiac or SMC subtypes exhibit differential myocardin requirements during development. Results of the present studies showed the virtual absence of myocardin−/− visceral SMCs or ventricular myocytes in chimeric myocardin knockout (KO) mice generated by injection of myocardin−/− embryonic stem cells (ESCs) into wild-type (WT; i.e., myocardin+/+ ESC) blastocysts. In contrast, myocardin−/− ESCs readily formed vascular SMC, albeit at a reduced frequency compared with WT ESCs. In addition, myocardin−/− ESCs competed equally with WT ESCs in forming atrial myocytes. The ultrastructural features of myocardin−/− vascular SMCs and cardiomyocytes were unchanged from their WT counterparts as determined using a unique X-ray microprobe transmission electron microscopic method developed by our laboratory. Myocardin−/− ESC-derived SMCs also showed normal contractile properties in an in vitro embryoid body SMC differentiation model, other than impaired thromboxane A2 responsiveness. Together, these results provide novel evidence that myocardin is essential for development of visceral SMCs and ventricular myocytes but is dispensable for development of atrial myocytes and vascular SMCs in the setting of chimeric KO mice. In addition, results suggest that as yet undefined defects in development and/or maturation of ventricular cardiomyocytes may have contributed to early embryonic lethality observed in conventional myocardin KO mice and that observed deficiencies in development of vascular SMC may have been secondary to these defects.

scholarly journals LOCALIZATION OF TRITIATED NOREPINEPHRINE IN VASCULAR SYMPATHETIC AXONS OF THE RAT INTESTINE AND MESENTERY BY ELECTRON MICROSCOPE RADIOAUTOGRAPHY

1968 ◽  
Vol 38 (1) ◽  
pp. 184-192 ◽  
Author(s):  
C. E. Devine ◽  
F. O. Simpson
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Close Contact ◽  
Short Interval ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Electron Microscopic ◽  
Granular Vesicles ◽  
Silver Grains

The distribution of infused tritiated norepinephrine (NE-3H) in small mesenteric arteries and intestinal arterioles in rats was investigated with electron microscopic radioautography. Silver grains, indicating the presence of the tritium label on the sections, were found lying mainly over axon bundles, but some were present over collagen and smooth muscle cells. Axons with the highest concentrations of silver grains had been sectioned at points where they were naked of Schwann cell sheath, were dilated into varicosities, and contained small granular vesicles. This finding was taken as confirmatory circumstantial evidence that the small granular vesicles were the sites of uptake and storage of NE. The short interval between the start of infusion and the fixation of the tissue appeared to rule out any process other than a direct uptake of NE by the peripheral axons. If axonal sites of uptake of NE-3H correspond to sites of release of NE, then the evidence suggests that such sites of release are widespread over the terminal part of the axon and are not confined to those parts of the axon which are in close contact with smooth muscle cells. Since the fixation and embedding procedures will remove NE which is not strongly bound to tissues, the localization of NE-3H in the radioautographs does not necessarily correspond to the distribution of all the NE present in vivo.

Calcium and contractions of isolated smooth muscle cells from rat myometrium

1987 ◽  
Vol 65 (9) ◽  
pp. 1966-1975 ◽  
Author(s):  
M. Kyozuka ◽  
J. Crankshaw ◽  
I. Berezin ◽  
S. M. Collins ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electron Microscopic Examination ◽  
Muscle Cells ◽  
Isolated Cells ◽  
Electron Microscopic ◽  
Cell Shortening ◽  
Before And After ◽  
Intracellular Ca ◽  
Small Muscle

Smooth muscle cells were isolated from estrogenized rat myometrium by collagenase digestion. Electron microscopic examination and measurement of cell lengths by image-splitting micrometry were carried out after fixation with acrolein. Mean lengths of cells before and after isolation were 81.7 and 66.9 μm, respectively. Responses of cells were compared with contractions of isolated strips recorded isometrically. Effects of carbachol and KCl were examined in 2 mM Ca, 2 mM Ca + 4 mM EGTA, and 2 mM Ca + 10−8 M nitrendipine solution. Carbachol and KCl produced concentration-dependent shortening of isolated cells maximal at 30 s after addition. The concentrations of carbachol required to produce shortenings were about 100-fold less than those required to produce isometric contractions; but no major difference was observed in the concentration dependence of cell shortening and isometric contraction produced by potassium-induced depolarization. In 2 mM Ca solution, there was a phasic response, followed by a tonic response such that more than 50% of maximum cell shortening was maintained for 10 min. However, in 2 mM Ca + 4 mM EGTA or 10−8 M nitrendipine, the tonic contraction was abolished and cells rapidly relaxed after 30 s. If carbachol was added to cells after varying times in the EGTA-containing solution, the ability to initiate a contraction declined exponentially with a half-time of 160 s. Effects of depolarization by KCl were examined in 2 mM Ca plus nitrendipine and 2 mM Ca + 4 mM EGTA solution. Shortening occurred in 2 mM Ca solution by depolarization but not if nitrendipine was added. Though shortening was not observed in 2 mM Ca + 4 mM EGTA solution by KCl, subsequent addition of carbachol induced shortening. These results suggested that there was an intracellular Ca store site from which Ca was released by carbachol and which was not affected by depolarization in the absence of external Ca. No evidence was obtained that the contraction persists in Ca2+-free medium in isolated cells, which is in agreement with previous findings in small muscle strips in which only a similar transient response was obtained.

Experimental Atherosclerosis: Surface Ultrastructural Studies in the Rabbit Aorta

1979 ◽  
Author(s):  
N.F. Rodman ◽  
S.N. Jagannathan ◽  
J.J. Jenkins ◽  
J.A. Rodman
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Rabbit Aorta ◽  
Muscle Cells ◽  
Experimental Atherosclerosis ◽  
Atherogenic Diet ◽  
Electron Microscopic ◽  
Ultrastructural Studies ◽  
Critical Point Drying ◽  
Lipid Vacuoles

Numerous techniques have been employed in the study of experimental atherosclerosis. This study employs critical point drying, cryofracture and transmission and and scanning electron microscopic studies of experimental atherosclerosis in New Zealand white rabbits. Rabbits were maintained on a diet containing 1% cholesterol and 5% Wesson oil and had serum cholesterol levels of 1800 to 2100 mg/dl. Animals were sacrificed at 100 days, 181 days, 217 days, 225 days and 246 days after starting the atherogenic diet. Animals were fixed by perfusion, using Tyrode’s solution followed by Trump’s fixative. Most severe lesions were in the ascending aorta. Least severe lesions were in the common iliac arteries. Very early lesions had widened intimal spaces containing free lipid and smooth muscle cells containing lipid vacuoles. These lesions had distinct borders or were irregular and diffuse. More severe lesions had micro-ulcers at irregular borders. Endothelium over the surface of such lesions was variable and usually intact. An occasional cell with microvilli was observed. By cryofracture cells contained lipid vacuoles with multiple intercommunications. In later lesions cholesterol clefts were also seen. Lipid vacuoles were also observed 1n endothelial cells and in smooth muscle cells of the superficial media. It seems reasonable to conclude that lipid is transported into the subendothelial intimal space and there taken up by smooth muscle cells.

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