scholarly journals Comparison of pain intensity, smooth muscle cells density, and alpha-smooth muscle actin expression in ovarial and peritoneal endometriosis

2021 ◽  
Vol 29 (3) ◽  
pp. 108
Author(s):  
Sutrisno Sutrisno ◽  
Muhammad Nooryanto ◽  
Shella Widya Gani
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Pain Intensity ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Alpha Smooth Muscle Actin ◽  
Cross Sectional ◽  
Muscle Density ◽  
Peritoneal Endometriosis

HIGHLIGHT1. Pain intensity, smooth muscle cells density, and alpha-SMA expression can be used to analyze the role of smooth muscle in endometriosis.2. Compared to healthy individuals, those with endometriosis have higher pain intensity, smooth muscle cells density, and alpha-SMA expression. 3. Among endometriotic patients, those with peritoneal endometriosis have higher pain intensity, smooth muscle cells density, and alpha-SMA expression than those with ovarial endometriosis.3. The expression of alpha-SMA, smooth muscle density, and pain intensity were found to correlate significantly in endometriosis. ABSTRACTObjectives: to identify the role of smooth muscle through the analysis of smooth muscle cells density, expression of a-SMA, and the pain intensity.Materials and Methods: Study design is a cross sectional analytic observational. Study sample consists of women with ovarial endometrios and women with peritoneal endometriosis that undergo laparoscopy and laparotomy in RSUD Saiful Anwar Malang and RSIA Melati Malang from January until December 2019. There are 16 samples: 8 samples of ovarial endometriosis and 8 samples of peritoneal endometriosis. Smooth muscle cell density was analyzed by comparing the number of smooth muscle cells with the total area of endometriosis tissue in one microscopical field. a-SMA expression obtained by immunohistochemistry. Degree of pain obatined by filling the part 1 point 1-11 of EHP-30 queistionnaire the day after the procedure. Data was analyzed by Independent T-test and Pearson correlation.Results: Pain intensity, smooth muscle cells density, and a-SMA expression is higher in the endometriosis patient compared to healthy individual. Pain intensity, smooth muscle cells density, and a-SMA expression is lower in the ovarial endometriosis compared to peritoneal endometriosis.Conclusion: There are a significant correlation between the expression of a-SMA, smooth muscle density, and pain intensity in endometriosis.

scholarly journals Renal afferent arteriolar and tubuloglomerular feedback reactivity in mice with conditional deletions of adenosine 1 receptors

2012 ◽  
Vol 303 (8) ◽  
pp. F1166-F1175 ◽  
Author(s):  
Lingli Li ◽  
En Yin Lai ◽  
Yuning Huang ◽  
Christoph Eisner ◽  
Diane Mizel ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mesangial Cells ◽  
Smooth Muscle Actin ◽  
Critical Role ◽  
Muscle Cells ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Actin Promoter

Adenosine 1 receptors (A1AR) have been shown in previous experiments to play a major role in the tubuloglomerular feedback (TGF) constrictor response of afferent arterioles (AA) to increased loop of Henle flow. Overexpression studies have pointed to a critical role of vascular A1AR, but it has remained unclear whether selective deletion of A1AR from smooth muscle cells is sufficient to abolish TGF responsiveness. To address this question, we have determined TGF response magnitude in mice in which vascular A1AR deletion was achieved using the loxP recombination approach with cre recombinase being controlled by a smooth muscle actin promoter (SmCre/A1ARff). Effective vascular deletion of A1AR was affirmed by absence of vasoconstrictor responses to adenosine or cyclohexyl adenosine (CHA) in microperfused AA. Elevation of loop of Henle flow from 0 to 30 nl/min caused a 22.1 ± 3.1% reduction of stop flow pressure in control mice and of 7.2 ± 1.5% in SmCre/A1ARff mice ( P < 0.001). Maintenance of residual TGF activity despite absence of A1AR-mediated responses in AA suggests participation of extravascular A1AR in TGF. Support for this notion comes from the observation that deletion of A1ARff by nestin-driven cre causes an identical TGF response reduction (7.3 ± 2.4% in NestinCre/A1ARff vs. 20.3 ± 2.7% in controls), whereas AA responsiveness was reduced but not abolished. A1AR on AA smooth muscle cells are primarily responsible for TGF activation, but A1AR on extravascular cells, perhaps mesangial cells, appear to contribute to the TGF response.

scholarly journals The alpha 6 and beta 4 integrin subunits are expressed by smooth muscle cells of human small vessels: a new localization in mesenchymal cells.

1994 ◽  
Vol 42 (9) ◽  
pp. 1221-1228 ◽  
Author(s):  
O Cremona ◽  
P Savoia ◽  
P C Marchisio ◽  
G Gabbiani ◽  
C Chaponnier
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Confocal Laser ◽  
Alpha Smooth Muscle Actin ◽  
Excitation Spectra ◽  
Small Vessels ◽  
Von Willebrand

The alpha 6 beta 4 integrin complex is generally thought to be expressed by epithelial cells, where it is localized in specific adhesion structures, the hemidesmosomes. Recent observations have suggested a new localization of the beta 4 integrin chain in small vessels, possibly in endothelial cells, i.e., in cells of mesenchymal origin. In the present study we show that (a) the alpha 6 and beta 4 integrin chains are not expressed by endothelial cells, since they are not localized in von Willebrand factor-producing cells; (b) instead, smooth muscle cells of small vessels are intensely positive to antibodies to both alpha 6 and beta 4 intergrin chains; and (c) in some restricted regions of these smooth muscle cells there is a clear colocalization between alpha-smooth muscle actin and alpha 6 and beta 4 integrin chains, suggesting that a new type of cytoskeletal linkage for the alpha 6 beta 4 integrin complex may occur in mesenchyme-derived cells. Our observations are supported by confocal laser microscopy (CLSM) images of specimens labeled by double immunofluorescence. This technical choice was made to take advantage of the higher resolution offered by CLSM in comparison with conventional immunofluorescence. A careful selection of barrier filters was necessary to separate accurately emission and excitation spectra of the fluorochromes used in this study, resulting in an efficient colocalization analysis.

scholarly journals Expression of PDGF alpha-receptor in renal arteriosclerosis and rejecting renal transplants.

1998 ◽  
Vol 9 (2) ◽  
pp. 211-223 ◽  
Author(s):  
J Floege ◽  
K L Hudkins ◽  
C L Davis ◽  
S M Schwartz ◽  
C E Alpers
Keyword(s):  
Smooth Muscle ◽  
Renal Disease ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Mature Adult ◽  
Receptor Mrna

Platelet-derived growth factor (PDGF) plays an important role in renal disease. We have recently demonstrated that in healthy mature human kidney, PDGF alpha-receptor expression is largely restricted to interstitial cells. The study presented here assesses the expression of PDGF alpha-receptor in 18 mature adult kidneys with arteriosclerosis from individuals with no clinically evident history of renal disease other than localized neoplasia, in 13 kidneys with irreversible transplant rejection, and in a series of renal transplant biopsies composed of examples of both severe and absent rejection, by in situ hybridization and immunocytochemistry. Strong focal or diffuse expression of PDGF alpha-receptor mRNA and protein was noted in some intimal cells of intrarenal arterial vessels exhibiting signs of arteriosclerosis and/or vascular rejection. By double immunostaining, it could be shown that these cells were neither endothelial cells nor infiltrating leukocytes. The cells were most often identified as smooth muscle by colabeling for the smooth muscle cell-specific protein SM22alpha and less commonly for alpha-smooth muscle actin. There was also a population of PDGF alpha-receptor-expressing cells that failed to colabel with any of these markers, and hence remain of uncertain histogenesis. These intimal cells were generally negative for several other markers of differentiated smooth muscle cells, i.e., calponin and desmin. Near these PDGF alpha-receptor-positive intimal cells, expression of PDGF A-chain, an alpha-receptor ligand, was demonstrated in endothelial, intimal, and/or medial cells. Prominent PDGF alpha-receptor mRNA and protein expression also was noted in areas of interstitial fibrosis and in some glomeruli, in particular those with segmental glomerulosclerosis or fibrotic crescents. Double immunolabeling for PDGF alpha-receptor and alpha-smooth muscle actin confirmed that most of these latter PDGF alpha-receptor-positive cells were interstitial myofibroblasts or mesangial cells, or both. In summary, these data demonstrate widespread expression of PDGF alpha-receptor in renal cell types involved in fibrotic and sclerosing processes. The data also show that PDGF alpha-receptor expression identifies a unique population of phenotypically altered vascular smooth muscle cells, which appear to be involved in the vascular response to injury.

scholarly journals Neutralization of S100A4 induces stabilization of atherosclerotic plaques: role of smooth muscle cells

2020 ◽  
Author(s):  
A Sakic ◽  
C Chaabane ◽  
N Ambartsumian ◽  
J Klingelhöfer ◽  
S Lemeille ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Atherosclerotic Plaques ◽  
Porcine Coronary Artery ◽  
Phenotypic Transition ◽  
Synthetic Phenotype

Abstract Aims During atherosclerosis, smooth muscle cells (SMCs) accumulate in the intima where they switch from a contractile to a synthetic phenotype. From porcine coronary artery, we isolated spindle-shaped (S) SMCs exhibiting features of the contractile phenotype and rhomboid (R) SMCs typical of the synthetic phenotype. S100A4 was identified as a marker of R-SMCs in vitro and intimal SMCs, in pig and man. S100A4 exhibits intra- and extracellular functions. In this study, we investigated the role of extracellular S100A4 in SMC phenotypic transition. Methods and Results S-SMCs were treated with oligomeric recombinant S100A4 (oS100A4), which induced nuclear factor (NF)-κB activation. Treatment of S-SMCs with oS100A4 in combination with platelet-derived growth factor (PDGF)-BB induced a complete SMC transition toward a pro-inflammatory R-phenotype associated with NF-κB activation, through toll-like receptor-4. RNA sequencing of cells treated with oS100A4/PDGF-BB revealed a strong upregulation of pro-inflammatory genes and enrichment of transcription factor binding sites essential for SMC phenotypic transition. In a mouse model of established atherosclerosis, neutralization of extracellular S100A4 decreased area of atherosclerotic lesions, necrotic core, and CD68 expression and increased α-smooth muscle actin and smooth muscle myosin heavy chain expression. Conclusion We suggest that the neutralization of extracellular S100A4 promotes the stabilization of atherosclerotic plaques. Extracellular S100A4 could be a new target to influence the evolution of atherosclerotic plaques. Translational perspective Our studies indicate that extracellular S100A4 is causally related to atherosclerotic plaque progression putting it forward as a prospective therapeutic target for plaque stabilization and/or regression.

scholarly journals Interferon gamma inhibits both proliferation and expression of differentiation-specific alpha-smooth muscle actin in arterial smooth muscle cells.

1989 ◽  
Vol 170 (5) ◽  
pp. 1595-1608 ◽  
Author(s):  
G K Hansson ◽  
M Hellstrand ◽  
L Rymo ◽  
L Rubbia ◽  
G Gabbiani
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Arterial Smooth Muscle ◽  
Ifn Gamma ◽  
Actin Mrna ◽  
Arterial Smooth Muscle Cells

Differentiation of muscle cells is characterized morphologically by the acquisition of contractile filaments and characteristic shape changes, and on the molecular level by induction of the expression of several genes, including those for the muscle-specific alpha-actin isoforms. IFN-gamma is an inhibitor of proliferation for several cells, including vascular smooth muscle, and is also an inducer of differentiated properties for several hematopoietic cells. We have therefore investigated whether IFN-gamma affects the expression of alpha-smooth muscle actin in cultured arterial smooth muscle cells. Cells exposed to IFN-gamma show a reduction of alpha-smooth muscle actin-containing stress fibers, as detected by immunofluorescence. The effect was observed in all phases of the cell cycle, and was caused by a reduction of the synthesis of alpha-smooth muscle actin protein as revealed by two-dimensional electrophoretic analysis of actin isoforms. RNA hybridization using a cRNA probe that hybridizes to all actin mRNAs showed that IFN-gamma-treated cells have a reduced content of the 1.7-kb mRNA that codes for alpha-smooth muscle actin, and to a lesser extent, also of the 2.1-kb mRNA encoding the beta and gamma-cytoplasmic actins. The reduction of alpha-smooth muscle actin mRNA was confirmed using an alpha-smooth muscle actin-specific cRNA probe. The reduction of alpha-smooth muscle actin mRNA occurs within 12 h, and is dependent on protein synthesis, since cycloheximide treatment reversed the effect. The inhibition of this mRNA species was dose dependent, and detectable by RNA hybridization at a dose of 50 U/ml IFN-gamma. These results suggest that the differentiation of arterial smooth muscle cells is not necessarily coupled to an inhibition of cellular proliferation. Instead, IFN-gamma may regulate the expression of several genes that control both proliferation and expression of differentiation markers.

scholarly journals Alpha-smooth muscle actin, a differentiation marker of smooth muscle cells, is present in microfilamentous bundles of pericytes.

1989 ◽  
Vol 37 (3) ◽  
pp. 315-321 ◽  
Author(s):  
O Skalli ◽  
M F Pelte ◽  
M C Peclet ◽  
G Gabbiani ◽  
P Gugliotta ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Cell Types ◽  
Electron Microscopic Level ◽  
Alpha Smooth Muscle Actin ◽  
Electron Microscopic ◽  
Microfilament Bundles ◽  
Differentiation Marker

alpha-Smooth muscle (alpha-sm) actin, an isoform typical of smooth muscle cells (SMC) and present in high amounts in vascular SMC, was demonstrated in the cytoplasm of pericytes of various rat and human organs by means of immunocytochemistry at the electron microscopic level. In SMC and pericytes, alpha-sm actin was localized in microfilament bundles, strengthening the assumption that it is the functional isoform in these cell types and supporting the assumption that pericytes exert contractile functions.

scholarly journals Smooth Muscle Cells of Penis in the Rat: Noninvasive Quantification with Shear Wave Elastography

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Jia-Jie Zhang ◽  
Xiao-Hui Qiao ◽  
Feng Gao ◽  
Ming Bai ◽  
Fan Li ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Shear Wave ◽  
Smooth Muscle Actin ◽  
Shear Wave Elastography ◽  
Muscle Cells ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Immunohistochemistry Analysis ◽  
Measurement Index

Purpose. Smooth muscle cells (SMCs) of cavernosum play an important role in erection. It is of great significance to quantitatively analyze the level of SMCs in penis. In this study, we investigated the feasibility of shear wave elastography (SWE) on evaluating the level of SMCs in penis quantitatively. Materials and Methods. Twenty healthy male rats were selected. The SWE imaging of penis was carried out and then immunohistochemistry analysis of penis was performed to analyze the expression of alpha smooth muscle actin in penis. The measurement index of SWE examination was tissue stiffness (TS). The measurement index of immunohistochemistry analysis was positive area percentage of alpha smooth muscle actin (AP). Results. Sixty sets of data of TS and AP were obtained. The results showed that TS was significantly correlated with AP and the correlation coefficient was −0.618 (p<0.001). The result of TS had been plotted against the AP measurements. The relation between the two results has been fitted with quadric curve; the goodness-of-fit index was 0.364 (p<0.001). Conclusions. The level of SMCs in penis was successfully quantified in vivo with SWE. SWE can be used clinically for evaluating the level of SMCs in penis quantitatively.

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