Pulmonary Myxoma in a Sheep

2009 ◽  
Vol 46 (3) ◽  
pp. 457-459 ◽  
Author(s):  
F. Ilhan ◽  
Z. Yener
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Left Lung ◽  
Stellate Cells ◽  
Muscle Actin ◽  
Neoplastic Cells ◽  
S 100 ◽  
Myxoid Matrix ◽  
Uncommon Neoplasm

Pulmonary myxoma is an uncommon neoplasm. A pale tan, lobulated, and well-circumscribed mass was discovered at slaughter in the left lung of a 5-year-old sheep. Histologically, the tumor was composed of spindloid to stellate cells in a myxoid matrix. Neoplastic cells were immunohistochemically positive for vimentin but did not express cytokeratins, S-100 protein, smooth muscle actin, desmin, or p53. On the basis of the histologic and immunohistochemical findings, this tumor was diagnosed as a myxoma.

scholarly journals Piloleiomyosarcoma in cats: Histological and immunohistochemical features

2021 ◽  
pp. 030098582110425
Author(s):  
Francisco Rodríguez Guisado ◽  
Pedro Luis Castro
Keyword(s):  
Smooth Muscle ◽  
Subcutaneous Tissue ◽  
Smooth Muscle Actin ◽  
Neuron Specific Enolase ◽  
Surgical Excision ◽  
Giant Cells ◽  
Hair Follicles ◽  
Muscle Actin ◽  
Neoplastic Cells ◽  
S 100

This study describes the histomorphology and immunohistochemical profile of 9 cases of feline piloleiomyosarcoma. Cats ranged in age from 7 to 16 years (mean 10), and tumors were 7 to 24 mm in diameter (mean 15). Tumors were composed of fusiform cells that were haphazardly arranged or in variably sized interwoven bundles. Neoplastic cells had eosinophilic and fibrillar cytoplasm, and elongated blunt-ended nuclei. Entrapment of hair follicles and absence of vascular components support an origin from the smooth muscle cells of the arrector pili. Additional findings included bizarre nuclei and giant cells (7/9 cases), atypical mitoses (7/9 cases), ulceration (3/9 cases), and intratumoral necrosis (6/9 cases). Neoplastic cells expressed calponin, desmin, α-smooth muscle actin, and vimentin, but not CD18, CD31, cytokeratins, glial fibrillary acidic protein, neuron-specific enolase, Melan A, p63, or S-100 protein. Surgical excision was curative in 6/9 cases, with local recurrence in 2/9 cases and metastasis to local lymph nodes in 1/9 case. Clinical outcome was influenced by mitotic count, infiltration of subcutaneous tissue, and intensity of nuclear immunolabeling for p53.

scholarly journals Ca2+-dependent regulation of vascular smooth-muscle caldesmon by S.100 and related smooth-muscle proteins

1991 ◽  
Vol 277 (3) ◽  
pp. 819-824 ◽  
Author(s):  
K Pritchard ◽  
S B Marston
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Bovine Brain ◽  
Protein Yield ◽  
Muscle Actin ◽  
Muscle Proteins ◽  
Related Protein ◽  
Thin Filaments ◽  
S 100 ◽  
Related Proteins

1. We have investigated the ability of bovine brain S.100, and of three related proteins from sheep aorta smooth muscle, to confer Ca(2+)-sensitivity on thin filaments reconstituted from smooth-muscle actin, tropomyosin and caldesmon. 2. At 37 degrees C in pH 7.0 buffer containing 120 mM-KCl, approximately stoichiometric amounts of S.100 reversed caldesmon's inhibition of the activation of myosin MgATPase by smooth-muscle actin-tropomyosin. The [S.100] which reversed by 50% the inhibition by caldesmon (the E.C.50) was 2.5 microM when [caldesmon] = 2-3 microM in the assay mixture. When [KCl] was decreased to 70 mM, E.C.50 = 11.5 microM; at 25 degrees C in 70 mM-KCl, up to 20 microM-S.100 had no effect. When skeletal-muscle actin rather than smooth-muscle actin was used to reconstitute thin filaments, 20 microM-S.100 did reverse inhibition by caldesmon, at 25 degrees C in buffer containing 70 mM-KCl. This dependence on conditions is also characteristic of the calmodulin-caldesmon interaction. 3. These results suggested that S.100 or a related protein might interact with caldesmon in smooth muscle. We therefore attempted to prepare such a protein from sheep aorta. Three proteins were purified: an Mr-17,000 protein (yield 16 mg/kg), an abundant Mr-11,000 protein (yield 48 mg/kg), and an Mr-9000 protein (yield 4 mg/kg). Neither of the last two low-Mr proteins had any effect on activation of myosin MgATPase by reconstituted thin filaments. The protein of Mr 17,000 had Ca(2+)-sensitizing activity, and behaved exactly like brain calmodulin in the assay system.

Gastrointestinal Stromal Tumors and Leiomyomas in the Dog: A Histopathologic, Immunohistochemical, and Molecular Genetic Study of 50 Cases

2003 ◽  
Vol 40 (1) ◽  
pp. 42-54 ◽  
Author(s):  
D. Frost ◽  
J. Lasota ◽  
M. Miettinen
Keyword(s):  
Smooth Muscle ◽  
Gastrointestinal Stromal Tumors ◽  
Smooth Muscle Actin ◽  
Abdominal Cavity ◽  
Clinical Signs ◽  
Muscle Actin ◽  
Molecular Genetic Study ◽  
Stromal Tumors ◽  
Pathologic Features ◽  
S 100

Fifty canine gastrointestinal (GI) mesenchymal tumors were examined to determine the occurrence of leiomyomas (LM) and GI stromal tumors and to compare their clinicopathologic features. Twenty-one tumors (42%) were histologically reclassified as gastrointestinal stromal tumors (GISTs) and 29 tumors (58%) as LMs on the basis of their histologic similarity with homologous human tumors. The GISTs occurred equally in males and females, with a mean age of 11 years (range 5–14 years). Five GISTs (24%) were associated with clinical signs and six (29%) had metastasis in liver or abdominal cavity. The GISTs occurred in large intestine (10, 48%), small bowel (six, 29%), stomach (four, 19%), and mesentery of small intestine (one, 5%). Histologically, they were highly cellular spindle, or less commonly epithelioid tumors with mitotic rates ranging from 0 to 19 per 10 HPF. Eleven tumors (52%) were positive for CD117 (KIT); seven (33%) were positive for smooth muscle actin but none for desmin and S-100 protein. Sequences of KIT exon 11, often mutated in human GISTs, were evaluated from four GISTs. Deletion of Try556-Lys557 coexisting with duplication of Gln555 in one case of GIST and T to C transition resulting in substitution of Pro for Leu575 in another were identified. The LMs occurred predominantly in males (82%) with a mean age of 11 years (range 8–17 years). Nine tumors (31%) had associated clinical signs. They occurred in the stomach (22, 76%), esophagus (four, 14%), and intestines (three, 10%); all were paucicellular, had no mitoses, and were composed of mature smooth muscle cells. Twenty-eight (97%) were positive for smooth muscle actin and 18(62%) for desmin but none for CD117 and S-100. Both GISTs and true LMs occur in the GI tract of dogs. Both tumors have distinctive pathologic features.

The hepatitis C virus core protein indirectly induces alpha-smooth muscle actin expression in hepatic stellate cells via interleukin-8

2010 ◽  
Vol 52 (5) ◽  
pp. 635-643 ◽  
Author(s):  
Sophie Clément ◽  
Stéphanie Pascarella ◽  
Stéphanie Conzelmann ◽  
Carmen Gonelle-Gispert ◽  
Kévin Guilloux ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Hepatitis C ◽  
Hepatic Stellate Cells ◽  
Core Protein ◽  
Smooth Muscle Actin ◽  
Stellate Cells ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Virus Core ◽  
Actin Expression

scholarly journals Effect of Caloric Restriction on Hepatic Sinusoidal System and Stellate Cells in Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Jian Chen ◽  
Kara King ◽  
Jian X. Zhang
Keyword(s):  
Smooth Muscle ◽  
Vitamin A ◽  
Caloric Restriction ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Cell Activity ◽  
Stellate Cells ◽  
Activity Level ◽  
Muscle Actin ◽  
Old Mice

Aging associated changes in liver include reduced hepatic blood flow, increased number of stellate cells, and collagen deposits in perisinusoidal space. We tested the possibility of mitigating these changes with caloric restriction. Two-month-old mice were subjected to 30 percent caloric restriction for 12 months and then examined for the effect of caloric restriction on the sinusoidal network, collagen deposition, and the number of stellate cells. Using intravital fluorescence microscopy, assessments were made on sinusoidal diameter, density, volumetric flow, perfusion index, and autofluorescence of vitamin A that was primarily stored with lipid droplets in stellate cells. A significant effect was observed in the vitamin A autofluorescence of stellate cells; stellate cell associated fluorescence was diminished in terms of number and size of fluorescent spots. Caloric restriction reduced collagen deposits in liver sections and lowered the gene expression ofα1-(I) collagen but notα-smooth muscle actin. No differences were detected in sinusoidal dimension measurements. Our results showed that caloric restriction was effective in ameliorating the increase in stellate cells and the mild fibrosis in old mice. However, caloric restriction had no impact on stellate cell activity level as indicated by the unaffectedα-smooth muscle actin expression.

Immunohistochemical Staining Characteristics of Canine Gastrointestinal Stromal Tumors

1997 ◽  
Vol 34 (4) ◽  
pp. 303-311 ◽  
Author(s):  
R. G. LaRock ◽  
P. E. Ginn
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Immunohistochemical Staining ◽  
Gastrointestinal Stromal Tumors ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Stromal Tumors ◽  
S 100 ◽  
Microscopic Features ◽  
Microscopic Diagnosis

Sections from 35 formalin-fixed, paraffin-embedded, canine gastrointestinal stromal tumors consisting of 14 leiomyomas (five stomach, three small intestine, two colon, four rectum), 18 leiomyosarcomas (one stomach, five small intestine, nine cecum, three rectum), two undifferentiated sarcomas (two stomach), and one neurofibrosarcoma (small intestine) were examined for the expression of vimentin, S-100 protein, α-smooth muscle actin, and desmin via immunoperoxidase methodology using an avidin-biotin complex technique. The leiomyomas were 4/14 (29%) vimentin-positive, 3/14 (21%) S-100 protein-positive, 10/14 (71%) α-smooth muscle actin-positive and 13/14 (93%) desmin-positive. Leiomyosarcomas were 18/18 (100%) vimentin-positive, 11/18 (61%) S-100 protein-positive, 9/18 (50%) α-smooth muscle actin-positive, and 15/18 (83%) desmin-positive. The undifferentiated sarcomas were 2/2 (100%) vimentin-positive, 2/2 (100%) S-100 protein-positive, 1/2 (50%) α-smooth muscle actin-positive, and 0/2 (0%) desmin-positive. The neurofibrosarcoma was vimentin and S-100 protein-positive and α-smooth muscle actin- and desmin-negative. Thirty-one of thirty-five (89%) of all neoplasms demonstrated reactivity for either desmin and/or α-smooth muscle actin. S-100 protein reactivity occurred in 17/35 (49%) of all specimens. Lack of desmin and α-smooth muscle actin reactivity occurred in 4/35 (11%) of all specimens, all of which were vimentin-positive. The immunohistochemical results indicate that the majority of canine gastrointestinal stromal tumors (GIST) with light microscopic features of smooth muscle cells have immunohistochemical staining patterns supporting smooth muscle differentiation. Vimentin reactivity correlated with a light microscopic diagnosis of malignancy. The lack of smooth muscle cell markers in some tumors and the high percentage of cases positive for S-100 protein may suggest a more complex histogenesis or differentiation for subgroups of these tumors.

scholarly journals Stellate cells in livers of dogs with portal vein hypoperfusion

2018 ◽  
Vol 74 (1) ◽  
pp. 6017-2018
Author(s):  
MAŁGORZATA SOBCZAK-FILIPIAK ◽  
JÓZEF SZAREK ◽  
MICHAŁ CZOPOWICZ ◽  
MAREK GALANTY ◽  
IZABELLA DOLKA ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Liver Fibrosis ◽  
Portal Vein ◽  
Lipid Droplets ◽  
Smooth Muscle Actin ◽  
Stellate Cells ◽  
Portosystemic Shunt ◽  
Muscle Actin ◽  
Healthy Dogs ◽  
Cytoplasmic Lipid Droplets

Hepatic stellate cells play a crucial role in the development of liver fibrosis. In a damaged liver, stellate cells undergo activation, which is manifested as a change of their phenotype: differentiation of stellate cells to myofibroblast-type cells, expression of alpha-Smooth Muscle Actin, their proliferation and a reduction in the size of cytoplasmic lipid droplets. The aim of this study was to determine the number and morphology of stellate cells in the canine liver affected by congenital portosystemic shunt (PSS) and portal vein hypoplasia – hepatic microvascular dysplasia (PVH-HMD). The material for investigation were archived paraffin blocks with liver samples collected supravitally from six dogs with PSS, six dogs with PVH-HMD and six healthy dogs. On the HE-stained sections, the number of stellate cells per 100 hepatocytes was counted (Sztark method) and the diameter of veins in the hepatic triads was measured (light microscope Olympus BX 43, SC30 camera, CellSens Entry 2011 Olympus). In addition, the diameter of lipid droplets in stellate cells was measured (computed image analysis system LUCIA 4.21). The results were analysed statistically (the Kruskal-Wallis test followed by Dunn’s post-hoc procedure; significance level (α) at 0.05; Statistica 12 StatSoft Inc.). The degree of liver fibrosis was determined (Masson’s method of slide stain; Scheuer scale). The liver samples from the dogs with PSS and PVH-HMD were stained immunohistochemically with Monoclonal Mouse Anti-Human Smooth Muscle Actin (α-SMA), clone 1A4, antibodies (DAKO). Portosystemic shunt and primary portal vein hypoplasia in the dog results in a reduction in the diameter of portal vein branches and in insufficient portal blood flow through the liver. In the material investigated, this was particularly evident in the animals affected by PSS: such dogs had a significantly smaller diameter of the veins than did the healthy dogs (p<0.001) or the dogs with PVH-HMD (p=0.023). Fibrosis and the expression of α-SMA were stronger in the dogs with PSS than in those with PVH-HMD. Moreover, the dogs with PSS had a significantly higher average number of stellate cells than the healthy animals (p=0.007) did. However, the examination of the material revealed an enlargement of cytoplasmic lipid droplets: the dogs with PSS had a significantly larger diameter of lipid vacuoles in the cytoplasm of stellate cells than did the healthy animals (p<0.001) or the dogs with PVH-HMD (p=0.043); the dogs with PVH-HMD had lipid droplets with a significantly larger diameter than the healthy animals (p<0.001) did. Hypoperfusion of the liver and the accompanying regressive lesions in hepatocytes result mainly in an increased number of stellate cells and stronger expression of α-SMA, while cytoplasmic lipid droplets in the stellate cells are not reduced in size. The present study indicates the need for detailed analyses of clinical cases and warrants further comprehensive studies of comparative hepatopathology because it demonstrates differences between humans and dogs in the morphological indicators of hepatic stellate cell activation in chronic liver damage.

scholarly journals Structural Changes and Detection of Liver Fibrosis–Related Protein Levels in Coculture of Alveolar Echinococcosis-Protoscoleces and Human Hepatic Stellate Cells

2021 ◽  
Author(s):  
DEping cao ◽  
Emad Shamsan ◽  
Bofan Jiang ◽  
Zhang Yaogang ◽  
Mustafa Abdo Saif Dehwah
Keyword(s):  
Smooth Muscle ◽  
Liver Fibrosis ◽  
Hepatic Stellate Cells ◽  
Structural Changes ◽  
Alveolar Echinococcosis ◽  
Smooth Muscle Actin ◽  
Stellate Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Muscle Actin ◽  
Related Protein

Abstract BackgroundEchinococcus multilocularis is a causative agent of human alveolar echinococcosis (AE). AE leads to cirrhosis in several organs, such as the liver, triggering severe conditions, including hepatic failure and encephalopathy. The main purpose of this study is to explore the interaction between treated hepatic stellate cells and AE-protoscoleces (AE-PSCs). The results of this study will be provided experimental basis for revealing the mechanisms of hepatic fibrosis after AE infection.MethodsWe investigated the role of alveolar echinococcosis-protoscoleces (AE-PSCs) in liver fibrosis and structural changes and liver fibrosis-related protein expression in a coculture of PSCs and human hepatic stellate cells (HSCs). Structural changes were detected by transmission electron microscopy, whereas liver fibrosis-related proteins, collagen I, alpha-smooth muscle actin, and osteopontin levels were measured by western blotting and enzyme-linked immunosorbent assay. ResultsPSCs exhibited morphological changes, specifically changes in shape, and showed slight changes in the cytoplasmic membrane, whereas structural modifications were observed in HSCs. Additionally, western blotting and enzyme-linked immunosorbent assay revealed that PSCs treated in vitro with HSC-LX2 showed significantly increased collagen-Ⅰ, α-smooth muscle actin, and osteopontin expression levels after 3–4 days of incubation in a coculture system. AE-PSCs induced liver fibrosis by inducing extracellular matrix expression and HSC activation.ConclusionsThese results provide insight into the pathogenesis of echinococcosis- induced hepatic fibrosis and introduce therapeutic targets and diagnostic criteria for managing echinococcosis-dependent liver fibrosis.

c-Myb modulates transcription of the α-smooth muscle actin gene in activated hepatic stellate cells

2000 ◽  
Vol 278 (2) ◽  
pp. G321-G328 ◽  
Author(s):  
Martina Buck ◽  
Dong Joon Kim ◽  
Karl Houglum ◽  
Tarek Hassanein ◽  
Mario Chojkier
Keyword(s):  
Smooth Muscle ◽  
Hepatic Stellate Cells ◽  
Cell Activation ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Stellate Cells ◽  
Dominant Negative ◽  
Muscle Actin ◽  
Muscle Actin Gene ◽  
High Level

Expression of α-smooth muscle actin (α-SMA) defines the phenotype of activated (myofibroblastic) hepatic stellate cells. These cells, but not quiescent stellate cells, have a high level of α-SMA and c-Myb expression, as well as increased c-Myb-binding activities to the proximal α-SMA E box. Therefore, we analyzed the role of c-Myb in α-SMA transcription and stellate cell activation. Activated primary rat stellate cells displayed a high expression of the −724 and −271 α-SMA/luciferase (LUC) chimeric genes, which contain c-Myb binding sites (−223/−216 bp). α-SMA/LUC minigenes with mutation (−219/−217 bp), truncation (−224 bp), or deletion (−191 bp) of the c-Myb binding site were not efficiently transcribed. Transfection of wild-type c-Myb into quiescent stellate cells, which do not express endogenous c-Myb, induced a ∼10-fold stimulation of −724 α-SMA/LUC expression. Conversely, expression of either a dominant-negative c-Myb basic domain mutant (Cys43 → Asp) or a c-Myb antisense RNA blocked transcription from the −724 α-SMA/LUC or −271 α-SMA/LUC in activated cells. Moreover, transfection of c- myb antisense, but not sense, RNA inhibited both expression of the endogenous α-SMA gene and stellate cell activation, whereas transfection of c- myb stimulated α-SMA expression in quiescent stellate cells. These findings suggest that c-Myb modulates the activation of stellate cells and that integrity of the redox sensor Cys43in c-Myb is required for this effect.

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