Collagen type IV, laminin, α-smooth muscle actin (αSMA), α1 and α6 integrins expression in the liver with metastases from malignant gastrointestinal tumours

Feline ocular sarcomas are malignant intraocular neoplasms that are frequently associated with a history of ocular trauma. They usually present as fibrosarcomas, but some have both epithelial and mesenchymal features. The purpose of this study was to determine the cell of origin of a subset of feline intraocular sarcomas that display a mixed epithelial-mesenchymal phenotype, with elaboration of basement membrane—type matrix. We examined the morphology and histochemical and immunohistochemical phenotypes of nine feline intraocular sarcomas. Immunohistochemistry and in situ hybridization were performed to detect expression of crystallin alpha A. In addition, tumors were examined for expression of vimentin, cytokeratin, smooth muscle actin, desmin, melan A, neural cell adhesion molecule, S-100, glial fibrillary acidic protein, nerve growth factor receptor, and collagen type IV. Animals ranged from 7 to 17 years of age—no breed or sex predilection for tumor occurrence was present. Tumors were characterized by mixed epithelial and mesenchymal phenotypes, both of which elaborated basement membrane-type material and expressed vimentin highly. On the basis of collagen type IV and crystallin alpha A immunopositivity, we established that three of nine tumors were of lens epithelial origin. Expression of desmin and smooth muscle actin identified one tumor as a leiomyosarcoma. The remainder were undifferentiated sarcomas of myofibroblastic origin. This is the first report of lens epithelial neoplasia in clinical material from any species. The history and morphologic features of feline ocular sarcomas are reminiscent of feline vaccine-induced sarcomas. These tumors may share pathophysiologic similarities unique to this species.

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Immunohistochemical Localization of Collagen Type III and Type IV, Laminin, Tenascin and α-Smooth Muscle Actin (αSMA) in the Human Liver in Peliosis

Pathology - Research and Practice ◽

10.1078/0344-0338-00339 ◽

2002 ◽

Vol 198 (12) ◽

pp. 803-812 ◽

Cited By ~ 12

Author(s):

Maya Gulubova

Keyword(s):

Smooth Muscle ◽

Human Liver ◽

Collagen Type ◽

Smooth Muscle Actin ◽

Immunohistochemical Localization ◽

Muscle Actin ◽

Collagen Type Iii ◽

Type Iii ◽

Type Iv

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Liraglutide suppresses production of extracellular matrix proteins and ameliorates renal injury of diabetic nephropathy by enhancing Wnt/β-catenin signaling

AJP Renal Physiology ◽

10.1152/ajprenal.00128.2020 ◽

2020 ◽

Vol 319 (3) ◽

pp. F458-F468 ◽

Cited By ~ 3

Author(s):

Linjing Huang ◽

Tingting Lin ◽

Meizhen Shi ◽

Xiuqing Chen ◽

Peiwen Wu

Keyword(s):

Diabetic Nephropathy ◽

Collagen Type ◽

Mesangial Cells ◽

Smooth Muscle Actin ◽

Diabetic Rats ◽

Collagen Type Iv ◽

Signaling Proteins ◽

Muscle Actin ◽

Type Iv

The Wnt/β-catenin signaling pathway is involved in production of the extracellular matrix (ECM) by mesangial cells (MCs). Recent studies by us and others have demonstrated that glucagon-like peptide-1 receptor agonists (GLP-1RAs) have protective effects against diabetic nephropathy. The purpose of the present study was to investigate whether the Wnt/β-catenin signaling in MCs contributes to GLP-1RA-induced inhibition of ECM accumulation and mitigation of glomerular injury in diabetic nephropathy. In cultured human mesangial cells, liraglutide (a GLP-1RA) treatment significantly reduced high glucose (HG)-stimulated production of fibronectin, collagen type IV, and α-smooth muscle actin, and the liraglutide effects were significantly attenuated by XAV-939, a selective inhibitor of Wnt/β-catenin signaling. Furthermore, HG treatment significantly decreased protein abundance of Wnt4, Wnt5a, phospho-glycogen synthase kinase-3β, and β-catenin. These HG effects on Wnt/β-catenin signaling proteins were significantly blunted by liraglutide treatment. For in vivo experiments, we administered liraglutide (200 μg·kg−1·12 h−1) by subcutaneous injection to streptozocin-induced type 1 diabetic rats for 8 wk. Administration of liraglutide significantly improved elevated blood urine nitrogen, serum creatinine, and urinary albumin excretion rate and alleviated renal hypertrophy, mesangial expansion, and glomerular fibrosis in type 1 diabetic rats, whereas blood glucose level and body weight did not have significant changes. Consistent with the in vitro experiments, liraglutide treatment significantly reduced the diabetes-induced increases in glomerular fibronectin, collagen type IV, and α-smooth muscle actin and decreases in glomerular Wnt/β-catenin signaling proteins. These results suggest that liraglutide alleviated glomerular ECM accumulation and renal injury in diabetic nephropathy by enhancing Wnt/β-catenin signaling.

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Cyclic Mechanical Stretch Induced Smooth Muscle Cell Changes in Cerebral Aneurysm Progress by Reducing Collagen Type IV and Collagen Type VI Levels

Cellular Physiology and Biochemistry ◽

10.1159/000487347 ◽

2018 ◽

Vol 45 (3) ◽

pp. 1051-1060 ◽

Cited By ~ 7

Author(s):

Peixi Liu ◽

Yaying Song ◽

Yingjie Zhou ◽

Yingjun Liu ◽

Tianming Qiu ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Collagen Type ◽

Cerebral Aneurysms ◽

Muscle Cells ◽

Mechanical Stretch ◽

Collagen Type Iv ◽

Type Iv

Background/Aims: Cerebral aneurysm growth is characterized by continuous structural weakness of local smooth muscle cells, though the mechanism is unclear. In this study, we examine protein changes in cerebral aneurysm and human brain vascular smooth muscle cells after cyclic mechanical stretch. We further explore the relationship between the smooth muscle cell changes and reductions in the levels of collagen types IV and VI. Methods: Saccular cerebral aneurysms (n=10) were collected, and temporal artery samples were used as controls. Quantitative proteomics were analyzed and histopathological changes were examined. Smooth muscle cells were cultured in a flexible silicone chamber and subjected to 15% cyclic mechanical stretch. The effect of stretch on the cell viability, function, gene and protein expression were further studied for the understanding the molecular mechanism of aneurysm development. Results: Proteomics analysis revealed 92 proteins with increased expression and 88 proteins with decreased expression compared to the controls (p<0.05). KEGG pathway analysis showed that the change in focal adhesion and extracellular matrix-receptor interaction, suggesting the involvement of collagen type IV and VI. The aneurysm tissue exhibited fewer smooth muscle cells and lower levels of collagen type IV and VI. Human brain vascular smooth muscle cell culture showed spindle-like cells and obvious smooth muscle cell layer. Cell proteomics analysis showed that decreased expression of 118 proteins and increased expression of 32 proteins in smooth muscle cells after cyclic mechanical stretch. KEGG pathway analysis indicated that focal adhesion and ECM-receptor interaction were involved. After cyclic mechanical stretch, collagen type IV and IV expression were decreased. Moreover, the stretch induced MMP-1 and MMP-3 expression elevation. Conclusion: We demonstrated that collagen type IV and VI were decreased in cerebral aneurysms and continuous cyclic mechanical stretch induced smooth muscle cell changes. Smooth muscle cell protection provides an additional therapeutic option to prevent the growth of cerebral aneurysms.

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Fibronectin and the basement membrane components laminin and collagen type IV influence the phenotypic properties of subcultured rat aortic smooth muscle cells differently

Cell and Tissue Research ◽

10.1007/s004410050089 ◽

1994 ◽

Vol 276 (2) ◽

pp. 263-271 ◽

Cited By ~ 7

Author(s):

Johan Thyberg ◽

Anna Hultgurdh-Nilsson

Keyword(s):

Smooth Muscle ◽

Basement Membrane ◽

Smooth Muscle Cells ◽

Collagen Type ◽

Collagen Type Iv ◽

Phenotypic Properties ◽

Aortic Smooth Muscle ◽

Type Iv ◽

Membrane Components ◽

Basement Membrane Components

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Stereotactic Radiosurgery of the Rete Mirabile in Swine: A Longitudinal Study of Histopathological Changes

Neurosurgery ◽

10.1227/01.neu.0000197335.93538.bd ◽

2006 ◽

Vol 58 (3) ◽

pp. 551-558 ◽

Cited By ~ 10

Author(s):

Reza Jahan ◽

Timothy D. Solberg ◽

Daniel Lee ◽

Paul Medin ◽

Satoshi Tateshima ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Stereotactic Radiosurgery ◽

Collagen Type ◽

Muscle Cells ◽

Collagen Type Iv ◽

Histopathological Changes ◽

Rete Mirabile ◽

Type Iv

Abstract OBJECTIVE: Stereotactic radiosurgery is an established, effective treatment for brain arteriovenous malformations. The mechanisms of vessel occlusion in arteriovenous malformations has not been extensively evaluated. To better understand these mechanisms, we report histopathological changes in the swine rete mirabile after stereotactic radiosurgery. METHODS: Thirty-five swine were used, 15 as nonradiated controls and 20 as radiated. Two in the control group and five in the radiated group were sacrificed before the study endpoint. Tissue was obtained from 13 nonradiated (4 at 3 mo, 5 at 6 mo, 4 at 9 mo) and 15 radiated swine (2 at 3 mo, 3 at 6 mo, 10 at 9 mo) for histological, immunohistochemical, and morphometric analysis. RESULTS: Radiated vessels showed increasing intimal hyperplasia over the follow-up period. Histometrical analysis confirmed this with evidence of progressive luminal narrowing over the follow-up period. Immunohistochemical analysis showed intimal cells to be proliferating smooth muscle cells with surrounding extracellular collagen Type IV. Adventitial fibrosis composed of collagen Type IV was also seen with smooth muscle cells interspersed within the collagen matrix. The nonradiated animals showed no intimal hyperplasia or change in the appearance or size of the vessels over the same follow-up period. Adventitial fibrosis was minimal in the nonradiated animals. CONCLUSION: The vessels show an intimal response to radiation with progressive occlusion caused by migrating, proliferating smooth muscle cells, a likely source of the extracellular collagen in the intima. Cytokine mediated pathways likely produce these morphological changes. Future studies will be directed toward elucidating these underlying molecular mechanisms.

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