Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q16637 (SMA)
 8,107 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the characteristics of the mesenchymal cells of ameloblastic fibrosarcoma (AFS), three cases of AFS were studied immunohistochemically and ultrastructurally. The results showed that the mesenchymal component of AFS consisted predominantly of fibroblastic cells with a small number of undifferentiated cells, a few histiocytes and occasionally myofibroblastic cells under electron microscope. The fibroblastic cells were Vimentin positive only, and myofibroblastic cells were positive for Vimentin, HHF35 and alpha-SMA. The histiocytes were positive both for kp1 and PG-M1, suggesting that these cells were infiltrating cells from peripheral blood rather than histiocytic differentiation of tumor cells. Compared with ameloblastic fibroma, AFS showed much higher PCNA labeling index, suggesting higher proliferation activity of AFS.
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PMID:[Ameloblastic fibrosarcoma: an immunohistochemical and ultrastructural study of the mesenchymal component]. 1221 96

Three canine osteosarcoma cell lines were established from spontaneous pelvic and radial osteosarcomas. The cell populations cultured exhibited characteristics of malignancy and consisted of adherent, pleomorphic, mostly large spindle-shaped or polyhedral cells, characterised by the presence of numerous cytoplasmic granules and vacuoles. The main ultrastructural features included the presence of abundant rough endoplasmic reticulum and numerous cytoplasmic vesicles, deposit vacuoles and small cytoplasmic protrusions. Zymography showed that the cell lines produce high levels of MMP-2 and MMP-9, enzymes directly involved in crucial aspects of the metastatic process. Consistent with their osteoblastic lineage and malignant phenotype, all cell lines were immunoreactive to vimentin, osteopontin, PCNA, p53, MMP-2 and MMP-9, while they were negative for cytokeratin, desmin, SMA, Factor VIII, NSE, GFAP, Rb and p21 protein. No retroviral particles or RNA were detected ultrastructurally or with RT-PCR, although the possibility of viral involvement in osteosarcoma cannot be excluded. The new cell lines provide excellent in vitro models that may allow further studies on the pathobiology of canine osteosarcoma to be undertaken.
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PMID:Characterisation of three novel canine osteosarcoma cell lines producing high levels of matrix metalloproteinases. 1519 3

Tonsillectomy often improves clinical features in immunoglobulin A nephropathy (IgAN), however, the mechanisms mediating clinical modifications are unclear. In the present study, we examined the immunohistological alterations in biopsy specimens obtained from IgAN patients before and after tonsillectomy. We investigated eight IgAN patients who underwent repeated renal biopsy in the present study. Immunohistochemistry for alpha-smooth muscle actin (alpha-SMA), CD68 and proliferating cell nuclear antigen (PCNA) were performed and histological findings were compared before and after tonsillectomy. None of the patients were treated with steroids or immunosuppressive drugs before second renal biopsy. The expression of alpha-SMA and the number of CD68 positive cells were significantly decreased in IgAN patients with improvement of proteinuria and hematuria after tonsillectomy. The degree of mesangial cell proliferation, expansion of mesangial area and the number of PCNA positive cells were not changed after tonsillectomy. These results suggest that the reduced number of activated mesangial cells and macrophages may be involved in the improvement of hematuria after tonsillectomy. They also suggest that tonsillectomy may improve proteinuria and hematuria in some patients with IgAN through reduction of mesangial cell activation and macrophage infiltration.
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PMID:Clinical and immunohistochemical study of immunoglobulin A nephropathy (IgAN) before and after tonsillectomy. 1576 92

Cystadenoma and cystadenocarcinoma of the salivary glands are rare tumors, approximately half of cases being diagnosed at the level of parotid. The studied tumor associated both benign and malign zones, with deep infiltrating character in the adjacent structures. In both areas the growing pattern was predominantly cystic and papillary, and the proliferated neoplastic cells were majority cubical or columnar, with low grade of nuclear pleomorphism in the becoming malign areas, discordant with the infiltrative character of the neoplasm. Immunohistochemically, we investigated the tumor with AE1-AE3, CEA, SMA, S-100 and PCNA.
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PMID:Histopathologic and immunohistochemical study in one case of cystadenoma of parotid gland becoming malignant. 1584 90

Although leptin is a key adipokine promoting liver fibrosis, adiponectin may prevent liver injury. To determine the role of these adipokines in liver fibrosis and to understand their expression in vivo, fa/fa rats and their lean littermates were subjected to bile duct ligation (BDL). Histomorphometry for collagen and alpha-smooth muscle actin (alpha-SMA) revealed that lean rats, but not fa/fa littermates, had significant fibrosis with abundant hepatic stellate cell (HSC) activation. The lean-BDL rats had significantly higher leptin concentrations in the hepatic vein than lean sham-operated, fa/fa BDL, or fa/fa sham-operated rats. Co-localization of leptin and alpha-SMA in activated HSCs was observed by immunohistochemistry. Real-time reverse transcriptase-polymerase chain reaction and Western blot analysis confirmed the presence of leptin and alpha-SMA in activated, but not quiescent, HSCs, whereas only quiescent HSCs synthesized adiponectin mRNA and protein. Adiponectin overexpression in activated HSCs reduced proliferation, augmented apoptosis, and reduced expression of alpha-SMA and proliferating cell nuclear antigen. Adiponectin receptors (AdipoR1 and AdipoR2) were detected in both activated and quiescent HSCs, but only activated HSCs produced significant apoptosis after treatment with either globular or full-length adiponectin. Adiponectin may act to reverse HSC activation, maintain HSC quiescence, or significantly, may have important therapeutic implications in liver fibrosis.
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PMID:The roles of leptin and adiponectin: a novel paradigm in adipocytokine regulation of liver fibrosis and stellate cell biology. 1592 Jan 51

This case report describes a rare case of canalicular adenoma arising in the upper lip of a 61-year-old male patient. Macroscopic examination of the tumor revealed a well-defined, smooth, firm, elastic hard, round nodule with a diameter of 1.0 cm. The cut surface was white. Histopathology showed that the tumor was an encapsulated mass with a complex cellular pattern of anastomosing duct-like or trabecular structures lined by a single layer of tall columnar epithelial cells, which were embedded in a loose, fibrous, and highly vascular connective tissue stroma. The tumor cells were immunoreactive to AE1/AE3, CK19 and S-100, were partially positive for CK7, CK8, GFAP and PCNA, but were negative for SMA, CK13, CK14 and vimentin.
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PMID:Canalicular adenoma arising in the upper lip: review of the pathological findings. 1596 Jan 60

The antifibrotic effects of the peptide hormone relaxin on cardiac and renal fibrosis were studied in 9- to 10-month-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Rats (n=8 to 9 per group) were allocated into 3 groups: WKY controls, vehicle-treated SHR (SHR-V), and relaxin-treated SHR (SHR-R). Relaxin (0.5 mg/kg per day) was administered via subcutaneously implanted osmotic mini-pumps over 2 weeks before hearts and kidneys were harvested for analysis. Collagen content was analyzed by hydroxyproline assay, gel electrophoresis, and quantitative histology. Zymography was used to determine matrix metalloproteinase (MMP) expression and Western blotting to determine proliferating cell nuclear antigen (PCNA) expression and alpha-smooth muscle actin (alpha-SMA)/myofibroblast expression, whereas cardiac hypertrophy was assessed by myocyte size and real-time polymerase chain reaction of associated genes. The left ventricular (LV) myocardium of SHR-V contained increased collagen levels (by 25+/-1%, P<0.01 using biochemical analysis and 3-fold; P<0.01 using quantitative histology), enhanced expression of PCNA (by 70+/-8%; P<0.01), alpha-SMA (by 32+/-2%; P<0.05), and the collagen-degrading enzyme MMP-9 (by 70+/-6%; P<0.05) versus respective levels measured in WKY controls. The kidneys of SHR-V also contained increased collagen (25+/-2%, P<0.05 using biochemical analysis and 2.4-fold; P<0.01 using quantitative histology). Relaxin treatment significantly normalized collagen content in the LV (P<0.01) and kidney (P<0.05), completely inhibited cell proliferation (P<0.01) and fibroblast differentiation (P<0.05) in the LV, and increased MMP-2 expression (by 25+/-1%; P<0.05) without affecting MMP-9 in the LV compared with that measured in SHR-V. Thus, relaxin is a potent antifibrotic hormone with a rapid-occurring efficacy that may have therapeutic potential for hypertensive disease.
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PMID:Relaxin reverses cardiac and renal fibrosis in spontaneously hypertensive rats. 1596 69

Intracellular signaling mechanisms regulating the turnover of alpha-SMA-positive myofibroblasts (myoFbs) at the site of myocardial infarction (MI) are poorly understood. Y-Box (YB)-1, a multifunctional protein, may be involved in regulation of proliferation, migration and apoptosis of myoFbs. Our objective was to study the expression of YB-1 in the infarcted rat heart and its localization in myoFbs. On days 3-28 following MI, we monitored YB-1 expression and its colocalization with alpha-SMA, and proliferation markers PCNA and Ki-67 in infarcted tissue by Western blot, immunohistochemistry, and immunofluorescent double-labeling. YB-1 is barely detectable in normal myocardium. At the infarct site, however, YB-1 is markedly elevated from day 3 post-MI concomitant with the induction of cell proliferation. MyoFbs are the major source of YB-1 and retain it up to day 28 post-MI. We suggest early expression of YB-1 promotes proliferation and migration of myoFbs, whereas prolonged expression may be responsible for scar formation.
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PMID:Expression of the multifunctional Y-box protein, YB-1, in myofibroblasts of the infarcted rat heart. 1600 47

This study compares the populations of liver mesenchymal cells (LMCs) and their proliferative activity in schistosomal periportal fibrosis and in hepatitis C virus-induced cirrhosis. LMCs were evaluated by immunohistochemical double staining for proliferating cell nuclear antigen (PCNA) and alpha-smooth muscle actin (alpha-SMA) or glial fibrillary acid protein (GFAP) in liver biopsies from humans with schistosomal fibrosis (n=40), hepatitis C virus-induced cirrhosis (n=20), and normal controls (n=20). The number of LMCs was found to be higher in schistosomal fibrosis than in the normal liver, but lower than in cirrhosis. alpha-SMA- and GFAP-positive cells were increased in both diseases, but more so in cirrhosis. In cirrhotic liver, alpha-SMA-positive cells were highly predominant in relation to GFAP-positive cells. However, there was an inverted ratio between these cells in schistosomiasis as compared to cirrhosis. The PCNA labeling index was higher in alpha-SMA-positive cells than in GFAP-positive cells, and did not differ between pipe-stem fibrosis and liver cirrhosis regarding alpha-SMA- or GFAP-positive cells. The predominance of GFAP-positive cells observed in schistosomiasis suggests that hepatic stellate cells (HSCs) have a major role in connective tissue deposition in the human schistosomal liver. On the other hand, the smaller number of LMCs in schistosomal fibrosis in comparison to liver cirrhosis may be related to mild and limited injury due to the schistosomal egg-induced inflammatory response. The granulomatous inflammation around Schistosoma mansoni eggs appears to mobilize and activate a reduced number of mesenchymal cells in comparison to the scattered necro-inflammatory reaction produced by the hepatitis C virus.
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PMID:Hepatic stellate cells in human schistosomiasis mansoni: a comparative immunohistochemical study with liver cirrhosis. 1647 18

We have previously shown that VEGF165 gene delivery into ischemic skeletal muscle exerts not only proangiogenic, but also remarkable antiapoptotic and proregenerative activity. The aim of this study was to determine whether recombinant adeno-associated virus (rAAV)-mediated gene delivery of VEGF165 into cardiac muscle, during acute myocardial infarction, exerts a protective effect to promote long-term functional recovery. Acute infarction of the anterior LV wall was induced in 12 chronically instrumented dogs by permanent occlusion of the LAD coronary artery. Four hours after occlusion, rAAV-VEGF165 or rAAV-LacZ (n=6 each; 5x10(12) viral particles per animal) was directly injected with an echo-guided needle into the dysfunctional cardiac wall. LV and arterial pressure, dP/dtmax, and ejection fraction were not significantly different between the two groups over time. In contrast, in the infarcted region, at four weeks after infarction, fractional shortening was 75+/-18% and -3+/-15% of baseline and length-pressure area was 54+/-15% and 0.8+/-15% of baseline in VEGF165 versus LacZ, respectively (P<0.05). Histological analysis of the border regions showed a marked increase in the number of alpha-SMA-positive arterioles (68+/-2.8 versus 100+/-3.8 vessels per microscopic field in LacZ and VEGF165 group, respectively; P<0.05). In both groups, the receptor VEGFR-2 was diffusely expressed on the surviving cardiomyocytes and, consistently, myocardial viability was significantly improved in the VEGF165-treated group, with several troponin T-expressing cardiomyocytes displaying nuclear positivity for the proliferation marker PCNA. Altogether, our results indicate that VEGF165 gene delivery exerts a marked beneficial action by enhancing both arteriologenesis and cardiomyocyte viability in infarcted myocardium.
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PMID:Adeno-associated virus-mediated transduction of VEGF165 improves cardiac tissue viability and functional recovery after permanent coronary occlusion in conscious dogs. 1733 32


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