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 assess the nutritional status of the patients with esophageal cancer, we measured the areas of sternocleidomastoid and rectus abdominis muscles (SMA, RAMA) on real time ultrasound imaging and calculated muscle index (MI = (SMA+RAMA/Height)). Eighty-three patients with esophageal cancer were included in the present study. Preoperatively, significant Spearman's coefficients were found between MI and the percentage of standard arm circumference (R = 0.52) and between MI and the percentage of standard arm muscle circumference (R = 0.51). Postoperatively, patients with wide muscle area showed high values of prealbumin, transferrin and fibronectin. To study the changes after surgery, we also measured the area of quadriceps muscle in patients with esophageal cancer. The areas of quadriceps muscle in patients with dysphagia were much diminished than in those without dysphagia. Measurement of areas of muscles such as SMA, RAMA and quadriceps muscle was proved to be a useful procedure in evaluating the nutritional status of patients with esophageal cancer.
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PMID:[Evaluation of nutritional status in patients with esophageal cancer by measurement of sternocleidomastoid, rectus abdominis and quadriceps muscles on ultrasound imaging]. 138 59

We have studied the sequential morphological changes that took place in the kidneys of 8 rats with nephrotoxic serum nephritis (NTN). Rats underwent kidney biopsies at different time intervals (days 7, 15, 30, 90 and 120). The tissues were processed for light microscopy as well as immunohistochemistry for inflammatory cellular infiltrate as well as for the components of the extracellular matrix (ECM) and myofibroblasts (cells expressing alpha-smooth muscle actin, alpha-SMA). Nephrotic rats developed severe proteinuria, impaired renal function as well as progressive renal scarring. However, the natural history of NTN was heterogeneous with some rats recovering (n = 5) and other progressing to end-stage renal failure (n = 3). The heterogeneous nature of the glomerulonephritis has established that those with a good outcome had a stabilisation, with some resolution, of the deposited ECM and of the scarring process. By contrast, rats with a poor outcome had a progressive increase in glomerular as well as interstitial ECM. Cells expressing alpha-SMA (myofibroblasts) were detected in the glomeruli as well as in the interstitium of nephritic rats. Changes in the expression of cells expressing alpha-SMA paralleled those of the components of the ECM in particular fibronectin. alpha-SMA immunostain was the best predictor of progression. Early glomerular alpha-SMA immunostain (days 7 and 30) was a strong predictor of the subsequent development of glomerulosclerosis and renal dysfunction. The predictive value of interstitial alpha-SMA immunostain on days 7 for subsequent tubulo-interstitial scarring and renal insufficiency was also strong and exceeded that of other histological or immunohistochemical parameters of scarring. This study establishes the natural history of experimental renal scarring and identifies a renal cell type, the myofibroblast, as a useful marker of progression. It also suggests a role for myofibroblasts in the progression of glomerulosclerosis and tubulo-interstitial fibrosis.
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PMID:Myofibroblasts and the progression of experimental glomerulonephritis. 758 53

Autoimmune myocarditis is considered to play a major role in the pathogenesis of dilated cardiomyopathy. A new autoimmune myocarditis model was attained by repeated immunization using murine cardiac C-protein with the immunological adjuvant, Klebsiella pneumoniae O3 lipopolysaccharide. For further analysis of a pathological epitope, the cDNA encoding C-protein was isolated; a fusion protein encoded by part of this cDNA induced myocarditis in SMA mice as well as in three other strains: DBA/1J (H-2q), O20/A (H-2pz1), and SJL (H-2s). The nucleotide sequence and its deduced amino acid analysis revealed that this protein had immunoglobulin-like and fibronectin-like repeats. This study provides a new animal model of autoimmune myocarditis which may shed light on the pathogenesis of dilated cardiomyopathy.
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PMID:Autoimmune myocarditis induced in mice by cardiac C-protein. Cloning of complementary DNA encoding murine cardiac C-protein and partial characterization of the antigenic peptides. 808 44

Interferon gamma (IFN-gamma) inhibits in vitro the activation of hepatic stellate cells (HSC), the primary extracellular matrix-producing cells in liver fibrosis. This study was undertaken to determine in vivo the effect of IFN-gamma in the rat model of liver fibrosis induced by dimethylnitrosamine (DMN), where HSC activation represents an early response to cell injury. Rats were killed after 1 or 3 weeks of treatment with DMN, IFN-gamma, DMN + IFN-gamma, or saline. Immunohistochemistry was used to identify proliferating (desmin-positive/bromodeoxyuridine (BrdU)-positive cells) and activated (alpha-smooth-muscle actin [alpha-SMA]-positive cells) HSCs. Collagen deposition was determined colorimetrically and by morphometry. The parenchymal extension of desmin- and actin-positive cells and of fibrotic tissue was measured by point-counting technique and expressed as a percentage of area. Western blot was used to determine laminin and fibronectin accumulation. The levels of messenger RNA (mRNA) for procollagen type I, fibronectin, and laminin were evaluated by Northern blot. No differences were observed in rats treated with either saline or IFN-gamma alone. IFN-gamma reduced HSC activation induced by liver injury, as shown by the decreased number of proliferating HSC and the reduction of parenchymal area occupied by alpha-SMA-positive cells observed in DMN + IFN-gamma-treated animals compared with the DMN group. This was associated with reduced collagen, laminin, and fibronectin accumulation and lower levels of mRNA for procollagen type I, fibronectin, and laminin in the DMN + IFN-gamma group. Thus, this study indicates that IFN-gamma reduces extracellular matrix deposition in vivo by inhibition of HSC activation.
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PMID:Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis. 862 Nov 53

Adherent cells derived from human palatine tonsils were isolated and cultivated. Exponentially growing adherent cells (TAC) were observed by phase-contrast microscopy and transmission electron microscopy. Immunocytochemical studies were also performed. TAC were composed of relatively monotonous cells with polygonal or spindle shapes and high proliferative activity. In addition to the development of rough endoplasmic reticulum and lysosomes, the TAC possessed a moderate amount of pinocytotic vesicles and a few microfilaments. All of the TAC strongly expressed fibroblastic markers and partial monocyte/macrophage markers, such as beta-subunit of prolyl 4-hydroxylase (DAKO-fibroblast), lysozyme, anti-alpha-1-antichymotrypsin (alpha ACT), and CD68 (KP-1, EBM/11). It was noted that, as the TAC were cultured for a longer period, they gradually increased the reactivity with the monoclonal antibody PG-M1. Furthermore, the TAC expressed myocytic phenotype, such as alpha-smooth muscle actin (alpha SMA) with various intensity. Moreover, as to extracellular matrix, TAC stained for collagen type I, collagen type III, laminin, and fibronectin. Collagen type IV was weakly positive. The results presented here showed that the TAC expressed three different phenotypes of fibroblasts, histiocytes and smooth muscle cells at the same time. The monoclonal antibody raised against the TAC reacted strongly with the subendothelial pericytes and/or smooth muscle cells in the extrafollicular area in human tonsils. The present results also suggested that the origin of the TAC was probably subendothelial pericytes and/or smooth muscle cells of the microvasculatures in the tonsil.
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PMID:Co-expression of fibroblastic, histiocytic and smooth muscle cell phenotypes on cultured adherent cells derived from human palatine tonsils: a morphological and immunocytochemical study. 880 95

To provide a better understanding of the role of fibroblastic cells during corneal wound-healing, we examined the expression of cytoskeleton components (i.e. smooth muscle alpha-actin (alpha-SMA), vimentin, desmin), adherens molecules (vinculin and talin) and cellular fibronectin in alkali-burned and lacerated rabbit corneas. Alkali-burned and lacerated corneas, which had healed for various periods of time (1 day to 45 days), were excised and subjected to immunohistochemical studies with monoclonal antibodies against alpha-SMA, vimentin, desmin, vinculin, talin and cellular fibronectin. Monoclonal antibody against alpha-SMA reacted with fibroblastic cells in injured corneas but did not react with keratocytes in normal corneas. Anti-desmin antibody did not react with any corneal cells in normal or injured corneas except the muscle cells in the newly-formed capillary of injured corneas. The results indicate that the fibroblastic cells in injured corneas have the characteristics of myofibroblasts. The number of myofibroblasts in granulation tissues increased and peaked within 3 weeks of injury and then declined. Electron microscopy revealed that some fibroblastic cells in the lacerated cornea which had healed for 4 weeks contained dense chromatins. In situ 3'-end labeling with terminal nucleotide transferase indicating that some of the fibroblastic cells contained nicked genomic DNA. These observations imply that apoptosis plays a role in regulating the number of myofibroblasts in the injured corneas. Antibodies against cellular fibronectin, vinculin and talin react with the fibroblastic cells in the injured corneas, but not with the keratocytes of normal corneas. Examination with transmission electron microscopy demonstrated the presence of microtendon and fibronexis associated with fibroblastic cells and the presence of stress fiber within fibroblastic cells. The results indicate that the fibroblastic cells may cause corneal wound contraction, which in turn contributes to the formation of opaque scar tissues.
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PMID:Dynamics of the expression of cytoskeleton components and adherens molecules by fibroblastic cells in alkali-burned and lacerated corneas. 949 55

In this study we examined if an association exists between expression of an alternatively spliced "embryonic" fibronectin isoform EIIIA (Fn-EIIIA) and alpha-smooth muscle actin (alpha-SMA) in the maturing and adult rat kidney and in two unrelated models of glomerular disease, passive accelerated anti-glomerular basement membrane (GBM) nephritis and Habu venom (HV)-induced proliferative glomerulonephritis, using immunohistochemistry and in situ hybridization. Fn-EIIIA and alpha-SMA proteins were abundantly expressed in mesangium and in periglomerular and peritubular interstitium of 20-day embryonic and 7-day (D-7) postnatal kidneys in regions of tubule and glomerular development. Staining was markedly reduced in these structures in maturing juvenile (D-14) kidney and was largely lost in adult kidney. Expression of Fn-EIIIA and alpha-SMA was reinitiated in the mesangium and the periglomerular and peritubular interstitium in both models and was also observed in glomerular crescents in anti-GBM nephritis. Increased expression of Fn-EIIIA mRNA by in situ hybridization corresponded to the localization of protein staining. Dual labeling experiments verified co-localization of Fn-EIIIA and alpha-SMA, showing a strong correlation of staining between location and staining intensity during kidney development, maturation, and disease. Expression of EIIIA mRNA corresponded to protein expression in developing and diseased kidneys and was lost in adult kidney. These studies show a recapitulation of the co-expression of Fn-EIIIA and alpha-SMA in anti-GBM disease and suggest a functional link for these two proteins.
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PMID:Expression of embryonic fibronectin isoform EIIIA parallels alpha-smooth muscle actin in maturing and diseased kidney. 1033 Apr 55

The extended exposure of proteins to reducing sugars leads to nonenzymatic glycation with the accumulation of advanced glycation end products (AGEs). Long-lived proteins, such as collagen and crystallins, are subjected to this modification, and are implicated as causal factors in several diseases including diabetic complications, cataracts, and arteriosclerosis. One means through which AGEs modulate cellular interactions is via binding to specific receptors. In the current study, the existence of AGEs in human anterior polar lens capsules of cataracts was confirmed using a combination of dot-immunoblot and fluorescent detection. Human lens epithelial cells (LECs) attached to anterior lens capsules expressed mRNA for the receptor for AGEs (RAGE). The interaction of LECs with AGEs using bovine lens epithelial explants demonstrated that AGEs induced mRNAs and proteins of fibronectin, collagen type I, aberrant extracellular matrix proteins, and alpha-SMA, a specific marker for myofibroblastic cells. These findings suggest that AGEs may alter cellular functions which induce mRNAs and proteins associated with fibrosis in LECs.
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PMID:Effect of advanced glycation end products on lens epithelial cells in vitro. 1094 40

This study investigated the immunocytochemical characteristics of normal myoepithelial cells (MECs) of human major and minor salivary glands using the LSAB method. Other human exocrine glands were used as controls. Immunoreactivity of MECs was observed exclusively with fully differentiated smooth muscle antibodies (a-SMA; SMMS-1; CALP; hCD) and with epithelial markers (cytokeratins) Ck14 and Ck17. This epithelial-muscular immunophenotype was similarly expressed in the MECs of other human exocrine glands used as control. In the salivary MECs, we did not observe evidence for neuroectodermic phenotype (S-100 protein, GFAP, NSE). On the contrary, positivity was observed for S-100 protein in Mecs of control glands (mammary, bronchial and sweat glands). Immunoreaction for extracellular matrix markers (fibronectin, laminin and collagen IV) and vimentin always were negative. Our data show that in normal "non transformed" MECs of the salivary glands the smooth muscle phenotype is in a state of complete differentiation, while the epithelial phenotype expresses only Ck14 and Ck17. This double and simultaneous immunoreactivity represents a differential marker of MECs from the epithelial basal cell (EBCs).
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PMID:On the myoepithelium of human salivary glands. An immunocytochemical study. 1098 Jun 76

Chronic pancreatitis is characterized by fibrosis. We reported an anti-inflammatory effect of the herbal medicine Saiko-keishi-to (TJ-10) on chronic pancreatitis. This study aimed to elucidate the antifibrotic effect of TJ-10. Four-week-old male WBN/Kob rats were fed a special pellet diet (MB-3) with or without TJ-10 (80 mg/100 g body weight) for 20 weeks. Pancreata were histopathologically examined at every 4 weeks, and the expression of fibrosis-related factors such as transforming growth factor beta1 (TGF-beta1), fibronectin (FN), alpha-smooth muscle actin (alpha-SMA), and type III collagen was analyzed. In untreated WBN/Kob rats, chronic pancreatitis developed at 12 weeks and progressed with marked fibrosis at 16 weeks, and the expression of TGF-beta1 and FN peaked at 12 weeks. However, in the TJ-10-treated rats, the rate of pancreatic fibrosis and the expression of TGF-beta1, FN, alpha-SMA, and type III collagen at 12 and 16 weeks decreased significantly compared to those in the untreated rats. These results suggest that TJ-10 inhibits the pancreatic fibrosis by the suppression of TGF-beta1 expression.
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PMID:Antifibrotic effect of the herbal medicine Saiko-keishi-to (TJ-10) on chronic pancreatitis in the WBN/Kob rat. 1113 77


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