Tenascin gene expression in rat liver and in rat liver cells In vivo and in vitro studies

Ramadori, Giuliano; Schwögler, S.; Veit, Th.; Rieder, H.; Chiquet‐Ehrismann, Ruth; Mackie, Eleanor J.; Büschenfelde, K H Meyer zum

doi:10.1007/bf02899540

Cited by 55 publications

(29 citation statements)

References 32 publications

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“…30,32,45 The localization of TN-C that we found in the normal canine liver is in agreement with that reported for man and rat. 19,35,48,49,53 In contrast to rat and man, quiescent canine HSC express a-SMA (Fig. 7).…”

Section: Discussionmentioning

confidence: 99%

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Tenascin-C in Chronic Canine Hepatitis: Immunohistochemical Localization and Correlation with Necro-Inflammatory Activity, Fibrotic Stage, and Expression of Alpha-Smooth Muscle Actin, Cytokeratin 7, and CD3+ Cells

2007

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Abstract. During fibrosis, the extracellular matrix (ECM) is continuously remodeled and increases in volume due to the production of various proteins. We studied the distribution of tenascin-C (TN-C) and the correlation of TN-C with the necro-inflammatory activity and expression of alpha-smooth muscle actin (a-SMA), cytokeratin 7 (CK7), and CD3+ T-lymphocytes in canine chronic hepatitis. This was analyzed using immunohistochemistry and semiquantitative scoring. We used 3 groups (n 5 19) of dogs: group 1 (n 5 5) with neonatal hepatitis/lobular dissecting hepatitis (NH/LDH), group 2 (n 5 8) with chronic hepatitis/cirrhosis (CH/CIRR), and group 3 (n 5 6) consisting of healthy animals. In normal livers, TN-C was localized in Disse's space and around bile ducts and blood vessels. In CH/CIRR livers, TN-C was localized at the periphery of the regenerating nodules and was conspicuous in the bridging fibrous bands. In NH/LDH, TN-C was diffusely distributed along the reticular fibers that dissected between single cells or groups of hepatocytes. a-SMA in the normal hepatic parenchyma showed an irregular distribution along the perisinusoidal linings. In other groups, a-SMA was increased in fibrotic septa and perisinusoidal linings. In normal livers, CK7 was positive in bile ducts. In other groups, CK7-expressing cells were conspicuous in the portal-parenchymal interface, the periphery of the regenerative nodules, and the degenerated parenchyma. The pattern of CD3+ lymphocytes was inversely proportional to that of TN-C. These results also showed that TN-C is strongly correlated with increased fibrotic stage, inflammatory activity, and expression of CK7 and a-SMA. TN-C, CK7, and CD3 expression did not differ between diagnostic groups.

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Section: Discussionmentioning

confidence: 99%

“…44,51,55 The ECM protein TN-C is expressed in normal and fibrotic livers of humans and rats. 19,35,48,49,53 TN-C serum level is reported to have a strong correlation with the progression of the fibrosis. 54 In canine hepatitis, there is lack of knowledge of the contribution of ECM proteins to the progression of hepatic fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Tenascin-C in Chronic Canine Hepatitis: Immunohistochemical Localization and Correlation with Necro-Inflammatory Activity, Fibrotic Stage, and Expression of Alpha-Smooth Muscle Actin, Cytokeratin 7, and CD3+ Cells

2007

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“…Frozen tissue sections (7 μm) of normal or acutely or chronically damaged rat liver specimens and of normal and cirrhotic human livers were fixed in methanol/acetone (5 min/ 10 s at -20°C), air-dried for 45 min, and stored at -20°C, as described elsewhere (Knittel et al 1992a(Knittel et al , b, 1996aRamadori et al 1990Ramadori et al , 1991. Cells cultured in LAB-TEK slide chambers were fixed by the same procedure.…”

Section: Immunochemistry and Cytochemistrymentioning

confidence: 99%

“…Rat hepatic stellate cells (HSCs), endothelial cells (ECs), and Kupffer cells of the liver (KCs) were isolated and purified as described previously (Knittel et al 1992a(Knittel et al , b, 1996aRamadori et al 1990Ramadori et al , 1991Neubauer et al 1995). Briefly, the liver was digested enzymatically with pronase and collagenase, and non-parenchymal liver cells were separated by a Nycodenz density gradient.…”

Section: Cell Isolation and Culturementioning

confidence: 99%

Expression of the ECM proteins fibulin-1 and -2 in acute and chronic liver disease and in cultured rat liver cells

Piscaglia¹,

Dudas²,

Knittel³

et al. 2009

Z Gastroenterol

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Fibulin-2 has previously been considered as a marker to distinguish rat liver myofibroblasts from hepatic stellate cells. The function of other fibulins in acute or chronic liver damage has not yet been investigated. The aim of this study has been to evaluate the expression of fibulin-1 and -2 in models of rat liver injury and in human liver cirrhosis. Their cellular sources have also been investigated. In normal rat liver, fibulin-1 and -2 were both mainly present in the portal field. Fibulin-1-coding transcripts were detected in total RNA of normal rat liver, whereas fibulin-2 mRNA was only detected by sensitive, real-time quantitative polymerase chain reaction. In acute liver injury, the expression of fibulin-1 was significantly increased (17.23-fold after 48 h), whereas that of fibulin-2 was not modified. The expression of both fibulin-1 and -2 was increased in experimental rat liver cirrhosis (19.16-and 26.47-fold, respectively). At the cellular level, fibulin-1 was detectable in hepatocytes, "activated" hepatic stellate cells, and liver myofibroblasts (2.71-, 122.65-, and 469.48-fold over the expression in normal rat liver), whereas fibulin-2 was restricted to liver myofibroblasts and was regulated by transforming growth factor beta-1 (TGF-β1) in 2-day-old hepatocyte cultures and in liver myofibroblasts. Thus, fibulin-1 and -2 respond differentially to single and repeated damaging noxae, and their expression is differently present in liver cells. Expression of the fibulin-2 gene is regulated by TGF-β1 in liver myofibroblasts.

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“…At the mRNA level, differences in matrix proteins expressed were found between sinusoidal endothelial cells isolated from normal and injured liver. Whereas sinusoidal endothelial cells of the normal liver express collagen type IV, entactin and von Willebrand factor, those from injured liver produce mRNA for collagen type I, III, IV and fibronectin [11,20].…”

mentioning

confidence: 99%

Fibrosis and Altered Matrix Synthesis

Ramadori

Knittel

Saile³

1998

Digestion

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Tenascin gene expression in rat liver and in rat liver cells In vivo and in vitro studies

Cited by 55 publications

References 32 publications

Tenascin-C in Chronic Canine Hepatitis: Immunohistochemical Localization and Correlation with Necro-Inflammatory Activity, Fibrotic Stage, and Expression of Alpha-Smooth Muscle Actin, Cytokeratin 7, and CD3+ Cells

Tenascin-C in Chronic Canine Hepatitis: Immunohistochemical Localization and Correlation with Necro-Inflammatory Activity, Fibrotic Stage, and Expression of Alpha-Smooth Muscle Actin, Cytokeratin 7, and CD3+ Cells

Expression of the ECM proteins fibulin-1 and -2 in acute and chronic liver disease and in cultured rat liver cells

Fibrosis and Altered Matrix Synthesis

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