Structural Motifs of the Extracellular Matrix Proteins Laminin and Tenascin
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Tenascin
Structural motif
Tenascin C
Type IV collagen
Dermoepidermal junction
Skin equivalent
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Abstract The extracellular matrix protein tenascin‐C is expressed in processes like embryogenesis and wound healing and in neoplasia. Tenascin‐C expression in gliomas has been described previously; however, the relation to clinical data remains inconsistent. Generally, analysis of tenascin‐C function is difficult due to different alternatively spliced isoforms. Our studies focus on changes in tenascin‐C expression in human gliomas, correlating these changes with tumor progression and elucidating the functional role of the glioma cell‐specific tenascin‐C isoform pool. Eighty‐six glioma tissues of different World Health Organization (WHO) grades were analyzed immunohistochemically for tenascin‐C expression. The influence of the specific tenascin‐C isoforms produced by glioblastoma cells on proliferation and migration was examined in vitro using blocking antibodies recognizing all isoforms. In general, tenascin‐C expression increased with tumor malignancy. Perivascular staining of tenascin‐C around tumor‐supplying blood vessels was observed in all glioblastoma tissues, whereas in WHO II and III gliomas, perivascular tenascin‐C staining appeared less frequently. The appearance of perivascular tenascin‐C correlated significantly with a shorter disease‐free time. Analysis of proliferation and migration in the presence of blocking antibodies revealed an inhibition of proliferation by around 30% in all 3 glioblastoma cell cultures, as well as a decrease in migration of 30.6–46.7%. Thus we conclude that the endogenous pool of tenascin‐C isoforms in gliomas supports both tumor cell proliferation and tumor cell migration. In addition, our data on the perivascular staining of tenascin‐C in WHO II and III gliomas and its correlation with a shorter disease‐free time suggest that tenascin‐C may be a new and potent prognostic marker for an earlier tumor recurrence. © 2002 Wiley‐Liss, Inc.
Tenascin C
Tenascin
Tumor progression
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Tenascin
Structural motif
Tenascin C
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Tenascin
Tenascin C
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AIM:To study the expression and significance of laminin in human colorectal carcinoma.METHODS:Using the monoclonal antibody to laminin and streptavidin-peroxidase immunohistochemical method, the expression of laminin in 63 cases of human colorectal carcinoma tissues was determined.RESULTS:In normal marge intestinal mucosa adjacent to carcinoma, laminin was largely restricted to basement membrane in continuous linear pattern. In contrast, human colorectal carcinomas exhibited a progressive loss of an intact basement membrane that was correlated with decreasing differentiation degree.Well and moderately differentiated tumors exhibited a thin basement membrane with intermittent disruptions, and poorly differentiated tumors exhibited no areas of intact basement membrane. An association was found between lack of basement membrane laminin immunohistochemical staining in colorectal carcinoma and poorly differentiated tumor (P < 0.01).CONCLUSION:Immunohistochemical staining for laminin could provide a very useful indexfor the determination of the differentiation degree of colorectal carcinoma.
Type IV collagen
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De novo formation of laminin-positive basement membranes was found to be a distinct morphologic feature of diethylnitrosamine/phenobarbital-induced hepatocellular carcinomas of the rat. The first appearance of extracellularly located laminin occurred in the pre-neoplastic liver lesions (corresponding to neoplastic nodules), and this feature became successively more prominent during the course of hepatocellular carcinoma development. Most groups of tumor cells were surrounded by laminin-positive basement membrane material. The laminin-positive material was also deposited along the sinusoids, a location where no laminin was seen in normal rat liver. The amount of extractable laminin from hepatocellular carcinomas was significantly higher (approximately 100 ng per mg tissue) than that of normal liver tissue (less than 20 ng per mg). In vitro experiments demonstrated that normal and pre-neoplastic rat hepatocytes had the capacity to lay down basement membrane-like material. This occurred, however, only when the hepatocytes were cocultured with certain feeder cells or when grown in the presence of their conditioned media. These results indicate that during experimental hepatocarcinogenesis in the rat some as yet undefined humoral factor(s) might influence the hepatocytes to turn on genes encoding the basement membrane components and further stimulate the assembly and deposition of basement membranes.
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Tenascin C
Tenascin
Tumor progression
Parenchyma
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The developmental localization patterns of collagen type IV alpha1-5 chains, laminin-1, laminin-5, and laminin alpha2 chain were analyzed in the embryonic mouse eye using isoform specific antibodies and immunofluorescence microscopy. Laminin-1 isoform and alpha1-2(IV) were ubiquitously expressed along the ocular surface basement membranes at a very early stage of eye development. Alpha3-5(IV) were first detected at later stages of development, and exhibited a variable distribution pattern along the ocular surface basement membrane. In contrast, expression of the laminin alpha2 chain was restricted to the conjunctival basement membrane, and was first detected during the same developmental period in which keratin K4-positive, differentiated conjunctival epithelial cells were observed. Although laminin-5 was uniformly expressed along the adult ocular surface basement membrane, during embryogenesis it was first incorporated into the conjunctival basement membrane structure. These data suggest that some of the laminin isoforms, including laminin alpha2 and laminin-5, may play a role in the formation of a conjunctival-type basement membrane. The temporal relationship between the localization of these molecules to the conjunctival basement membrane and the appearance of differentiated conjunctival epithelial cells suggests a role for external influence on the differentiation pathways of ocular surface epithelium.
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Tenascin-C is an extracellular matrix glycoprotein with a dynamic and restricted distribution during organ development and in disease. Tenascin-C is up-regulated in response to several pathological conditions, including cancer, and a number of studies have implicated it in the regulation of glioma cell migration, invasion and angiogenesis. In a recent article published in the journal Cancer Research , Sarkar and colleagues present evidence indicating that Tenascin-C can also sustain proliferation of brain tumor initiating cells by promoting expression of the Notch ligand Jagged1 (1).
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Objective: To observe the changes of extracellular matrix in type Ⅱ cells and thickness of basement membrane beneath type Ⅱ cells in old rats. Methods: Inmmunocytochemistry and image analysis were used to measure the relative contents of laminin and fibronectin in type Ⅱ cells in young (1 2 months), adult (8 9 months) and old (25 28 months) rats. Results: There were less laminin, more fibronectin in type Ⅱ cells and thicker basement membrane beneath type Ⅱ cells in old rats. Conclusion: These results suggest the altered metabolism of extracellular matrix from type Ⅱ cells in old rats, which may result in abnormal recovery of alveoli after being injured.
Type IV collagen
Matrix (chemical analysis)
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