Role of IL-10 in Hepatocyte Tight Junction Alteration in Mouse Model of Experimental Colitis

Mazzon, Emanuela; Puzzolo, Domenico; Caputi, Achille P.; Cuzzocrea, Salvatore

doi:10.1007/bf03402016

Cited by 57 publications

(47 citation statements)

References 62 publications

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“…Anomalies in claudin expression are responsible for aberrant barrier function Aberrant TJ barrier function and increased tissue permeability are common characteristics of several diseases, such as pulmonary edema, jaundice, inflammatory bowel disease, diarrhea, several kidney diseases, diabetic retinopathy inflammation, blood-borne metastasis and numerous pathological conditions (Mazzon et al, 2002;Wolburg et al, 2003). In experimental autoimmune encephalomyelitis, brain and spinal cord sections reveal the selective loss of claudin-3 from the TJs of venules surrounded by inflammatory cuffs (Wolburg et al, 2001).…”

Section: Claudin Genes and Claudin Gene Expressionmentioning

confidence: 99%

“…This is consistent with studies showing that Snail is a transcriptional repressor that plays a central role in the epithelial-mesenchymal transition, during which epithelial cells lose their polarity during development. This also points to a role for claudins in both normal epithelial cytoarchitecture and the epithelial-mesenchymal transition during metastasis.Anomalies in claudin expression are responsible for aberrant barrier function Aberrant TJ barrier function and increased tissue permeability are common characteristics of several diseases, such as pulmonary edema, jaundice, inflammatory bowel disease, diarrhea, several kidney diseases, diabetic retinopathy inflammation, blood-borne metastasis and numerous 2440 Journal of Cell Science 117 (12) (Mazzon et al, 2002;Wolburg et al, 2003). In experimental autoimmune encephalomyelitis, brain and spinal cord sections reveal the selective loss of claudin-3 from the TJs of venules surrounded by inflammatory cuffs (Wolburg et al, 2001).…”

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Barriers built on claudins

Turksen¹,

Troy²

2004

Journal of Cell Science

361

288

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We wish to correct some errors that we inadvertently introduced in revising and editing our recent Commentary. In the text, we incorrectly cited (Wolburg et al., 2003) in reference to the downregulation of claudin-23 in gastric cancer; the reference should be (Katoh and Katoh, 2003) as correctly cited in Table 3. (Peacock et al., 1997) was mistakenly inserted in relation to the discussion of the number of claudin genes. We also wrote the number of human claudin genes as 24, the number currently ascribed to the mouse claudin genes (GenBank). The correct number ascribed to human claudin genes by (Katoh and Katoh, 2003) is 23, up from the originally predicted 20 (Venter et al., 2001). In this regard, it is worth noting that, since our Commentary was published, (Loh et al., 2004) have annotated the claudins in the teleost Fugu rubripes genome and reported 56 claudin genes, of which only 35 can be assigned orthology to 17 mammalian claudin genes, with the remaining 21 being specific to the fish lineage and most of the 56 expressed in a more or less tissue-specific fashion, or at particular developmental stages. This, along with other issues we raised, suggests that additional annotation of multiple other genomes and other functional genomics approaches will be useful to advance our understanding of claudin biology and physiology. Finally, based on a Clustal analysis of full-length claudins, we reported that there is a highly conserved WWCC motif of unknown function within the first loop of the claudins analysed; a motif also reported in alignments of claudins carried out by (Katoh and Katoh, 2003). IntroductionIn multicellular organisms, certain tissues must be separated from each other and protected against the external environment. Epithelial and endothelial sheets achieve this by providing cellular borders that cover external and internal surfaces throughout the body. Complexes between adjacent cells in these sheets include gap junctions, desmosomes, adherence junctions and tight junctions (TJs) -also known as the zonula occludens. Early ultrastructural and morphological data revealed TJs as continuous circumferential intercellular contacts between epithelial cells (Farquhar and Palade, 1963) that create a barrier to the paracellular movement of water, solutes and immune cells (Madara, 1998;Nusrat et al., 2000). Later work showed that this epithelial barrier is heterogeneous in tightness and dynamics depending on the tissue. In addition it is physiologically regulated, and its disruption contributes to human disease. Numerous in-depth reviews on TJs exist (Begley and Brightman, 2003;Fanning et al., 1999; GonzalezMariscal et al., 2003;Heiskala et al., 2001;Madara, 1989;Mitic and Anderson, 1998;Stevenson, 1999;Tsukita and Furuse, 2000a;Tsukita and Furuse, 2000b;Tsukita et al., 2001;Zahraoui et al., 2000). Here we therefore only briefly summarize their essential features and then focus on the recent identification of claudins and our evolving understanding of their contribution to TJ structure and function. Tight...

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Section: Claudin Genes and Claudin Gene Expressionmentioning

confidence: 99%

mentioning

confidence: 99%

Barriers built on claudins

Turksen¹,

Troy²

2004

Journal of Cell Science

361

288

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“…These proteins can form homodimers or heterodimers to produce paired strands between adjacent cells, thereby determining the characteristic permeability properties of different epithelial tissues (7). Disruption of tight junction barrier function and changes in permeability properties have been shown to be associated with a number of pathologic conditions such as kidney disorders, inflammatory bowel disease, pulmonary edema, diarrhea, and jaundice (8)(9)(10)(11)(12). In addition, mutations in claudin genes are also linked to genetic disorders.…”

Section: Introductionmentioning

confidence: 99%

Claudin-3 and Claudin-4 Expression in Ovarian Epithelial Cells Enhances Invasion and Is Associated with Increased Matrix Metalloproteinase-2 Activity

2005

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Claudin proteins form a large family of integral membrane proteins crucial for tight junction formation and function. Our previous studies have revealed that claudin-3 and claudin-4 proteins are highly overexpressed in ovarian cancer. To clarify the roles of claudins in ovarian tumorigenesis, we have generated human ovarian surface epithelial (HOSE) cells constitutively expressing wild-type claudin-3 and claudin-4. Expression of these claudins in HOSE cells increased cell invasion and motility as measured by Boyden chamber assays and wound-healing experiments. Conversely, small interfering RNA (siRNA)-mediated knockdown of claudin-3 and claudin-4 expression in ovarian cancer cell lines reduced invasion. Claudin expression also increased cell survival in HOSE cells but did not significantly affect cell proliferation. Moreover, the claudin-expressing ovarian epithelial cells were found to have increased matrix metalloproteinase-2 (MMP-2) activity indicating that claudin-mediated increased invasion might be mediated through the activation of MMP proteins. However, siRNA inactivation of claudins in ovarian cancer cell lines did not have a significant effect on the high endogenous MMP-2 activity present in these cells, showing that malignant cells have alternative or additional pathways to fully activate MMP-2. Taken together, our results suggest that claudin overexpression may promote ovarian tumorigenesis and metastasis through increased invasion and survival of tumor cells. (Cancer Res 2005; 65(16): 7378-85)

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“…Dinitrobenzene sulfonic acid (DNBS)-induced colitis in experimental animals (eg mouse and rats) has proven to be a useful model of IBD, as it possesses many of the cell and humoral immunity characteristics found in human IBD. 6,7 Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors that are related to retinoid, steroid and thyroid hormone receptors. 8 All members of this superfamily have a similar structure: the amino-terminal (N-terminal) region allows ligand-independent activation, confers constitutive activity on the receptor and is negatively regulated by phosphorylation.…”

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Role of endogenous and exogenous ligands for the peroxisome proliferators activated receptors alpha (PPAR-α) in the development of inflammatory bowel disease in mice

Cuzzocrea

Paola

Mazzon

et al. 2004

Laboratory Investigation

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The peroxisome proliferator-activated receptor-a (PPAR-a) is a member of the nuclear receptor superfamily of ligand-dependent transcription factors related to retinoid, steroid and thyroid hormone receptors. The aim of the present study was to examine the effects of endogenous and exogenous PPAR-a ligand on the development of experimental colitis. To address this question, we used an experimental model of colitis, induced by dinitrobenzene sulfonic acid (DNBS). When compared to DNBS-treated PPAR-a wild-type (WT) mice, DNBStreated PPAR-a knockout mice (PPAR-aKO) mice experienced a higher rate of the extent and severity of the histological signs of colon injury. After administration of DNBS PPAR-aWT mice experienced hemorrhagic diarrhea, weight loss and large areas of necrosis in the mucosa of the colon were also observed. Neutrophil infiltration was associated with upregulation of ICAM-1. Immunohistochemistry for nitrotyrosine showed an intense staining in the inflamed colon. Absence of a functional PPAR-a gene in PPAR-aKO mice resulted in a significant augmentation of all the above-described parameters. On the contrary, the treatment of PPAR-aWT with Wy-14643 (1 mg/kg daily i.p) significantly reduced: (i) the degree of hemorrhagic diarrhea and weight loss, (ii) the degree of colon injury, (iii) the rise in MPO activity (mucosa), (iv) the increase in staining (immunohistochemistry) for nitrotyrosine, as well as (v) the upregulation of ICAM-1 caused by DNBS in the colon. In order to elucidate whether the protective effects of Wy-14643 is related to activation of the PPAR-a receptor, we also investigated the effect the of Wy-14643 treatment on PPAR-a-deficient mice. The absence of the PPAR-a receptor significantly abolished the protective effect of the PPAR-a agonist against DNBS-induced colitis. Thus, endogenous and exogenous PPAR-a ligands reduce the degree of colitis caused by DNBS. We propose that PPAR-a ligand may be useful in the treatment of inflammatory bowel disease.

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Role of IL-10 in Hepatocyte Tight Junction Alteration in Mouse Model of Experimental Colitis

Cited by 57 publications

References 62 publications

Barriers built on claudins

Barriers built on claudins

Claudin-3 and Claudin-4 Expression in Ovarian Epithelial Cells Enhances Invasion and Is Associated with Increased Matrix Metalloproteinase-2 Activity

Role of endogenous and exogenous ligands for the peroxisome proliferators activated receptors alpha (PPAR-α) in the development of inflammatory bowel disease in mice

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