Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions

Imamura, Masafumi; Kojima, Takashi; Lan, Mengdong; Son, Seiichi; Murata, Masaki; Osanai, Makoto; Chiba, Hideki; Hirata, Koichi; Sawada, Norimasa

doi:10.1016/j.yexcr.2007.03.010

Cited by 13 publications

(9 citation statements)

References 45 publications

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“…Thus, fetal lung explants were cultured with increasing concentrations of IL-11, CLC, CNTF, CT-1 or OSM, selected according to literature [26]–[35]. Supplementation studies showed that cytokines within the gp130 family can elicit opposite effects in lung explant growth.…”

Section: Discussionmentioning

confidence: 99%

The Role of Glycoprotein 130 Family of Cytokines in Fetal Rat Lung Development

et al. 2013

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The glycoprotein 130 (gp130) dependent family of cytokines comprises interleukin-6 (IL-6), IL-11, leukemia inhibitory factor (LIF), cardiotrophin-like cytokine (CLC), ciliary neurotrophic factor (CNTF), cardiotrophin-1 (CT-1) and oncostatin M (OSM). These cytokines share the membrane gp130 as a common signal transducer. Recently, it was demonstrated that IL-6 promotes, whereas LIF inhibits fetal lung branching. Thus, in this study, the effects on fetal lung morphogenesis of the other classical members of the gp130-type cytokines (IL-11, CLC, CNTF, CT-1 and OSM) were investigated. We also provide the first description of these cytokines and their common gp130 receptor protein expression patterns during rat lung development. Fetal rat lung explants were cultured in vitro with increasing concentrations of IL-11, CLC, CNTF, CT-1 and OSM. Treated lung explants were morphometrically analyzed and assessed for MAPK, PI3K/AKT and STAT3 signaling modifications. IL-11, which similarly to IL-6 acts through a gp130 homodimer receptor, significantly stimulated lung growth via p38 phosphorylation. On the other hand, CLC, CNTF, CT-1 and OSM, whose receptors are gp130 heterodimers, inhibited lung growth acting in different signal-transducing pathways. Thus, the present study demonstrated that although cytokines of the gp130 family share a common signal transducer, there are specific biological activities for each cytokine on lung development. Indeed, cytokine signaling through gp130 homodimers stimulate, whereas cytokine signaling through gp130 heterodimers inhibit lung branching.

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Section: Discussionmentioning

confidence: 99%

The Role of Glycoprotein 130 Family of Cytokines in Fetal Rat Lung Development

et al. 2013

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“…In primary cultures of adult rat hepatocytes, interleukin‐1β regulated expression of claudin‐2 via p38 MAPK and PI3K (42). In primary cultured rat hepatocytes, upregulation of claudin‐2 by oncostatin M was controlled through PKC and PI3K (43). In hepatocytes derived from occludin‐deficient mice, claudin‐2 expression was increased via MAPK and PI3K (44).…”

Section: Discussionmentioning

confidence: 99%

Transforming growth factor‐β induces epithelial to mesenchymal transition by down‐regulation of claudin‐1 expression and the fence function in adult rat hepatocytes

Kojima

Takano

Yamamoto

et al. 2007

Liver International

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“…3D). Oncostatin M, possibly regulated by TNFα (Kamiya and Gonzalez, 2004), appears to elicit metabolic maturation of hepatocytes by activation of JAK/STAT signaling through its receptor gp130 (Kamiya et al, 1999) and promotes adhesion and polarity through upregulation of the tight junction protein claudin-2 (Imamura et al, 2007) and the adherens junction protein E-cadherin (Battle et al, 2006). Glucocorticoids may act to suppress growth and induce expression of critical hepatocyte transcription factors HNF4α (Li et al, 2000) and C/EBPα (Tomizawa et al, 1998; Michalopoulos et al, 2003; Yamasaki et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Beta‐catenin signaling in hepatic development and progenitors: Which way does the WNT blow?

Lade

Monga

2010

Developmental Dynamics

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The Wnt/β-catenin pathway is an evolutionarily conserved signaling cascade that plays key roles in development and adult tissue homeostasis and is aberrantly activated in many tumors. Over a decade of work in mouse, chick, xenopus, and zebrafish models has uncovered multiple functions of this pathway in hepatic pathophysiology. Specifically, beta-catenin, the central component of the canonical Wnt pathway, is implicated in the regulation of liver regeneration, development, and carcinogenesis. Wnt-independent activation of beta-catenin by receptor tyrosine kinases has also been observed in the liver. In liver development across various species, through regulation of cell proliferation, differentiation, and maturation, beta-catenin directs foregut endoderm specification, hepatic specification of the foregut, and hepatic morphogenesis. Its role has also been defined in adult hepatic progenitors or oval cells especially in their expansion and differentiation. Thus, beta-catenin undergoes tight temporal regulation to exhibit pleiotropic effects during hepatic development and in hepatic progenitor biology.

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Oncostatin M induces upregulation of claudin-2 in rodent hepatocytes coinciding with changes in morphology and function of tight junctions

Cited by 13 publications

References 45 publications

The Role of Glycoprotein 130 Family of Cytokines in Fetal Rat Lung Development

The Role of Glycoprotein 130 Family of Cytokines in Fetal Rat Lung Development

Transforming growth factor‐β induces epithelial to mesenchymal transition by down‐regulation of claudin‐1 expression and the fence function in adult rat hepatocytes

Beta‐catenin signaling in hepatic development and progenitors: Which way does the WNT blow?

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