Up-Regulation of the Claudin-6 Gene in Adipogenesis

Hong, Yeon Hee; Hishikawa, Daisuke; Miyahara, Hisae; Nishimura, Yukihiko; Tsuzuki, Hiroaki; Gotoh, Chizu; Iga, Tomoyo; Suzuki, Yasuki; Song, Sung-Moo; Choi, Ki Choon; Lee, Hong Gu; Sasaki, Shinichi; Roh, Sang Gun

doi:10.1271/bbb.69.2117

Cited by 8 publications

(8 citation statements)

References 23 publications

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“…Although the in vivo contribution of CLDN6 and CLDN9 to HCV infection is unresolved, there are several lines of evidence suggesting that CLDN6 and CLDN9 are potential HCV coreceptors. Previous reports have shown that the expression of CLDN6 and CLDN9 in liver is detectable by RT-PCR (11,12). Our study also detected the expression of CLDN6 and CLDN9 in liver by real-time PCR (Fig.…”

Section: Discussionsupporting

confidence: 74%

Claudin-6 and Claudin-9 Function as Additional Coreceptors for Hepatitis C Virus

Zheng

Yuan

et al. 2007

J Virol

193

189

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Hepatitis C virus (HCV) is a global challenge to public health. Several factors have been proven to be critical for HCV entry, including the newly identified claudin-1 (CLDN1). However, the mechanism of HCV entry is still obscure. Presently, among the 20 members of the claudin family identified in humans so far, CLDN1 has been the only member shown to be necessary for HCV entry. Recently, we discovered that Bel7402, an HCV-permissive cell line, does not express CLDN1 but expresses other members of claudin family. Among these claudins, CLDN9 was able to mediate HCV entry just as efficiently as CLDN1. We then examined if other members of the claudin family could mediate entry. We show that CLDN6 and CLDN9, but not CLDN2, CLDN3, CLDN4, CLDN7, CLDN11, CLDN12, CLDN15, CLDN17, and CLDN23, were able to mediate the entry of HCV into target cells. We found that CLDN6 and CLDN9 are expressed in the liver, the primary site of HCV replication. We also showed that CLDN6 and CLDN9, but not CLDN1, are expressed in peripheral blood mononuclear cells, an additional site of HCV replication. Through sequence comparison and mutagenesis studies, we show that residues N38 and V45 in the first extracellular loop (EL1) of CLDN9 are necessary for HCV entry.Hepatitis C virus (HCV) is the major cause of liver cirrhosis and hepatocellular carcinoma worldwide. Approximately 3% of the global population is infected with HCV, and at least 70% develop chronic hepatitis (13,17,32). In patients with chronic HCV infection, about 20% develop liver cirrhosis, about 5% of which go on to develop hepatocellular carcinoma (17). While HCV is generally confined to the liver, there is growing evidence suggesting that HCV can replicate in extrahepatic tissues including peripheral blood mononuclear cells (PBMCs) (4,15,23,24

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Section: Discussionsupporting

confidence: 74%

Claudin-6 and Claudin-9 Function as Additional Coreceptors for Hepatitis C Virus

Zheng

Yuan

et al. 2007

J Virol

193

189

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“…The claudin (CLDN) family plays a major role in tight junction-specific obliteration of the intercellular space through calcium-independent dell-adhesion activity. CLDN6 is known to be an important regulator in adipogenesis and fat deposition but is not detected in this study [55]. Genetic manipulation of CLDN1 expression induced changes in cellular phenotype [56].…”

Section: Discussionmentioning

confidence: 68%

Comparative Transcriptome Analysis of Adipose Tissues Reveals that ECM-Receptor Interaction Is Involved in the Depot-Specific Adipogenesis in Cattle

et al. 2013

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Adipocytes mainly function as energy storage and endocrine cells. Adipose tissues showed the biological and genetic difference based on their depots. The difference of adipocytes between depots might be influenced by the inherent genetic programing for adipogenesis. We used RNA-seq technique to investigate the transcriptomes in 3 adipose tissues of omental (O), subcutaneous (S) and intramuscular (I) fats in cattle. Sequence reads were obtained from Illumina HiSeq2000 and mapped to the bovine genome using Tophat2. Differentially expressed genes (DEG) between adipose tissues were detected by EdgeR. We identified 5797, 2156, and 5455 DEGs in the comparison between OI, OS, and IS respectively and also found 5657 DEGs in the comparison between the intramuscular and the combined omental and subcutaneous fats (C) (FDR<0.01). Depot specifically up- and down- regulated DEGs were 853 in S, 48 in I, and 979 in O. The numbers of DEGs and functional annotation studies suggested that I had the different genetic profile compared to other two adipose tissues. In I, DEGs involved in the developmental process (eg. EGR2, FAS, and KLF7) were up-regulated and those in the immune system process were down-regulated. Many DEGs from the adipose tissues were enriched in the various GO terms of developmental process and KEGG pathway analysis showed that the ECM-receptor interaction was one of commonly enriched pathways in all of the 3 adipose tissues and also functioned as a sub-pathway of other enriched pathways. However, genes involved in the ECM-receptor interaction were differentially regulated depending on the depots. Collagens, main ECM constituents, were significantly up-regulated in S and integrins, transmembrane receptors, were up-regulated in I. Different laminins were up-regulated in the different depots. This comparative transcriptome analysis of three adipose tissues suggested that the interactions between ECM components and transmembrane receptors of fat cells depend on the depot specific adipogenesis.

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“…Recent reports show that CLDN6 plays important roles in cells under both physiological and pathological conditions. For example, CLDN6 can regulate adipogenesis and fat deposition [22], it is required for normal blastocyst formation [23], and its expression occurs in early development, with particular attention to definitive endoderm derivatives [24]. CLDN6 is expressed very early in epidermal morphogenesis [1], and it is important for maintaining permeability barriers and transepithelial resistance in epidermal cells [11].…”

Section: Discussionmentioning

confidence: 99%

Role of Estrogen Receptor-α in the Regulation of Claudin-6 Expression in Breast Cancer Cells

Liu

Ren

et al. 2011

J Breast Cancer

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PurposeIn our previous studies we showed that upregulating claudin-6 (CLDN6) expression may contribute to preventing breast cancer, and that 17β-estradiol induces a concentration- and time-related effect on CLDN6 mRNA and protein expression in MCF-7 cells. However, the mechanisms of 17β-estradiol regulation of CLDN6 are still unclear. We determined the role of estrogen receptors in the regulation of CLDN6 expression in human breast cancer tissues and a cell line.MethodsCLDN6, estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) expression in breast cancer tissues were examined using immunohistochemistry. The human breast cancer cell line, MCF-7, which expresses ERα but not ERβ was used. CLDN6 and ERα expression were measured by reverse transcriptase-PCR, Western blotting and immunofluorescent staining. Treatments with propyl pyrazole triol (PPT) and ICI 182, 780 (ICI) were performed.ResultsThe results revealed that CLDN6 expression was related to ERα in breast cancer tissues (p=0.033). PPT, an ERα-selective ligand, upregulated CLDN6 expression at 10-5 mol/L after 24 hours. The effect of PPT on regulating CLDN6 expression in MCF-7 cells was blocked by ICI.ConclusionThese findings suggest that Erα reulates CLDN6 expression in breast cancer tissues and that 17β-estradiol induces CLDN6 expression through an ERα pathway in MCF-7 cells.

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Up-Regulation of the Claudin-6 Gene in Adipogenesis

Cited by 8 publications

References 23 publications

Claudin-6 and Claudin-9 Function as Additional Coreceptors for Hepatitis C Virus

Claudin-6 and Claudin-9 Function as Additional Coreceptors for Hepatitis C Virus

Comparative Transcriptome Analysis of Adipose Tissues Reveals that ECM-Receptor Interaction Is Involved in the Depot-Specific Adipogenesis in Cattle

Role of Estrogen Receptor-α in the Regulation of Claudin-6 Expression in Breast Cancer Cells

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