Expression of claudin-7 and -8 along the mouse nephron

Li, Wing Y.; Huey, Catherine L; Yu, Alan

doi:10.1152/ajprenal.00384.2003

Cited by 169 publications

(157 citation statements)

References 49 publications

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“…Besides, Claudins have been described as essential modulators of paracellular permeability (Matter and Balda 2007;Günzel and Yu 2013). Claudin-8 is restricted to the proximal tubule (PST), distal tubule and collecting duct in the mouse nephron (Li et al 2004). In addition, Claudin-8 plays an important role in the paracellular cation barrier of the distal renal tubule (Hou et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Transcription Factor SOX9 Promotes Osteosarcoma Cell Growth by Repressing Claudin-8 Expression [Retraction]

Yang

Hao

et al. 2017

Tohoku J. Exp. Med.

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Osteosarcoma is a malignant bone cancer that mainly affects children. SOX9 plays a key role in bone formation and osteosarcoma, and Claudin-8 (CLDN8), a tight junction protein, contributes to proliferation of osteosarcoma cells. The aim of this study was to investigate the relationship between SOX9 and CLDN8 in osteosarcoma. The expression levels of SOX9 and CLDN8 were determined in osteosarcoma specimens (n = 25) by qRT-PCR and Western blot analyses. The levels of SOX9 mRNA and protein were significantly higher in osteosarcoma tissues than those in adjacent non-tumor tissues, whereas the expression levels of CLDN8 mRNA and protein were significantly lower in osteosarcoma tissues. Immunohistochemical analysis showed the high expression of SOX9 in 56 out of 97 osteosarcoma tissues (57.7%). By contrast, the low expression of immunoreactive CLDN8 was observed in 62 of 97 osteosarcoma tissues (63.9%). There was the inverse correlation between the expression levels of SOX9 and CLDN8 proteins (R = −0.633, P < 0.001). The overall survival was poorer in the patients with high SOX9 expression. Subsequently, using two human osteosarcoma cell lines, we showed that knockdown of SOX9 inhibited cell proliferation and migration but promoted cell apoptosis. Importantly, knockdown of SOX9 increased the expression levels of CLDN8 protein. The transient luciferase-reporter assays suggest that SOX9 may inhibit the promoter activity of the CLDN8 gene in osteosarcoma cells. In conclusion, we provide the evidence demonstrating that SOX9 may promote cell growth by repressing the expression of CLDN8. Thus, SOX9 may be a therapeutic target for osteosarcoma.

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Section: Introductionmentioning

confidence: 99%

Transcription Factor SOX9 Promotes Osteosarcoma Cell Growth by Repressing Claudin-8 Expression [Retraction]

Yang

Hao

et al. 2017

Tohoku J. Exp. Med.

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“…Thus, CLDN8 is required for the paracellular Cl -channel in the collecting duct. Immunofluorescence analyses have shown that CLDN3 and 7 are also expressed in the collecting ducts of mouse and rat kidneys (12,14), although one study described CLDN7 in the collecting ducts as located primarily on the basolateral membrane (13). Both M-1 and mIMCD3 cells express endogenous CLDN3 and CLDN7.…”

Section: Mutagenesis Identifies a Locus Of Amino Acids Critical For Cmentioning

confidence: 99%

“…CLDN3, 4, 7, and 8 are expressed primarily along the ASDN (12)(13)(14). In cultured renal epithelial MDCK cells, CLDN4 or CLDN8 overexpression selectively decreased the permeability of cations through TJs, specifically to Na + , K + , H + , and ammonium (15,16).…”

mentioning

confidence: 99%

Claudin-4 forms paracellular chloride channel in the kidney and requires claudin-8 for tight junction localization

Hou

Renigunta²,

Yang³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

209

233

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Tight junctions (TJs) play a key role in mediating paracellular ion reabsorption in the kidney. The paracellular pathway in the collecting duct of the kidney is a predominant route for transepithelial chloride reabsorption that determines the extracellular NaCl content and the blood pressure. However, the molecular mechanisms underlying the paracellular chloride reabsorption in the collecting duct are not understood. Here we showed that in mouse kidney collecting duct cells, claudin-4 functioned as a Cl -channel. A positively charged lysine residue at position 65 of claudin-4 was critical for its anion selectivity. Claudin-4 was observed to interact with claudin-8 using several criteria. In the collecting duct cells, the assembly of claudin-4 into TJ strands required its interaction with claudin-8. Depletion of claudin-8 resulted in the loss of paracellular chloride conductance, through a mechanism involving its recruitment of claudin-4 during TJ assembly. Together, our data show that claudin-4 interacts with claudin-8 and that their association is required for the anion-selective paracellular pathway in the collecting duct, suggesting a mechanism for coupling chloride reabsorption with sodium reabsorption in the collecting duct.C hloride is the predominant extracellular ionic constituent and thereby determines extracellular fluid volume (ECFV) and blood pressure (1-3). Although only responsible for the reabsorption of 2-3% filtered chloride, the aldosterone-sensitive distal nephron (ASDN) plays a vital regulatory role in renal handling of salt, ECFV control, and managing blood pressure (4). The ASDN comprises the distal convoluted tubule (DCT), the connecting tubule (CNT), and the collecting duct. The collecting duct is characterized by a heterogeneous epithelium-the principal cells and intercalated cells (5). Sodium reabsorption in the collecting duct is an active process driven by the basolateral Na + /K + -ATPase; acts through the apical epithelial sodium channel (ENaC) in the principal cell (6); and is responsible for generating the lumen-negative transepithelial potential. This electrogenic transport step creates a favorable electrical driving force for luminal reabsorption of chloride and secretion of potassium and proton. Chloride is transported by two major mechanisms (1). Chloride is actively reabsorbed by an electroneutral Cl − /HCO − exchanger (Slc26a4: pendrin) localized to the apical membrane of the β-type intercalated cell (7). Choride exits this cell via a basolateral Cl − channel (2) and diffuses passively down electrochemical gradients via the paracellular channel in the tight junction (TJ).The TJ is the most apical member of the junctional complex found in vertebrate epithelia responsible for the barrier to movement of ions and molecules between apical and basal compartments, the paracellular pathway (8). TJs are composed of three transmembrane proteins: occludin, claudins, and junctional adhesion molecule (JAM). The claudins (CLDNs) are a 28-member family of tetraspan proteins that range in m...

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“…A striking example is claudin-7, which is predominantly basolateral in the connecting tubule and collecting duct (68), as it is in airway, intestinal, and epididymal epithelia (23,42,51). At least in the epididymis it is not polymerized into strands (51).…”

Section: Expression and Localization Of Claudins In The Kidneymentioning

confidence: 99%

Biology of claudins

Angelow¹,

Ahlstrom²,

Yu³

2008

American Journal of Physiology-Renal Physiology

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304

294

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Claudins are a family of tight junction membrane proteins that regulate paracellular permeability of epithelia, likely by forming the lining of the paracellular pore. Claudins are expressed throughout the renal tubule, and mutations in two claudin genes are now known to cause familial hypercalciuric hypomagnesemia with nephrocalcinosis. In this review, we discuss recent advances in our understanding of the physiological role of various claudins in normal kidney function, and in understanding the fundamental biology of claudins, including the molecular basis for selectivity of permeation, claudin interactions in tight junction formation, and regulation of claudins by protein kinases and other intracellular signals.

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Expression of claudin-7 and -8 along the mouse nephron

Abstract: Expression of claudin-7 and -8 along the mouse nephron.

Cited by 169 publications

References 49 publications

Transcription Factor SOX9 Promotes Osteosarcoma Cell Growth by Repressing Claudin-8 Expression [Retraction]

Transcription Factor SOX9 Promotes Osteosarcoma Cell Growth by Repressing Claudin-8 Expression [Retraction]

Claudin-4 forms paracellular chloride channel in the kidney and requires claudin-8 for tight junction localization

Biology of claudins

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