Suppression of renal fibrosis by galectin-1 in high glucose-treated renal epithelial cells

Okano, Kazuhiro; Tsuruta, Yuki; Yamashita, Tetsuri; Takano, Mari; Echida, Yoshihisa; Nitta, Kosaku

doi:10.1016/j.yexcr.2010.08.015

Cited by 18 publications

(26 citation statements)

References 35 publications

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“…A human tubular epithelial cells, probably originating from proximal tubules, contains Galectin-1 in agreement with this finding (Lai et al, 2011). Although galectins may be secreted without identifiable signal sequence, intracellular and nuclear Galectin-1 are important in suppressing TGFb/Smad signaling in renal epithelial cells (Okano et al, 2010). Although galectins may be secreted without identifiable signal sequence, intracellular and nuclear Galectin-1 are important in suppressing TGFb/Smad signaling in renal epithelial cells (Okano et al, 2010).…”

Section: Introductionsupporting

confidence: 70%

“…In human, Galectin-1 is identified in renal mesangial and epithelial cells of the fetal kidney (Van Den Br et al, 1997) and disappears in normal adult kidney (Wasano et al, 1990). Galectin-1, however, seems to be reexpressed under pathological renal conditions, including renal tumors, fibrosis, autosomal recessive polycystic kidney disease (ARPKD), and DN (Valkova et al, 2005;Saussez et al, 2005;Okano et al, 2010;Masui et al, 2013). Galectin-1, however, seems to be reexpressed under pathological renal conditions, including renal tumors, fibrosis, autosomal recessive polycystic kidney disease (ARPKD), and DN (Valkova et al, 2005;Saussez et al, 2005;Okano et al, 2010;Masui et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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High glucose‐induced Galectin‐1 in human podocytes implicates the involvement of Galectin‐1 in diabetic nephropathy

Liu

Long²,

Fang

et al. 2014

Cell Biology International

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The diabetic milieu is believed to change the activity, or result in damage of podocytes-a key component of the glomerular filtration barrier and known to secrete matrix for glomerular basement membrane. This in turn contributes to diabetic nephropathy. However, how podocyte dysfunction is triggered in diabetic nephropathy remains ambiguous. Galectin-1 belongs to Galectin family that bind to β-galactoside residues of glycosylated proteins. We explored whether Galectin-1 is dysregulated in diabetic nephropathy using three different techniques, namely real-time polymerase chain reaction, western blotting, and immunofluorescent staining, to follow the expression of Galectin-1 under high glucose levels in podocytes. High glucose consistently induced Galectin-1 expression. Immunohistochemistry using a Galectin-1-specific antibody also showed elevated Galectin-1 in renal tissues of diabetic patients with manifestation of nephropathy, indicating a correlation of Galectin-1 overexpression with diabetic nephropathy. Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression.

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Section: Introductionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

High glucose‐induced Galectin‐1 in human podocytes implicates the involvement of Galectin‐1 in diabetic nephropathy

Liu

Long²,

Fang

et al. 2014

Cell Biology International

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“…Surprisingly, immunofluorescence and immunohistochemistry results revealed a marked increase in the accumulation of Col 1 and α-SMA+ myofibroblasts in the kidneys of the 5-week BDL-watertreated group, as determined by real-time PCR. It has been reported that TGF-β1/Smad signaling is a key mediator of renal tubular interstitial fibrosis (Nishida et al, 2007;Okano et al, 2010;Choi et al, 2011;Falke et al, 2012;Huen et al, 2013). Consistent with these reports, renal fibrosis was also observed in this study.…”

Section: Discussionsupporting

confidence: 92%

Xiayuxue decoction reduces renal injury by promoting macrophage apoptosis in hepatic cirrhotic rats

et al. 2015

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ABSTRACT. Renal pathological changes in cirrhotic rat have not been extensively reported. The aim of this study was to investigate whether Xiayuxue decoction (XYXD) could attenuate renal injury induced by bile duct ligation (BDL), with special focus on the mechanisms promoting renal macrophage apoptosis. The rats were treated with BDL for 5 weeks and administered 0.36 g/kg XYXD intragastrically from day 1 of initiating BDL. Renal tissue was monitored by hematoxylin-eosin and Sirius red staining. Macrophage infiltration and proinflammatory cytokines such as tumor necrosis factor and chemokine ligand 2 were detected by quantitative polymerase chain reaction. Macrophage apoptosis was detected by double immunofluorescence staining. Blood urea nitrogen, creatinine, and glomerulus diameter increased significantly after a 5-week BDL treatment in XYXD (BDL-XYXD) rats. CD68 and pro-inflammatory cytokine (2015) mRNA increased in the kidneys of control (BDL-water) rats. Fluorescence microscopy analysis showed that XYXD promoted apoptosis in renal CD68+ macrophages. Collogen1 (Col 1), pro-fibrogenic cytokines, and α-smooth muscle actin in kidneys of BDL-water rats increased significantly compared to the sham group. XYXD inhibited Col 1 and pro-fibrotic factors in BDL-XYXD rats. Our results demonstrated that XYXD significantly reduced renal injury by, at least in part, promoting macrophage apoptosis in rats with damaged renal histopathology due to BDL-induced cirrhosis.

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“…In the latter, Lim et al () found that TGF‐β 1 treatment also triggered nuclear translocation of Gal1. Moreover, this lectin was strongly increased and translocated to nucleus in renal epithelial cells treated with high glucose and TGF‐β 1 (Okano et al, ). In contrast, TGF‐β 1 ‐treated HepG2 cells evidenced a major localization of Gal1 close to the cell membrane, whereas no apparent changes in localization were observed in HuH‐7 cells.…”

Section: Discussionmentioning

confidence: 99%

Galectin-1 Controls the Proliferation and Migration of Liver Sinusoidal Endothelial Cells and Their Interaction With Hepatocarcinoma Cells

et al. 2015

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Galectin-1 (Gal1), a β-galactoside-binding protein elevated in hepatocellular carcinoma (HCC), promotes epithelial-mesenchymal transition (EMT) and its expression correlates with HCC growth, invasiveness, and metastasis. During the early stages of HCC, transforming growth factor β1 (TGF-β1 ) acts as a tumor suppressor; however in advanced stages, HCC cells lose their cytostatic response to TGF-β1 and undergo EMT. Here, we investigated the role of Gal1 on liver endothelial cell biology, and the interplay between Gal1 and TGF-β1 in HCC progression. By Western blot and immunofluorescence, we analyzed Gal1 expression, secretion and localization in HepG2 and HuH-7 human HCC cells, and in SK-HEP-1 human liver sinusoidal endothelial cells (SECs). We used loss-of-function and gain-of-function experiments to down- or up-regulate Gal1 expression, respectively, in HepG2 cells. We cultured SK-HEP-1 cells with conditioned media from HCC cells secreting different levels of Gal1, and demonstrated that Gal1 derived from tumor hepatocytes induced its own expression in SECs. Colorimetric and scratch-wound assays revealed that secretion of Gal1 by HCC cells induced SEC proliferation and migration. Moreover, by fluorescence microscopy we demonstrated that Gal1 promoted glycan-dependent heterotypic adhesion of HepG2 cells to SK-HEP-1 SECs. Furthermore, TGF-β1 induced Gal1 expression and secretion by HCC cells, and promoted HepG2 cell adhesion to SK-HEP-1 SECs through a Gal1-dependent mechanism. Finally, Gal1 modulated HepG2 cell proliferation and sensitivity to TGF-β1 -induced growth inhibition. Our results suggest that Gal1 and TGF-β1 might function coordinately within the HCC microenvironment to regulate tumor growth, invasion, metastasis, and angiogenesis.

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Suppression of renal fibrosis by galectin-1 in high glucose-treated renal epithelial cells

Cited by 18 publications

References 35 publications

High glucose‐induced Galectin‐1 in human podocytes implicates the involvement of Galectin‐1 in diabetic nephropathy

High glucose‐induced Galectin‐1 in human podocytes implicates the involvement of Galectin‐1 in diabetic nephropathy

Xiayuxue decoction reduces renal injury by promoting macrophage apoptosis in hepatic cirrhotic rats

Galectin-1 Controls the Proliferation and Migration of Liver Sinusoidal Endothelial Cells and Their Interaction With Hepatocarcinoma Cells

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