Visfatin: An adipokine activator of rat hepatic stellate cells

Liang, Ning-Lin; Men, Ruoting; Zhu, Yongjun; Yuan, Cong; Yan, Wei; Liu, Xiaojing; Yang, Li

doi:10.3892/mmr.2014.2795

Cited by 9 publications

(9 citation statements)

References 41 publications

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“…The progressive accumulation of fibrosis is the hallmark of NASH disease progression 1 . Liang et al 52 . reported that visfatin upregulated the gene and protein production of α‐SMA, a marker of HSC activation, and increased the mRNA and protein expression of collagen types I and III in the rat HSC.…”

Section: Discussionmentioning

confidence: 99%

Visfatin exacerbates hepatic inflammation and fibrosis in a methionine‐choline‐deficient diet mouse model

Heo

Choi

Lee

et al. 2021

J of Gastro and Hepatol

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Background and Aim Non‐alcoholic fatty liver disease (NAFLD) ranges from simple steatosis to non‐alcoholic steatohepatitis, which is characterized by hepatic inflammation that can progress to fibrosis, cirrhosis, and hepatocellular carcinoma. Visfatin, an adipocytokine, was reported to induce pro‐inflammatory cytokines and can be associated with liver fibrosis. We investigated the role of visfatin on hepatic inflammation and fibrosis in a methionine‐choline‐deficient (MCD)‐diet‐induced steatohepatitis mouse model. Methods Eight‐week‐old male C57BL/6 J mice were randomly assigned into one of three groups: (1) saline‐injected control diet group; (2) saline‐injected MCD diet group; and (3) visfatin‐injected MCD diet group (n = 8 per group). Mice were administered intravenous saline or 10 μg/kg of recombinant murine visfatin for 2 weeks. Histologic assessment of liver and biochemical and molecular measurements of endoplasmic reticulum (ER) stress, reactive oxidative stress (ROS), inflammation, and fibrosis were performed in livers from these animals. Results Visfatin injection aggravated hepatic steatosis and increased plasma alanine aminotransferase and aspartate aminotransferase concentrations. Visfatin increased inflammatory cell infiltration (as indicated by F4/80, CD68, ly6G, and CD3 mRNA expression) and expression of chemokines in the liver. Visfatin also increased the expression of pro‐inflammatory cytokines (IL‐1β, TNF‐α, and IL‐6) and activated fibrosis markers (CTGF, TIMP1, collagen 1α2, collagen 3α2, αSMA, fibronectin, and vimentin) in liver. Livers of visfatin‐injected mice showed upregulation of ER stress and ROS and activation of JNK signaling. Conclusions These results suggest that visfatin aggravates hepatic inflammation together with induction of ER and oxidative stress and exacerbates fibrosis in an MCD‐diet‐fed mouse model of NAFLD.

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Section: Discussionmentioning

confidence: 99%

Visfatin exacerbates hepatic inflammation and fibrosis in a methionine‐choline‐deficient diet mouse model

Heo

Choi

Lee

et al. 2021

J of Gastro and Hepatol

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“…Visfatin is an adipocytokine, which has an insulinlike effect, can promote nicotinamide adenine dinucleotide synthesis, and is involved in mediating inflammation and immunity (23)(24)(25). In recent years, studies have shown that visfatin can stimulate tumorigenesis and metastasis by stimulating inflammatory mediators and proinflammatory cytokines that are involved in tumor development (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Visfatin increases miR-21 to promote migration in HCC

Liang

Chen

Yang

et al. 2018

Cell Mol Biol (Noisy-le-grand)

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Hepatocellular carcinoma (HCC) is a common human malignancy. In this study, we aimed to investigate the serum levels of visfatin and miR-21 in HCC patients, to analysis the relationship between the pathological features and the plasma level of visfatin or miR-21, and to explore the roles of visfatin and miR-21 in migration of HCC cells. Our results showed that the serum levels of visfatin and miR-21 were significant higher in HCC patients than healthy subjects. The diagnostic sensitivity of serum visfatin was 82.5% and the specificity was 65.0%. The serum visfatin was significantly associated with the histology and metastasis. Visfatin induced miR-21 expression and cell migration in HepG2 cells. Transfection of miR-21 inhibitor suppressed the visfatin-induced migration in HCC cells. These results suggested that visfatin induced HCC cell migration via upregulation of miR-21, which provides a novel basis for the diagnosis of HCC.

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“…These cells release IL-6 and TNF in high quantity, and this is further induced by visfatin [ 161 ] ( Figure 2 ). In hepatic stellate cells synthesis of α‑smooth muscle actin, collagens and connective tissue growth factor are induced by visfatin, indicating profibrotic activity of this cytokine [ 162 ] ( Figure 2 ). In line with this in vitro study, an in vivo analysis shows reduced hepatic collagen and α‑smooth muscle actin upon suppression of hepatic visfatin in tetracarbon chloride and ethanol-treated rodents [ 163 ].…”

Section: Adipokines In Liver Cirrhosismentioning

confidence: 99%

Adipokines in Liver Cirrhosis

Buechler

Haberl

Rein-Fischboeck

et al. 2017

IJMS

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Liver fibrosis can progress to cirrhosis, which is considered a serious disease. The Child-Pugh score and the model of end-stage liver disease score have been established to assess residual liver function in patients with liver cirrhosis. The development of portal hypertension contributes to ascites, variceal bleeding and further complications in these patients. A transjugular intrahepatic portosystemic shunt (TIPS) is used to lower portal pressure, which represents a major improvement in the treatment of patients. Adipokines are proteins released from adipose tissue and modulate hepatic fibrogenesis. These proteins affect various biological processes that are involved in liver function, including angiogenesis, vasodilation, inflammation and deposition of extracellular matrix proteins. The best studied adipokines are adiponectin and leptin. Adiponectin protects against hepatic inflammation and fibrogenesis, and leptin functions as a profibrogenic factor. These and other adipokines are supposed to modulate disease severity in patients with liver cirrhosis. Consequently, circulating levels of these proteins have been analyzed to identify associations with parameters of hepatic function, portal hypertension and its associated complications in patients with liver cirrhosis. This review article briefly addresses the role of adipokines in hepatitis and liver fibrosis. Here, studies having analyzed these proteins in systemic blood in cirrhotic patients are listed to identify adipokines that are comparably changed in the different cohorts of patients with liver cirrhosis. Some studies measured these proteins in systemic, hepatic and portal vein blood or after TIPS to specify the tissues contributing to circulating levels of these proteins and the effect of portal hypertension, respectively.

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Visfatin: An adipokine activator of rat hepatic stellate cells

Cited by 9 publications

References 41 publications

Visfatin exacerbates hepatic inflammation and fibrosis in a methionine‐choline‐deficient diet mouse model

Visfatin exacerbates hepatic inflammation and fibrosis in a methionine‐choline‐deficient diet mouse model

Visfatin increases miR-21 to promote migration in HCC

Adipokines in Liver Cirrhosis

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