Literature DB >> 27097355

Screening for and validation of a hepatic fibrosis-related pathway induced by insulin-like growth factor-binding protein-related protein 1.

XiaoHong Guo1, HaiYan Zhang, QianQian Zhang, XiuQing Li, LiXin Liu.   

Abstract

OBJECTIVE: Our previous studies characterized insulin-like growth factor-binding protein-related protein 1 (IGFBPrP1) as a molecule that promotes hepatic fibrogenesis, but its mechanism has not been fully elucidated. Here, we have investigated the effect of IGFBPrP1 on gene expression in the hepatic fibrosis-related pathway.
MATERIALS AND METHODS: Sprague-Dawley rats received injections of an adenovirus carrying IGFBPrP1 or EGFP cDNA into their tail veins. In hepatic preparations, hepatic stellate cell activation was determined by α-smooth muscle actin expression and hepatic fibrosis by Sirius red staining and hydroxyproline content analysis. IGFBPrP1-inducible genes of the hepatic fibrosis-related pathway were assessed by PCR array. Expression of IGFBPrP1 and transforming growth factor β1 (TGFβ1) and array results were evaluated by quantitative real-time PCR and western blotting.
RESULTS: IGFBPrP1-overexpressing rats showed an increase in α-smooth muscle actin expression and collagen and hydroxyproline content in the liver. The PCR array results indicated that some genes were upregulated and some were downregulated in Ad-IGFBPrP1-infected rats. Among these, Egr1, MAP2K2 (MEK2) and MAPK3 (ERK1) expression increased, whereas PTEN and Hhip mRNA expression decreased. Egr1 protein levels increased and peaked 2 weeks after infection and then decreased gradually. PTEN protein decreased gradually in Ad-IGFBPrP1-infected rats with a concurrent increase in the degree of hepatic fibrosis. TGFβ1 levels increased during hepatic fibrosis development in liver tissues.
CONCLUSION: Egr1, PTEN, Hhip, MAP2K2 (MEK2) and MAPK3 (ERK1) were identified as candidate genes of the IGFBPrP1-induced hepatic fibrosis-related pathway. IGFBPrP1 promoted hepatic fibrosis mainly by enhancing the TGFβ1 expression that it triggered.

Entities:  

Mesh:

Substances:

Year:  2016        PMID: 27097355     DOI: 10.1097/MEG.0000000000000631

Source DB:  PubMed          Journal:  Eur J Gastroenterol Hepatol        ISSN: 0954-691X            Impact factor:   2.566


  5 in total

1.  IGFBP-6/sonic hedgehog/TLR4 signalling axis drives bone marrow fibrotic transformation in primary myelofibrosis.

Authors:  Lucia Longhitano; Daniele Tibullo; Nunzio Vicario; Cesarina Giallongo; Enrico La Spina; Alessandra Romano; Sofia Lombardo; Marina Moretti; Francesco Masia; Anna Rita Daniela Coda; Santina Venuto; Paolo Fontana; Rosalba Parenti; Giovanni Li Volti; Michelino Di Rosa; Giuseppe A Palumbo; Arcangelo Liso
Journal:  Aging (Albany NY)       Date:  2021-12-14       Impact factor: 5.682

2.  IGFBP7 remodels the tumor microenvironment of esophageal squamous cell carcinoma by activating the TGFβ1/SMAD signaling pathway.

Authors:  Xiuqing Li; Ji Zhang; Youshan Wu; Chuntao Ma; Dongying Wei; Lijuan Pan; Liangliang Cai
Journal:  Oncol Lett       Date:  2022-06-10       Impact factor: 3.111

3.  Kidney and lung tissue modifications after BDL-induced liver injury in mice are associated with increased expression of IGFBPrP1 and activation of the NF-κB inflammation pathway.

Authors:  Zhi-Hui Hu; Yang-Yang Kong; Jun-Jie Ren; Ting-Juan Huang; Yan-Qin Wang; Li-Xin Liu
Journal:  Int J Clin Exp Pathol       Date:  2020-02-01

4.  Insulin-Like Growth Factor Binding Protein-Related Protein 1 Activates Primary Hepatic Stellate Cells via Autophagy Regulated by the PI3K/Akt/mTOR Signaling Pathway.

Authors:  Yuzheng Zhou; Qianqian Zhang; Yangyang Kong; Xiaohong Guo; Haiyan Zhang; Huiqin Fan; Lixin Liu
Journal:  Dig Dis Sci       Date:  2019-08-29       Impact factor: 3.199

Review 5.  The Roles and Mechanisms of lncRNAs in Liver Fibrosis.

Authors:  Zhi He; Deying Yang; Xiaolan Fan; Mingwang Zhang; Yan Li; Xiaobin Gu; Mingyao Yang
Journal:  Int J Mol Sci       Date:  2020-02-21       Impact factor: 5.923

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.