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Interaction between insulin-like growth factor binding protein-related protein 1 and transforming growth factor beta 1 in primary hepatic stellate cells.
Hepatobiliary Pancreat Dis Int. 2017 Aug 15; 16(4):395-404.HP

Abstract

BACKGROUND

We previously showed that insulin-like growth factor binding protein-related protein 1 (IGFBPrP1) is a novel mediator in liver fibrosis. Transforming growth factor beta 1 (TGFβ1) is known as the strongest effector of liver fibrosis. Therefore, we aimed to investigate the detailed interaction between IGFBPrP1 and TGFβ1 in primary hepatic stellate cells (HSCs).

METHODS

We overexpressed TGFβ1 or IGFBPrP1 and inhibited TGFβ1 expression in primary HSCs for 6, 12, 24, 48, 72, and 96 hours to investigate their interaction and observe the accompanying expressions of α-smooth muscle actin (α-SMA), collagen I, fibronectin, and phosphorylated-mothers against decapentaplegic homolog 2/3 (p-Smad2/3).

RESULTS

We found that the adenovirus vector encoding the TGFβ1 gene (AdTGFβ1) induced IGFBPrP1 expression while that of α-SMA, collagen I, fibronectin, and TGFβ1 increased gradually. Concomitantly, AdIGFBPrP1 upregulated TGFβ1, α-SMA, collagen I, fibronectin, and p-Smad2/3 in a time-dependent manner while IGFBPrP1 expression was decreased at 96 hours. Inhibition of TGFβ1 expression reduced the IGFBPrP1-stimulated expression of α-SMA, collagen I, fibronectin, and p-Smad2/3.

CONCLUSIONS

These findings for the first time suggest the existence of a possible mutually regulation between IGFBPrP1 and TGFβ1, which likely accelerates liver fibrosis progression. Furthermore, IGFBPrP1 likely participates in liver fibrosis in a TGFβ1-depedent manner, and may act as an upstream regulatory factor of TGFβ1 in the Smad pathway.

Authors+Show Affiliations

Department of Gastroenterology and Hepatology, Taiyuan 030001, China.Department of Gastroenterology and Hepatology, Taiyuan 030001, China; Experimental Center of Science and Research, Taiyuan 030001, China; The First Clinical Hospital of Shanxi Medical University; and Key Laboratory of Cell Physiology, Provincial Department of the Ministry of Education, Shanxi Medical University, Taiyuan 030001, China.Department of Gastroenterology and Hepatology, Taiyuan 030001, China; Experimental Center of Science and Research, Taiyuan 030001, China; The First Clinical Hospital of Shanxi Medical University; and Key Laboratory of Cell Physiology, Provincial Department of the Ministry of Education, Shanxi Medical University, Taiyuan 030001, China.Department of Gastroenterology and Hepatology, Taiyuan 030001, China; Experimental Center of Science and Research, Taiyuan 030001, China; The First Clinical Hospital of Shanxi Medical University; and Key Laboratory of Cell Physiology, Provincial Department of the Ministry of Education, Shanxi Medical University, Taiyuan 030001, China.Department of Gastroenterology and Hepatology, Taiyuan 030001, China; Experimental Center of Science and Research, Taiyuan 030001, China; The First Clinical Hospital of Shanxi Medical University; and Key Laboratory of Cell Physiology, Provincial Department of the Ministry of Education, Shanxi Medical University, Taiyuan 030001, China.Department of Gastroenterology and Hepatology, Taiyuan 030001, China; Experimental Center of Science and Research, Taiyuan 030001, China; The First Clinical Hospital of Shanxi Medical University; and Key Laboratory of Cell Physiology, Provincial Department of the Ministry of Education, Shanxi Medical University, Taiyuan 030001, China. Electronic address: lixinliu6@hotmail.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28823370

Citation

Li, Xiu-Qing, et al. "Interaction Between Insulin-like Growth Factor Binding Protein-related Protein 1 and Transforming Growth Factor Beta 1 in Primary Hepatic Stellate Cells." Hepatobiliary & Pancreatic Diseases International : HBPD INT, vol. 16, no. 4, 2017, pp. 395-404.
Li XQ, Zhang QQ, Zhang HY, et al. Interaction between insulin-like growth factor binding protein-related protein 1 and transforming growth factor beta 1 in primary hepatic stellate cells. HBPD INT. 2017;16(4):395-404.
Li, X. Q., Zhang, Q. Q., Zhang, H. Y., Guo, X. H., Fan, H. Q., & Liu, L. X. (2017). Interaction between insulin-like growth factor binding protein-related protein 1 and transforming growth factor beta 1 in primary hepatic stellate cells. Hepatobiliary & Pancreatic Diseases International : HBPD INT, 16(4), 395-404. https://doi.org/10.1016/S1499-3872(17)60013-4
Li XQ, et al. Interaction Between Insulin-like Growth Factor Binding Protein-related Protein 1 and Transforming Growth Factor Beta 1 in Primary Hepatic Stellate Cells. HBPD INT. 2017 Aug 15;16(4):395-404. PubMed PMID: 28823370.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interaction between insulin-like growth factor binding protein-related protein 1 and transforming growth factor beta 1 in primary hepatic stellate cells. AU - Li,Xiu-Qing, AU - Zhang,Qian-Qian, AU - Zhang,Hai-Yan, AU - Guo,Xiao-Hong, AU - Fan,Hui-Qin, AU - Liu,Li-Xin, PY - 2016/06/20/received PY - 2016/12/30/accepted PY - 2017/8/22/entrez PY - 2017/8/22/pubmed PY - 2018/5/9/medline KW - Smad pathway KW - extracellular matrix KW - insulin-like growth factor binding protein-related protein 1 KW - primary hepatic stellate cells KW - transforming growth factor β1 KW - α-smooth muscle actin SP - 395 EP - 404 JF - Hepatobiliary & pancreatic diseases international : HBPD INT JO - HBPD INT VL - 16 IS - 4 N2 - BACKGROUND: We previously showed that insulin-like growth factor binding protein-related protein 1 (IGFBPrP1) is a novel mediator in liver fibrosis. Transforming growth factor beta 1 (TGFβ1) is known as the strongest effector of liver fibrosis. Therefore, we aimed to investigate the detailed interaction between IGFBPrP1 and TGFβ1 in primary hepatic stellate cells (HSCs). METHODS: We overexpressed TGFβ1 or IGFBPrP1 and inhibited TGFβ1 expression in primary HSCs for 6, 12, 24, 48, 72, and 96 hours to investigate their interaction and observe the accompanying expressions of α-smooth muscle actin (α-SMA), collagen I, fibronectin, and phosphorylated-mothers against decapentaplegic homolog 2/3 (p-Smad2/3). RESULTS: We found that the adenovirus vector encoding the TGFβ1 gene (AdTGFβ1) induced IGFBPrP1 expression while that of α-SMA, collagen I, fibronectin, and TGFβ1 increased gradually. Concomitantly, AdIGFBPrP1 upregulated TGFβ1, α-SMA, collagen I, fibronectin, and p-Smad2/3 in a time-dependent manner while IGFBPrP1 expression was decreased at 96 hours. Inhibition of TGFβ1 expression reduced the IGFBPrP1-stimulated expression of α-SMA, collagen I, fibronectin, and p-Smad2/3. CONCLUSIONS: These findings for the first time suggest the existence of a possible mutually regulation between IGFBPrP1 and TGFβ1, which likely accelerates liver fibrosis progression. Furthermore, IGFBPrP1 likely participates in liver fibrosis in a TGFβ1-depedent manner, and may act as an upstream regulatory factor of TGFβ1 in the Smad pathway. SN - 1499-3872 UR - https://www.unboundmedicine.com/medline/citation/28823370/Interaction_between_insulin_like_growth_factor_binding_protein_related_protein_1_and_transforming_growth_factor_beta_1_in_primary_hepatic_stellate_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1499-3872(17)60013-4 DB - PRIME DP - Unbound Medicine ER -