Analysis of Gene Expression Profiles of Liver Stellate Cells During Liver Regeneration in Rats

Xu, Chi; Chen, Xiaoguang; Chang, Cuifang; Wang, Gaiping; Wang, Wenbo; Zhang, Lianxing; Zhu, Qian; Wang, Lei; Zhang, Fuchun

doi:10.1007/s10059-011-0003-0

Cited by 7 publications

(5 citation statements)

References 21 publications

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“…However, Seth et al (2014) demonstrated that OPN could mediate the activation of HSCs in alcoholic liver diseases. Thus, it is inferred that OPN signaling cascade might inhibit inflammation in HSCs during LR, which was not contrary to our previous report that HSCs had suppressed immunity/ inflammation after PH in rats (Xu et al, 2011b). With respect to the effects of OPN on DCs, Shao et al (2014) revealed that OPN had a pro-chemotactic sequence for DCs and could promote the migration of DCs.…”

Section: Regulatory Roles Of Each Branch Of Opn Signaling Pathway In contrasting

confidence: 71%

Expression profiles uncover the correlation of OPN signaling pathways with rat liver regeneration at cellular level

Wang

Chen

et al. 2015

Cell Biology International

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Osteopontin (OPN) could participate in the occurrence of multiple liver diseases via promoting inflammation, cell activation, proliferation, and migration. However, the correlation of OPN with liver regeneration (LR) is poorly defined. Previous studies from us and others revealed that OPN was probably involved in the activation and proliferation of various hepatic cell types during LR. In this study, to further investigate the underlined mechanism of OPN in regulating LR, eight hepatic cell types were isolated and purified from rat regenerative livers at 10 time points. The gene expression profiles of above hepatic cells were assayed by Rat Genome 230 2.0 chips, and then IPA software was used to uncover the correlations of gene expression changes with physiological activities. The findings demonstrated that the majority of the OPN pathway-related genes were up-regulated in hepatocytes (HCs), pit cells (PCs), oval cells (OCs), and biliary epithelial cells (BECs) but down-regulated in other four cell types including sinusoidal endothelial cells (SECs), Kupffer cells (KCs), dendritic cells (DCs), and hepatic stellate cells (HSCs). Thereafter, functional enriched analysis by IPA indicated that OPN signaling pathway might promote cell proliferation, activation, migration, and inflammation in HCs, OCs, BECs, and PCs, and slightly boost proliferation and migration of SECs and KCs but inhibit inflammation response and chemotaxis in SECs and KCs and almost all physiological processes in DCs and HSCs. Morever, apoptosis, cell death, and necrosis were remarkably inhibited through JAK/STAT, ERK1/2, and NF-kB branches in almost every cell type. These above results suggest that OPN signaling pathway is closely related to HCs, OCs, BECs, and PCs but has less regulatory effect on SECs, KCs, HSCs, and DCs during rat LR.

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Section: Regulatory Roles Of Each Branch Of Opn Signaling Pathway In contrasting

confidence: 71%

Expression profiles uncover the correlation of OPN signaling pathways with rat liver regeneration at cellular level

Wang

Chen

et al. 2015

Cell Biology International

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“…Therefore, increased CXCR3 ligands could promote activated T cell migration and rejection. CXCR3 and IL-10 were found to be down-regulated in the proliferative phase during liver regeneration in rats ( Xu et al, 2011 ), suggesting that up-regulated CXCR ligands and IL-10 might have regulatory roles in liver regeneration, thereby delaying graft accommodation.…”

Section: Discussionmentioning

confidence: 99%

Combined Detection of Serum IL-10, IL-17, and CXCL10 Predicts Acute Rejection Following Adult Liver Transplantation

Kim¹,

Yoon²,

Yoo³

et al. 2016

Molecules and Cells

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Discovery of non-invasive diagnostic and predictive biomarkers for acute rejection in liver transplant patients would help to ensure the preservation of liver function in the graft, eventually contributing to improved graft and patient survival. We evaluated selected cytokines and chemokines in the sera from liver transplant patients as potential biomarkers for acute rejection, and found that the combined detection of IL-10, IL-17, and CXCL10 at 1-2 weeks post-operation could predict acute rejection following adult liver transplantation with 97% specificity and 94% sensitivity.

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“…On the other hand, studies with Lrat-deficient mice raised a question whether loss of lipid droplets causally contributes to liver fibrosis (Kluwe et al, 2011). Thus, further studies are required to elucidate the underlying mechanisms of HSC activation and to examine how RA synthesis and metabolism are regulated in the livers of Lratdeficient mice and during liver regeneration (Xu et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Retinol Binding Protein-Albumin Domain III Fusion Protein Deactivates Hepatic Stellate Cells

Park

Choi

Lee

et al. 2012

Molecules and Cells

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Liver fibrosis is characterized by accumulation of extracellular matrix, and activated hepatic stellate cells (HSCs) are the primary source of the fibrotic neomatrix and considered as therapeutic target cells. We previously showed that albumin in pancreatic stellate cells (PSCs), the key cell type for pancreatic fibrogenesis, is directly involved in the formation of vitamin A-containing lipid droplets, inhibiting PSC activation. In this study, we evaluated the anti-fibrotic activity of both albumin and retinol binding protein-albumin domain III fusion protein (R-III), designed for stellate cell-targeted delivery of albumin III, in rat primary HSCs and investigated the underlying mechanism. Forced expression of albumin or R-III in HSCs after passage 2 (activated HSCs) induced lipid droplet formation and deactivated HSCs, whereas point mutations in high-affinity fatty acid binding sites of albumin domain III abolished their activities. Exogenous R-III, but not albumin, was successfully internalized into and deactivated HSC-P2. When HSCs at day 3 after plating (pre-activated HSCs) were cultured in the presence of purified R-III, spontaneous activation of HSCs was inhibited even after passage 2, suggestive of a potential for preventive effect. Furthermore, treatment of HSCs-P2 with R-III led to a significant reduction in both cytoplasmic levels of all-trans retinoic acid and the subsequent retinoic acid signaling. Therefore, our data suggest that albumin deactivates HSCs with reduced retinoic acid levels and that R-III may have therapeutic and preventive potentials on liver fibrosis.

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Analysis of Gene Expression Profiles of Liver Stellate Cells During Liver Regeneration in Rats

Cited by 7 publications

References 21 publications

Expression profiles uncover the correlation of OPN signaling pathways with rat liver regeneration at cellular level

Expression profiles uncover the correlation of OPN signaling pathways with rat liver regeneration at cellular level

Combined Detection of Serum IL-10, IL-17, and CXCL10 Predicts Acute Rejection Following Adult Liver Transplantation

Retinol Binding Protein-Albumin Domain III Fusion Protein Deactivates Hepatic Stellate Cells

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