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Chen X.,Xinjiang University | Chen X.,Co constructing Key Laboratory for Cell Differentiation Regulation | Xu C.,Co constructing Key Laboratory for Cell Differentiation Regulation | Xu C.,Henan Normal University | And 2 more authors.
Journal of Interferon and Cytokine Research | Year: 2010

The immunomodulator interferons are assumed not only to fight tumor progress but also to inhibit liver regeneration by inactivating Kupffer cells. The potential mechanism is still poorly characterized. In particular, the relevance of interferon signaling to liver regeneration at cellular level still remains unknown. In this study, 8 types of rat liver cells from the regenerating liver at 10 recovery time points were separately isolated by percoll density gradient centrifugation and immunomagnetic bead. Transcription profiles of interferon-signaling pathway genes in each cell type along the time course of liver restoration were detected using Rat Genome 230 2.0 Array covering about 12, 727 known genes. The chip data demonstrated that hepatocyte mainly up-regulated the IFN-α1-mediated JAK/STAT pathway genes; biliary epithelial cell mostly expressed the IFN-β1-mediated p38 MAPK pathway genes; while the IFN-γ-activated JAK/STAT pathway genes were down-regulated particularly in HSC, KC, and DC during liver regeneration. It is inferred that STAT3, in contrast to STAT1, seemingly takes a more active role in IFN-α1-mediated JAK/STAT pathway in hepatocyte; IFN-β1-mediated p38 MAPK pathway possibly to some extent affects inflammation and apoptosis of biliary epithelial cell during liver regeneration; IFN-γ-induced JAK/STAT pathway may be associated with the attenuated apoptosis induction in HSC, KC, and DC. Our data suggested that a better understanding about how interferon signals at liver cell level might be helpful in developing an effective approach to protecting against the inhibition of regeneration. © Mary Ann Liebert, Inc. Source


Chen X.,Xinjiang University | Chen X.,Co constructing Key Laboratory for Cell Differentiation Regulation | Xu C.,Co constructing Key Laboratory for Cell Differentiation Regulation | Xu C.,Henan Normal University | And 2 more authors.
Genome | Year: 2010

It has been documented that chemokines can positively regulate liver regeneration at the tissue level after partial hepatectomy. However, the precise mechanism of the effects of chemokines on regeneration at the cellular level remains poorly defined. In this study, 8 cell types from rat regenerating liver at 8 recovery time points after 2/3 hepatectomy were isolated and purified using Percoll density gradient centrifugation and immunomagnetic bead methods. The expression profiles of each cell type were monitored using a microarray. RT-PCR analysis was performed to validate the reliability of the microarray results. The results showed that, on the whole, the expression profiles of chemokine and receptor genes varied among different cell types; most genes involved in chemokine signaling pathways showed an increase in expression across the 8 liver cell types during liver regeneration. The implication of these genes in regeneration was analyzed by bioinformatics and systems biology methods. According to the microarray results and gene synergy, activation of chemokine signaling pathways at 24 h in biliary epithelial cells and at 2-12 h in dendritic cells may be triggered by CCL2-CCR2 and CCL7-CCR3, respectively; activation of Plc/Pkc and Pi3k/Akt pathways at 2-12 h in sinusoidal endothelial cells might be caused by CCL7-CCR1; and activation of the Src/Ptk, Src/Vav, and Plc/Pkc pathways at the priming stage may be related to the inductive effect of CCL7. These data suggest the potential relevance of the pro-inflammatory chemokines for liver regeneration at the cellular level. Source


Xu C.,Henan Normal University | Xu C.,Co constructing Key Laboratory for Cell Differentiation Regulation | Chen X.,Co constructing Key Laboratory for Cell Differentiation Regulation | Chen X.,Xinjiang University | And 8 more authors.
Genes and Genomics | Year: 2012

It has been widely accepted that hepatocytes are critical for liver regeneration (LR), but very little is known about the role of biliary epithelial cells (BECs) in this event, so this study aims to manifest the relevance of BECs with LR. High purity population of BECs was obtained using Percoll gradient centrifugation combined with immunomagnetic-bead separation technique. Transcriptional profiles of BECs from rat regenerating liver after 2/3 hepatectomy were monitored with rat genome 230 2.0 array. Microarray analysis results were evaluated by RT-PCR assays. Of all the genes on the array, 1262 known genes and 1026 unknown genes were related to LR. 79 of 1262 known genes showed a 20-fold change in expression level, mainly participating in primary metabolism and inflammatory response. In contrast to the regenerating liver, BEC division did not occur at proliferative phase of LR; alterations in nucleic acid, lipid and protein metabolism were significantly different from each other or within the same substance metabolism at different phases; the active signaling pathways in priming phase were mediated mainly by G protein-coupled receptor, small GTPase and Wnt receptor. Transport-related genes showed up-regulated expression mainly in priming and proliferative phases, possibly linked to cell membrane formation and transport function recovery of BECs in the late phase. In brief, comparative analysis of biological activities of BECs and the regenerating liver reveals that bio-logical activities at the cellular level are not always consistent with those at tissue level, suggesting the necessity of cell level investigation on liver regeneration. Finally, expression of BEC markers in hepatocytes may suggest the potential of hepatocytes to transdifferentiate into BEC. © 2012 The Genetics Society of Korea and Springe. Source

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