Proteome analysis of hepatic non-parenchymal cells of immune liver fibrosis rats

Zhao, Qianqian; Feng, Yinchang; Jia, Xiaofang; Li, Yin; Zheng, Yi; Ouyang, DongSheng; Zhou, Hong‐Hao; Zhang, Lijun

doi:10.1007/s11427-014-4619-0

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…Until now, it has been discovered several possible anti-viral roles of Kupffer cells, including binding and/or uptake of virus inducing immune recognition and the production of pro-inflammatory factors resulting in inhibition of viral replication in hepatocytes, activation of neighboring cells, and attraction, activation, and interaction with other immune cells, which will further increase the anti-viral and inflammatory response. These immune activating roles of Kupffer cells are beneficial to combat viruse infection in the early stage after infection, but may also contribute to tissue damage and the development of fibrosis and cirrhosis during chronic viral hepatitis (Zhao et al, 2014). Furthermore, Kupffer cells also have immune regulatory functions, either through direct virus-Kupffer cells interaction, or as a component of the complex tolerogenic liver environment.…”

Section: Introductionmentioning

confidence: 99%

Inflammation-induced CD69+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Zhang

Jiang

et al. 2016

Sci. China Life Sci.

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Kupffer cells, the bone marrow-derived population. Hepatic CD69 + Kupffer cells suppressed Ag-nonspecific and OVA-specific CD4 T cell proliferation through mTGF-β1 both in vitro and in vivo, meanwhile, they did not interfere with activation of CD4 T cells. Thus, we have identified a new subset of inflammation-induced CD69 + Kupffer cells which can feedback inhibit CD4 T cell response via cell surface TGF-β1 at the late stage of immune response against infection. CD69 + Kupffer cells may contribute to protect host from pathological injure by preventing overactivation of immune response.

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Section: Introductionmentioning

confidence: 99%

Inflammation-induced CD69+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Zhang

Jiang

et al. 2016

Sci. China Life Sci.

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“…According to previously published protocols [ 15 , 16 ], hepatic non-parenchymal cells (NPCs) were obtained from liver tissues by collagenase type IV digestion (0.05 mg/mL) and gradient centrifugation. In brief, liver tissues were infused with perfusion buffer for up to 20 min then perfused with collagenase until digested.…”

Section: Methodsmentioning

confidence: 99%

Treatment with β-Adrenoceptor Agonist Isoproterenol Reduces Non-parenchymal Cell Responses in LPS/D-GalN-Induced Liver Injury

Wu,

Ni,

Zhang

et al. 2023

Inflammation

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There is an increasing evidence indicating the involvement of the sympathetic nervous system (SNS) in liver disease development. To achieve an extensive comprehension of the obscure process by which the SNS alleviates inflammatory damage in non-parenchymal liver cells (NPCs) during acute liver failure (ALF), we employ isoproterenol (ISO), a beta-adrenoceptor agonist, to mimic SNS signaling. ISO was administered to C57BL/6J mice to establish an acute liver failure (ALF) model using LPS/D-GalN, which was defined as ISO + ALF. Non-parenchymal cells (NPCs) were isolated from liver tissues and digested for tandem mass tag (TMT) labeled proteomics to identify differentially expressed proteins (DEPs). The administration of ISO resulted in a decreased serum levels of pro-inflammatory cytokines, e.g., TNF-α, IL-1β, and IL-6 in ALF mice, which alleviated liver damage. By using TMT analysis, it was possible to identify 1587 differentially expressed proteins (DEPs) in isolated NPCs. Notably, over 60% of the DEPs in the ISO + ALF vs. ALF comparison were shared in the Con vs. ALF comparison. According to enrichment analysis, the DEPs influenced by ISO in ALF mice were linked to biological functions of heme and fatty acid metabolism, interferon gamma response, TNFA signaling pathway, and mitochondrial oxidation function. Protein-protein interaction network analysis indicated Mapk14 and Caspase3 may serve as potentially valuable indicators of ISO intervention. In addition, the markers on activated macrophages, such as Mapk14, Casp1, Casp8, and Mrc1, were identified downregulated after ISO initiation. ISO treatment increased the abundance of anti-inflammatory markers in mouse macrophages, as evidenced by the immunohistochemistry (IHC) slides showing an increase in Arg + staining and a reduction in iNOS + staining. Furthermore, pretreatment with ISO also resulted in a reduction of LPS-stimulated inflammation signaling markers, Mapk14 and NF-κB, in human THP-1 cells. Prior treatment with ISO may have the potential to modify the biological functions of NPCs and could serve as an innovative pharmacotherapy for delaying the pathogenesis and progression of ALF.

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“…The upper supernatant was discarded and the remaining sediment washed with phosphate-buffered saline (PBS, Sangon Biotech, Shanghai, China) at 1,500 x g for 5 min; the deposit was then resuspended in fresh PBS. Subsequently, density gradient centrifugation was performed using Percoll (Biodee Biotechnology, Beijing, China) to isolate the cells as previously described (18,19) with slight modifications. The cell suspension was processed using a 60 and 40% Percoll gradient (1:1:1 volume ratio) at 3,000 x g for 30 min at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Establishment of a highly metastatic model with a newly isolated lung adenocarcinoma cell line

Cui

Geng

et al. 2015

International Journal of Oncology

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Abstract. Lung cancer is the leading cause of malignancyrelated death worldwide, and metastasis always results in a poor prognosis. However, therapeutic progress is hampered by a deficiency of appropriate pre-clinical metastatic models. To bridge this experimental gap, we developed an in vivo metastatic model via subcutaneous (s.c.) injection. The original cell line (XL-2) adopted in this model was newly isolated from the ascites of a patient with extensive metastases of lung adenocarcinoma, thereby avoiding any alteration of its initial molecular biology features from artificial serial cultivation. After comprehensive phenotypical and histological analysis, it was identified as a lung adenocarcinoma cell line. Additionally, the drug test showed that XL-2 cell line was sensitive to docetaxel, and resistant to doxorubicin, indicating it might serve as a cell line model of drug resistance for identifying mechanisms of tumors resistant to doxorubicin. Through this s.c. model, we further obtained a highly metastatic cell line (designated XL-2sci). The metastatic rate of mice in XL-2 group was 3/10, in contrast to the rate of 9/10 in XL-2sci group. Optical imaging, micro-computed tomography (micro-CT) scanning and Transwell assays were further applied to identify the enhanced metastatic capacity of Xl-2sci cells both in vivo and in vitro. Compared with XL-2 cells, ITRAQ labeled proteomics profiling study showed that some tumor metastasisassociated proteins were upregulated in XL-2sci cells, which also indicated the reliability of our model. Proliferation ability of XL-2 and XL-2sci were also evaluated. Results showed that highly metastatic XL-2sci possessed a decreased proliferation capacity versus XL-2, which demonstrated that its increased metastatic activity was not facilitated by a faster growth rate.In conclusion, we successfully developed an in vivo metastatic model using a newly established lung adenocarcinoma cell line, which will be beneficial to further investigations of lung cancer metastasis and to the development of anti-metastasis drugs.

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Proteome analysis of hepatic non-parenchymal cells of immune liver fibrosis rats

Cited by 8 publications

References 32 publications

Inflammation-induced CD69+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Inflammation-induced CD69+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Treatment with β-Adrenoceptor Agonist Isoproterenol Reduces Non-parenchymal Cell Responses in LPS/D-GalN-Induced Liver Injury

Establishment of a highly metastatic model with a newly isolated lung adenocarcinoma cell line

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