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Hepatic stellate cell

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https://www.readbyqxmd.com/read/28531915/bone-marrow-stem-cells-anti-liver-fibrosis-potency-inhibition-of-hepatic-stellate-cells-activity-and-extracellular-matrix-deposition
#1
Ervina Julien Sitanggang, Radiana Dhewayani Antarianto, Sri Widia A Jusman, Jeanne Adiwinata Pawitan, Ahmad Aulia Jusuf
Transplantation of bone marrow derived stem cells (BMSCs) has been reported inhibits liver fibrosis. Several in vitro studies by co-culturing BMSCs and hepatic stellate cells (HSCs) indirectly or directly in 2D models showed inhibition of HSC as the key player in liver fibrosis. In this study, we investigated direct effect of BMSCs on HSCs by co-culturing BMSCs and HSCs in 3D model as it represents the liver microenvironment with intricate cell-cell and cell-matrix interactions. Primary isolated rat HSCs and BMSCs were directly co-cultured at 1:1 ratio with hanging drop method...
May 30, 2017: International Journal of Stem Cells
https://www.readbyqxmd.com/read/28527913/von-willebrand-factor-deficiency-reduces-liver-fibrosis-in-mice
#2
Nikita Joshi, Anna K Kopec, Jessica L Ray, Holly Cline-Fedewa, Dafna J Groeneveld, Ton Lisman, James P Luyendyk
Liver diseases are associated with complex changes in the hemostatic system and elevated levels of the platelet-adhesive protein Von Willebrand factor (VWF) are reported in patients with acute and chronic liver damage. Although elevated levels of VWF are associated with fibrosis in the general population, the role of VWF in acute and chronic liver injury has not been examined in depth in experimental settings. We tested the hypothesis that VWF deficiency inhibits experimental liver injury and fibrosis. Wild-type (WT) and VWF-deficient mice were challenged with carbon tetrachloride (CCl4) and the impact of VWF deficiency on acute liver injury and chronic liver fibrosis was determined...
May 17, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/28526827/activated-hepatic-stellate-cells-secrete-periostin-to-induce-stem-cell-like-phenotype-of-residual-hepatocellular-carcinoma-cells-after-heat-treatment
#3
Rui Zhang, Rong-Rong Yao, Jing-Huan Li, Gang Dong, Min Ma, Qiong-Dan Zheng, Dong-Mei Gao, Jie-Feng Cui, Zheng-Gang Ren, Rong-Xin Chen
Some evidences show that residual tumor after thermal ablation will progress rapidly. However, its mechanisms remain unclear. Here, we assessed whether activated HSCs could regulate stem cell-like property of residual tumor after incomplete thermal ablation to promote tumor progression. Human HCC cell lines were exposed to sublethal heat treatment to simulate the peripheral zone of thermal ablation. After residual HCC cells were cultured with conditional medium (CM) from activated HSCs, parameters of the stem cell-like phenotypes were analyzed...
May 19, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28525892/rasal1-is-a-potent-regulator-of-hepatic-stellate-cell-activity-and-liver-fibrosis
#4
Akemi Takata, Motoyuki Otsuka, Takahiro Kishikawa, Mari Yamagami, Rei Ishibashi, Kazuma Sekiba, Tatsunori Suzuki, Motoko Ohno, Yui Yamashita, Takaya Abe, Ryota Masuzaki, Tsuneo Ikenoue, Kazuhiko Koike
Liver fibrosis, leading to cirrhosis and liver failure, can occur after chronic liver injury. The transition of hepatic stellate cells (HSCs) from quiescent cells into proliferative and fibrogenic cells is a central event in liver fibrosis. Here, we show that RAS protein activator like-1 (RASAL1), a RAS-GTPase-activating protein, which switches off RAS activity, is significantly decreased during HSC activation, and that HSC activation can be antagonized by forced expression of the RASAL1 protein. We demonstrate that RASAL1 suppresses HSC proliferation by regulating the Ras-MAPK pathway, and that RASAL1 suppresses HSC fibrogenic activity by regulating the PKA-LKB1-AMPK-SRF pathway by interacting with angiotensin II receptor, type 1...
May 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28520165/targeting-ccl4-induced-liver-fibrosis-by-rna-interference-mediated-inhibition-of-cyclin-e1-in-mice
#5
Jörg-Martin Bangen, Linda Hammerich, Roland Sonntag, Maike Baues, Ute Haas, Daniela Lambertz, Thomas Longerich, Twan Lammers, Frank Tacke, Christian Trautwein, Christian Liedtke
Initiation and progression of liver fibrosis requires proliferation and activation of resting hepatic stellate cells (HSC). Cyclin E1 (CcnE1) is the regulatory subunit of the Cyclin-dependent Kinase 2 (Cdk2) and controls cell cycle re-entry. We have recently shown that genetic inactivation of CcnE1 prevents activation, proliferation and survival of HSC and protects from liver fibrogenesis. The aim of the present study was to translate these findings into pre-clinical applications using an RNAi-based approach...
May 18, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28518142/mir-130a-3p-attenuates-activation-and-induces-apoptosis-of-hepatic-stellate-cells-in-nonalcoholic-fibrosing-steatohepatitis-by-directly-targeting-tgfbr1-and-tgfbr2
#6
Yang Wang, Jinghua Du, Xuemin Niu, Na Fu, Rongqi Wang, Yuguo Zhang, Suxian Zhao, Dianxing Sun, Yuemin Nan
Nonalcoholic fibrosing steatohepatitis is a uniform process that occurs throughout nonalcoholic fatty liver disease (NAFLD). MicroRNAs (miRNAs) have been shown to be involved in the biological processes, but the role and molecular mechanism of miRNAs in NAFLD are not entirely clear. In this study, we observed a significant reduction in the expression of miR-130a-3p in livers of a mouse model with fibrosis induced by a methionine-choline-deficient diet, of NAFLD patients, and in activated hepatic stellate cells (HSCs)...
May 18, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28508586/role-and-regulation-of-autophagy-and-apoptosis-by-nitric-oxide-in-hepatic-stellate-cells-during-acute-liver-failure
#7
Li Jin, Heng Gao, JiuPing Wang, ShuJuan Yang, Jing Wang, JingFeng Liu, Yuan Yang, TaoTao Yan, Tianyan Chen, Yingren Zhao, Yingli He
BACKGROUND & AIMS: We previously found that hepatic stellate cell (HSC) activation induced by autophagy maintains the liver architecture to prevent collapse during acute liver failure (ALF). Nitric oxide (NO) has shown to induce HSC apoptosis. Whether and how NO is involved in ALF and autophagy remains unclear. METHODS: ALF patients were recruited to investigate the correlation between plasma NO levels and clinical features. Liver tissues were collected from chronic hepatitis patients by biopsy and from ALF patients who had undergone liver transplantation...
May 15, 2017: Liver International: Official Journal of the International Association for the Study of the Liver
https://www.readbyqxmd.com/read/28506744/hepatic-stellate-cells-as-key-target-in-liver-fibrosis
#8
Takaaki Higashi, Scott L Friedman, Yujin Hoshida
Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or "activation") of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation...
May 12, 2017: Advanced Drug Delivery Reviews
https://www.readbyqxmd.com/read/28506098/long-term-influence-of-sialoadenectomy-on-the-liver-of-male-albino-rat
#9
Abeer A Mahmoud, Ebtehal Z Hassan, Eman M Askar
Epidermal growth factor is an endocrine product of the submandibular gland; the liver is an important target of its action and is affected by sialoadenectomy. Thirty rats were used in this study and divided into group I (sham-operated animals), group II (sialoadenectomy after 4 weeks), and group III (sialoadenectomy after 10 weeks). Liver samples were processed for light and electron microscope examination. Sialoadenectomy induced mild-to-moderate liver damage which persists up to 10 weeks after the operation...
May 16, 2017: Ultrastructural Pathology
https://www.readbyqxmd.com/read/28504959/casticin-attenuates-liver-fibrosis-and-hepatic-stellate-cell-activation-by-blocking-tgf-%C3%AE-smad-signaling-pathway
#10
Ling Zhou, Xiaoying Dong, Linlin Wang, Lanlan Shan, Ting Li, Wanfu Xu, Yan Ding, Mingqiang Lai, Xiaojun Lin, Meng Dai, Xiaochun Bai, Chunhong Jia, Hang Zheng
Although many advances have been made in understanding the pathogenesis of liver fibrosis, few options are available for treatment. Casticin, one of the major flavonoids in Fructus Viticis extracts, has shown hepatoprotective potential, but its effects on liver fibrosis are not clear. In this study, we investigated the antifibrotic activity of casticin and its underlying mechanism in vivo and in vitro. Male mice were injected intraperitoneally with carbon tetrachloride (CCl4) or underwent bile duct ligation (BDL) to induce liver fibrosis, followed by treatment with casticin or vehicle...
April 27, 2017: Oncotarget
https://www.readbyqxmd.com/read/28504685/spleen-derived-lipocalin-2-in-the-portal-vein-regulates-kupffer-cells-activation-and-attenuates-the-development-of-liver-fibrosis-in-mice
#11
Tomonori Aoyama, Kyoko Kuwahara-Arai, Akira Uchiyama, Kazuyoshi Kon, Hironao Okubo, Shunhei Yamashina, Kenichi Ikejima, Shigehiro Kokubu, Akihisa Miyazaki, Sumio Watanabe
The liver has an immune tolerance against gut-derived products from the portal vein (PV). A disruption of the gut-liver axis leads to liver injury and fibrosis. The spleen is connected to the PV and regulates immune functions. However, possible splenic effects on liver fibrosis development are unclear. Lipocalin-2 (Lcn2) is an antimicrobial protein that regulates macrophage activation. To clarify the role of the spleen in liver fibrosis development, we induced liver fibrosis in mice after splenectomy, and investigated liver fibrosis development...
May 15, 2017: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/28502477/knockdown-of-hepatic-gonadotropin-releasing-hormone-by-vivo-morpholino-decreases-liver-fibrosis-in-multidrug-resistance-gene-2-knockout-mice-by-down-regulation-of-mir-200b
#12
Konstantina Kyritsi, Fanyin Meng, Tianhao Zhou, Nan Wu, Julie Venter, Heather Francis, Lindsey Kennedy, Paolo Onori, Antonio Franchitto, Francesca Bernuzzi, Pietro Invernizzi, Kelly McDaniel, Romina Mancinelli, Domenico Alvaro, Eugenio Gaudio, Gianfranco Alpini, Shannon Glaser
Hepatic fibrosis occurs during the progression of primary sclerosing cholangitis (PSC) and is characterized by accumulation of extracellular matrix proteins. Proliferating cholangiocytes and activated hepatic stellate cells (HSCs) participate in the promotion of liver fibrosis during cholestasis. Gonadotropin-releasing hormone (GnRH) is a trophic peptide hormone synthesized by hypothalamic neurons and the biliary epithelium and exerts its biological effects on cholangiocytes by interaction with the receptor subtype (GnRHR1) expressed by cholangiocytes and HSCs...
May 11, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28501125/direct-orthotopic-implantation-of-hepatic-organoids
#13
Vivian X Zhou, Macarena Lolas, Tammy T Chang
BACKGROUND: Liver organoids show potential for development as a tissue replacement therapy for patients with end-stage liver disease, but efficient methods for introducing organoids into host livers have not been established. In this study, we aimed to develop a surgical technique to implant hepatic organoids into the liver and assess their engraftment. METHODS: Donor hepatocytes were isolated from ROSA26 C57BL/6 mice, so that engrafted cells, when implanted into wild-type mice, could be easily identified by X-gal staining...
May 1, 2017: Journal of Surgical Research
https://www.readbyqxmd.com/read/28498509/molecular-interplays-in-hepatic-stellate-cells-apoptosis-senescence-and-phenotype-reversion-as-cellular-connections-that-modulates-liver-fibrosis
#14
REVIEW
Silva B O, Ramos L F, Moraes K C M
Liver fibrosis is a pathophysiological process correlated with intense repair and cicatrization mechanisms in injured liver, and over the past few years, the characterization of the fine-tuning of molecular interconnections that support the development of liver fibrosis has been investigated. In this cellular process, the hepatic stellate cells (HSCs) support the organ fibrogenesis. The HSCs are found in two distinct morpho-physiological states: quiescent and activated. In normal liver, most HSCs are found in quiescent state, presenting a considerable amount of lipid droplets in the cytoplasm, while in injured liver the activated phenotype of HSCs is a myofibroblast,that secretes extracellular matrix elements and contributes to the establishment of the fibrotic process...
May 12, 2017: Cell Biology International
https://www.readbyqxmd.com/read/28496142/src-homology-protein-tyrosine-phosphatase-1-agonist-sc-43-reduces-liver-fibrosis
#15
Tung-Hung Su, Chung-Wai Shiau, Ping Jao, Nian-Jie Yang, Wei-Tien Tai, Chun-Jen Liu, Tai-Chung Tseng, Hung-Chih Yang, Chen-Hua Liu, Kai-Wen Huang, Ting-Chen Hu, Yu-Jen Huang, Yao-Ming Wu, Li-Ju Chen, Pei-Jer Chen, Ding-Shinn Chen, Kuen-Feng Chen, Jia-Horng Kao
This study aimed to investigate the role of src-homology protein tyrosine phosphatase-1 (SHP-1)-signal transducer and activator of transcription 3 (STAT3) pathway in liver fibrogenesis and the anti-fibrotic effect of SHP-1 agonist. The antifibrotic activity of SC-43, a sorafenib derivative with an enhanced SHP-1 activity, was evaluated in two fibrosis mouse models by carbon tetrachloride induction and bile duct ligation. Rat, human, and primary mouse hepatic stellate cells (HSCs) were used for mechanistic investigations...
May 11, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28496045/cholic-acid-enhances-visceral-adiposity-atherosclerosis-and-nonalcoholic-fatty-liver-disease-in-microminipigs
#16
Sohsuke Yamada, Hiroaki Kawaguchi, Tomonobu Yamada, Xin Guo, Kei Matsuo, Taiji Hamada, Naoki Miura, Takashi Tasaki, Akihide Tanimoto
AIM: We have recently established a novel swine model for studies of atherosclerosis using Microminipigs(TM) (µMPs) fed a high-fat/high-cholesterol diet (HcD). Using this swine model, we re-evaluated the effects of dietary cholic acid (CA) on serum lipid profile, atherosclerosis and hepatic injuries. METHODS: The µMPs were fed HcD supplemented with 0.7% CA (HcD+CA) for eight weeks, and the effect of CA on serum lipoprotein levels, expression of oxidative stress markers, adiposity and lesion formation in the aorta, liver, and other organs was investigated...
May 11, 2017: Journal of Atherosclerosis and Thrombosis
https://www.readbyqxmd.com/read/28494550/-regulatory-effect-of-vitamin-d-on-proliferation-and-apoptosis-of-hepatic-stellate-cells
#17
J Li, H X Wang, Z Q Cui
No abstract text is available yet for this article.
April 20, 2017: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
https://www.readbyqxmd.com/read/28494543/-effects-of-anluohuaxianwan-on-transforming-growth-factor-%C3%AE-1-and-related-signaling-pathways-in-rats-with-carbon-tetrachloride-induced-liver-fibrosis
#18
W Lu, Y H Gao, Z Z Wang, Y S Cai, Y Q Yang, Y Q Miao, F Pei, X E Liu, H Zhuang
Objective: The traditional Chinese medicine Anluohuaxianwan (ALHXW) has been used to treat liver fibrosis induced by chronic hepatitis B virus (HBV) infection. However, the anti-fibrosis mechanisms of ALHXW remain to be investigated. This study used a rat model of carbon tetrachloride (CCl(4))-induced liver fibrosis to explore the potential antifibrogenic mechanisms of ALHXW. Methods: Twenty-seven male Wistar rats were randomly assigned to control group, model group, and treatment group (n = 9 per group). Rats in the model and treatment group were injected intraperitoneally with 40% CCl(4)(2 ml/kg), and rats in the control group were administered saline twice a week for 6 weeks...
April 20, 2017: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
https://www.readbyqxmd.com/read/28489573/recombinant-sjp40-protein-enhances-p27-promoter-expression-in-hepatic-stellate-cells-via-an-e2f1-dependent-mechanism
#19
Yinong Duan, Lei Lyu, Dandan Zhu, Jianxin Wang, Jinling Chen, Liuting Chen, Chunzhao Yang, Xiaolei Sun
The p27 protein plays a critical role in cell cycle arrest. Our previous studies have demonstrated that recombinant P40 protein from Schistosoma japonicum (rSjP40) could induce G1 phase arrest of cell cycle. We, therefore, attempted to observe the effect of rSjP40 on p27 promoter activity in LX-2 cells and to explore its potential mechanisms in this study. Using both Western blot and dual-luciferase reporter assay, we demonstrated that rSjP40 could enhance the expression of p27 in LX-2 cells. Results obtained using truncated fragments of p27 promoter showed that rSjP40 increased p27 promoter activity in LX-2 cells, mainly via some transcription factors that bind to the -1740/-873 region of p27 promoter...
April 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/28487545/mechanisms-of-hepatic-stellate-cell-activation
#20
REVIEW
Takuma Tsuchida, Scott L Friedman
Hepatic fibrosis is a dynamic process characterized by the net accumulation of extracellular matrix resulting from chronic liver injury of any aetiology, including viral infection, alcoholic liver disease and NASH. Activation of hepatic stellate cells (HSCs) - transdifferentiation of quiescent, vitamin-A-storing cells into proliferative, fibrogenic myofibroblasts - is now well established as a central driver of fibrosis in experimental and human liver injury. Yet, the continued discovery of novel pathways and mediators, including autophagy, endoplasmic reticulum stress, oxidative stress, retinol and cholesterol metabolism, epigenetics and receptor-mediated signals, reveals the complexity of HSC activation...
May 10, 2017: Nature Reviews. Gastroenterology & Hepatology
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