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Crispr/cas9 hepatitis

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https://www.readbyqxmd.com/read/29097363/interrogation-of-the-atherosclerosis-associated-sort1-sortilin-1-locus-with-primary-human-hepatocytes-induced-pluripotent-stem-cell-hepatocytes-and-locus-humanized-mice
#1
Xiao Wang, Avanthi Raghavan, Derek T Peters, Evanthia E Pashos, Daniel J Rader, Kiran Musunuru
OBJECTIVE: The noncoding single-nucleotide polymorphism rs12740374 has been hypothesized to be the causal variant responsible for liver-specific modulation of SORT1(sortilin 1) expression (ie, expression quantitative trait locus) and, by extension, the association of the SORT1 locus on human chromosome 1p13 with low-density lipoprotein cholesterol levels and coronary heart disease. The goals of this study were to compare 3 different hepatocyte models in demonstrating that the rs12740374 minor allele sequence is responsible for transcriptional activation of SORT1 expression...
November 2, 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/29091957/hepatitis-e-virus-hev-egress-role-of-bst2-tetherin-and-interferon-induced-long-non-coding-rna-lncrna-bispr
#2
Daizy Paliwal, Prashant Joshi, Subrat Kumar Panda
BACKGROUND: The biology of Hepatitis E Virus (HEV), a common cause of epidemic and sporadic hepatitis, is still being explored. HEV exits liver through bile, a process which is essential for its natural transmission by feco-oral route. Though the process of this polarised HEV egress is not known in detail, HEV pORF3 and hepatocyte actin cytoskeleton have been shown to play a role. METHODS: Our transcriptome analysis in Hepatitis E virus (HEV) replicon transfected Huh7 cells at 24 and 72 hrs indicated that at 24hrs, both LncBISPR and BST2, expressed by a bidirectional promoter were highly upregulated whereas at 72 hrs, BST2 expression was comparatively reduced accompanied by normal levels of BISPR...
2017: PloS One
https://www.readbyqxmd.com/read/29034887/generation-of-three-mir-122-knockout-lines-from-a-human-embryonic-stem-cell-line
#3
Yanli Liu, Feima Wu, Yuanqi Zhuang, Dongsheng Guo, Nasir Abbas, Ruzi Wei, Kepin Wang, Yan Chen, Jiawang Tao, Yuhang Wu, Fang Yuan, Tingcai Pan, Fan Yang, Keyu Lai, Liangxue Lai, Yin-Xiong Li
miR-122 is the most abundant miRNA in the human liver, accounting for 52% of the entire hepatic miRNome. Previous studies have demonstrated that miR-122 plays key roles in hepatocyte growth, metabolism, and homeostasis. Here, we created three miR-122 knockout human embryonic stem cell line lines, WAe001-A-7, WAe001-A-8, and WAe001-A-9, using the CRISPR/Cas9 technique. These mutated cell lines retained their pluripotency, in vitro differentiation potential, normal morphology, and karyotype.
October 2017: Stem Cell Research
https://www.readbyqxmd.com/read/29029439/microrna-149-suppresses-hepatic-inflammatory-response-through-antagonizing-stat3-signaling-pathway
#4
Qiqi Zhang, Jia Su, Ziwei Wang, Hui Qi, Zeyong Ge, Zhijun Li, Wei-Dong Chen, Yan-Dong Wang
Chronic inflammation is increasingly recognized as an important component of tumorigenesis and metabolic diseases. The roles of microRNA149* (miRNA149*) in inflammation remain poorly understood. Here, we demonstrate that miR-149* is a suppressor of STAT3-mediated inflammation. MiR-149*(-/-) mice were generated with CRISPR/CAS9 technique. In a lipopolysaccharide (LPS)-induced inflammation model, miR-149*(-/-) mice show more severe liver injury and inflammation, compared with wild-type (WT) mice. MiR-149*(-/-) mice also displayed elevated messenger RNA (mRNA) levels of interleukin (IL)-6, inducible nitric oxide synthase (iNOS), complement C3 (C3) and IL-4 in response to LPS...
September 12, 2017: Oncotarget
https://www.readbyqxmd.com/read/28956740/genetic-correction-and-hepatic-differentiation-of-hemophilia-b-specific-human-induced-pluripotent-stem-cells
#5
Qiong He, Hui-Hui Wang, Tao Cheng, Wei-Ping Yuan, Yu-Po Ma, Yong-Ping Jiang, Zhi-Hua Ren
Objective To genetically correct a disease-causing point mutation in human induced pluripotent stem cells (iPSCs) derived from a hemophilia B patient. Methods First, the disease-causing mutation was detected by sequencing the encoding area of human coagulation factor IX (F IX) gene. Genomic DNA was extracted from the iPSCs, and the primers were designed to amplify the eight exons of F IX. Next, the point mutation in those iPSCs was genetically corrected using CRISPR/Cas9 technology in the presence of a 129-nucleotide homologous repair template that contained two synonymous mutations...
September 27, 2017: Chinese Medical Sciences Journal, Chung-kuo i Hsüeh K'o Hsüeh Tsa Chih
https://www.readbyqxmd.com/read/28944845/efficient-inhibition-of-duck-hepatitis-b-virus-dna-by-the-crispr-cas9-system
#6
Qingfen Zheng, Li Bai, Sujun Zheng, Mei Liu, Jinyan Zhang, Ting Wang, Zhongwei Xu, Yu Chen, Jiansheng Li, Zhongping Duan
Current therapeutic strategies cannot eradicate hepatitis B virus covalently closed circular DNA (HBV cccDNA), which accounts for the persistence of HBV infection. Very recently, the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR‑associated protein 9 (Cas9) system has been used as an efficient and powerful tool for viral genome editing. Given that the primary duck hepatocyte (PDH) infected with duck hepatitis B virus (DHBV) has been widely used to study human HBV infection in vitro, the present study aimed to demonstrate the targeted inhibition of DHBV DNA, especially cccDNA, by the CRISPR/Cas9 system using this model...
November 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28939663/hepatoma-intrinsic-ccrk-inhibition-diminishes-myeloid-derived-suppressor-cell-immunosuppression-and-enhances-immune-checkpoint-blockade-efficacy
#7
Jingying Zhou, Man Liu, Hanyong Sun, Yu Feng, Liangliang Xu, Anthony W H Chan, Joanna H Tong, John Wong, Charing Ching Ning Chong, Paul B S Lai, Hector Kwong-Sang Wang, Shun-Wa Tsang, Tyler Goodwin, Rihe Liu, Leaf Huang, Zhiwei Chen, Joseph Jy Sung, King Lau Chow, Ka Fai To, Alfred Sze-Lok Cheng
OBJECTIVE: Myeloid-derived suppressor cells (MDSCs) contribute to tumour immunosuppressive microenvironment and immune-checkpoint blockade resistance. Emerging evidence highlights the pivotal functions of cyclin-dependent kinases (CDKs) in tumour immunity. Here we elucidated the role of tumour-intrinsic CDK20, or cell cycle-related kinase (CCRK) on immunosuppression in hepatocellular carcinoma (HCC). DESIGN: Immunosuppression of MDSCs derived from patients with HCC and relationship with CCRK were determined by flow cytometry, expression analyses and co-culture systems...
September 22, 2017: Gut
https://www.readbyqxmd.com/read/28874468/tim1-havcr1-is-not-essential-for-cellular-entry-of-either-quasi-enveloped-or-naked-hepatitis-a-virions
#8
Anshuman Das, Asuka Hirai-Yuki, Olga González-López, Bethany Rhein, Sven Moller-Tank, Rachel Brouillette, Lucinda Hensley, Ichiro Misumi, William Lovell, John M Cullen, Jason K Whitmire, Wendy Maury, Stanley M Lemon
Receptor molecules play key roles in the cellular entry of picornaviruses, and TIM1 (HAVCR1) is widely accepted to be the receptor for hepatitis A virus (HAV), an unusual, hepatotropic human picornavirus. However, its identification as the hepatovirus receptor predated the discovery that hepatoviruses undergo nonlytic release from infected cells as membrane-cloaked, quasi-enveloped HAV (eHAV) virions that enter cells via a pathway distinct from naked, nonenveloped virions. We thus revisited the role of TIM1 in hepatovirus entry, examining both adherence and infection/replication in cells with clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9-engineered TIM1 knockout...
September 5, 2017: MBio
https://www.readbyqxmd.com/read/28859855/degradation-of-phlpp2-by-kctd17-via-a-glucagon-dependent-pathway-promotes-hepatic-steatosis
#9
KyeongJin Kim, Dongryeol Ryu, Paola Dongiovanni, Lale Ozcan, Shruti Nayak, Beatrix Ueberheide, Luca Valenti, Johan Auwerx, Utpal B Pajvani
BACKGROUND & AIMS: Obesity-induced non-alcoholic fatty liver disease (NAFLD) develops, in part, via excess insulin-stimulated hepatic de novo lipogenesis, which increases, paradoxically, in patients with obesity-induced insulin resistance. Pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2) terminates insulin signaling by dephosphorylating Akt; levels of PHLPP2 are reduced in livers from obese mice. We investigated whether loss of hepatic PHLPP2 is sufficient to induce fatty liver in mice, mechanisms of PHLPP2 degradation in fatty liver, and expression of genes that regulate PHLPP2 in livers of patients with NAFLD...
August 28, 2017: Gastroenterology
https://www.readbyqxmd.com/read/28839466/the-grna-mirna-grna-ternary-cassette-combining-crispr-cas9-with-rnai-approach-strongly-inhibits-hepatitis-b-virus-replication
#10
Jie Wang, Ran Chen, Ruiyang Zhang, Shanlong Ding, Tianying Zhang, Quan Yuan, Guiwen Guan, Xiangmei Chen, Ting Zhang, Hui Zhuang, Frederick Nunes, Timothy Block, Shuang Liu, Zhongping Duan, Ningshao Xia, Zhongwei Xu, Fengmin Lu
The CRISPR/Cas9 system is a novel genome editing technology which has been successfully used to inhibit HBV replication. Here, we described a novel gRNA-microRNA (miRNA)-gRNA ternary cassette driven by a single U6 promoter. With an anti-HBV pri-miR31 mimic integrated between two HBV-specific gRNAs, both gRNAs could be separated from the long transcript of gRNA-miR-HBV-gRNA ternary cassette through Drosha/DGCR8 processing. The results showed that the gRNA-miR-HBV-gRNA ternary cassette could efficiently express two gRNAs and miR-HBV...
2017: Theranostics
https://www.readbyqxmd.com/read/28636533/microrna-149-suppresses-hepatic-inflammatory-response-through-antagonizing-stat3-signaling-pathway
#11
Qiqi Zhang, Jia Su, Ziwei Wang, Hui Qi, Zeyong Ge, Zhijun Li, Wei-Dong Chen, Yan-Dong Wang
Chronic inflammation is increasingly recognized as an important component of tumorigenesis and metabolic diseases. The roles of microRNA149* (miRNA149*) in inflammation remain poorly understood. Here, we demonstrate that miR-149* is a suppressor of STAT3-mediated inflammation. MiR-149*-/- mice were generated with CRISPR/CAS9 technique. In a lipopolysaccharide (LPS)-induced inflammation model, miR-149*-/- mice show more severe liver injury and inflammation, compared with wild-type (WT) mice. MiR-149*-/- mice also displayed elevated messenger RNA (mRNA) levels of interleukin (IL)-6, inducible nitric oxide synthase (iNOS), complement C3 (C3) and IL-4 in response to LPS...
June 16, 2017: Oncotarget
https://www.readbyqxmd.com/read/28627393/the-potential-and-challenges-of-crispr-cas-in-eradication-of-hepatitis-b-virus-covalently-closed-circular-dna
#12
REVIEW
Hung-Chih Yang, Pei-Jer Chen
Current antiviral therapy fails to cure chronic hepatitis B virus (HBV) infection, primarily because of the persistence of covalently closed circular DNA (cccDNA). Although nucleos(t)ide analogues (NAs) can inhibit the reverse transcriptase of HBV and suppress its replication to levels below the detection limit, viremia often rebounds after cessation of therapy. Nuclear cccDNA serves as the HBV replicative template and exhibits extraordinary stability, and is not affected by NAs. Therefore, curing chronic hepatitis B (CHB) requires novel therapy for purging cccDNA from patients...
June 13, 2017: Virus Research
https://www.readbyqxmd.com/read/28584302/crispr-cas9-mediated-p53-and-pten-dual-mutation-accelerates-hepatocarcinogenesis-in-adult-hepatitis-b-virus-transgenic-mice
#13
Yongzhen Liu, Xuewei Qi, Zhenzhen Zeng, Lu Wang, Jie Wang, Ting Zhang, Qiang Xu, Congle Shen, Guangde Zhou, Shaomin Yang, Xiangmei Chen, Fengmin Lu
The p53 mutation and altered Pten expression are two most common genetic events in Hepatitis B virus (HBV) infection related hepatocellular carcinoma (HCC). To confirm the causative role of p53 and Pten somatic mutation in HCC development, we established CRISPR/Cas9-mediated somatic gene disruption via hydrodynamic tail vein injection, allowing for in vivo targeting p53 and Pten simultaneously in adult HBV transgenic mice. Here we demonstrated that the utility of this approach resulted in macroscopic liver tumors as early as 4 months' post injection and most tumors harbored both p53 and Pten loss-of-function alterations...
June 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28574502/hepatitis-b-virus-x-protein-promotes-creb-mediated-activation-of-mir-3188-and-notch-signaling-in-hepatocellular-carcinoma
#14
Shao-Jun Zhou, Yue-Ling Deng, Hui-Fang Liang, Jonathan C Jaoude, Fu-Yao Liu
Familiar clustering of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) has been frequently reported. However, limited information is available about the underlying molecular mechanisms in HBV-related HCC patients with family history of HCC. In our previous study, Agilent miRNA Base 16.0 microarray showed miRNA profiles of the plasma of HBV-related HCC patients who had a family history of HCC. This study aims to explore the expression, function, and mechanisms of miR-3188 in HCC that might provide novel insights into the role of family history on the risk of HCC...
September 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28557353/generation-of-carbamoyl-phosphate-synthetase-1-reporter-cell-lines-for-the-assessment-of-ammonia-metabolism
#15
Yi Wang, Le Chang, Jiahui Zhai, Qiao Wu, Donggen Wang, Yunfang Wang
Both primary hepatocytes and stem cells-derived hepatocyte-like cells (HLCs) are major sources for bioartificial liver (BAL). Maintenance of hepatocellular functions and induction of functional maturity of HLCs are critical for BAL's support effect. It remains difficult to assess and improve detoxification functions inherent to hepatocytes, including ammonia clearance. Here, we aim to assess ammonia metabolism and identify ammonia detoxification enhancer by developing an imaging strategy. In hepatoma cell line HepG2, and immortalized hepatic cell line LO2, carbamoyl phosphate synthetase 1 (CPS1) gene, the first enzyme of ammonia-eliminating urea cycle, was labelled with fluorescence protein via CRISPR/Cas9 system...
May 30, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28513320/crispr-cas9-based-pten-knock-out-and-sleeping-beauty-transposon-mediated-nras-knock-in-induces-hepatocellular-carcinoma-and-hepatic-lipid-accumulation-in-mice
#16
Mingming Gao, Dexi Liu
Both Pten and Nras are downstream mediators of receptor tyrosine kinase activation that plays important roles in controlling cell survival and proliferation. Here, we investigated whether and how Pten loss cross-talks with Nras activation in driving liver cancer development in mice. Somatic disruption of hepatic Pten and overexpression of Nras were achieved in out-bred immunocompetent CD-1 mice through a hydrodynamic delivery of plasmids carrying Sleeping Beauty transposon-based integration of Nras and the CRISPR/Cas9-mediated Pten knockout system...
July 3, 2017: Cancer Biology & Therapy
https://www.readbyqxmd.com/read/28442604/hepatitis-c-virus-indirectly-disrupts-dna-damage-induced-p53-responses-by-activating-protein-kinase-r
#17
Jonathan K Mitchell, Bentley R Midkiff, Benjamin Israelow, Matthew J Evans, Robert E Lanford, Christopher M Walker, Stanley M Lemon, David R McGivern
Many DNA tumor viruses promote cellular transformation by inactivating the critically important tumor suppressor protein p53. In contrast, it is not known whether p53 function is disrupted by hepatitis C virus (HCV), a unique, oncogenic RNA virus that is the leading infectious cause of liver cancer in many regions of the world. Here we show that HCV-permissive, liver-derived HepG2 cells engineered to constitutively express microRNA-122 (HepG2/miR-122 cells) have normal p53-mediated responses to DNA damage and that HCV replication in these cells potently suppresses p53 responses to etoposide, an inducer of DNA damage, or nutlin-3, an inhibitor of p53 degradation pathways...
April 25, 2017: MBio
https://www.readbyqxmd.com/read/28404852/attachment-and-postattachment-receptors-important-for-hepatitis-c-virus-infection-and-cell-to-cell-transmission
#18
Huahao Fan, Luhua Qiao, Kyung-Don Kang, Junfen Fan, Wensheng Wei, Guangxiang Luo
Hepatitis C virus (HCV) requires multiple receptors for its attachment to and entry into cells. Our previous studies found that human syndecan-1 (SDC-1), SDC-2, and T cell immunoglobulin and mucin domain-containing protein 1 (TIM-1) are HCV attachment receptors. Other cell surface molecules, such as CD81, Claudin-1 (CLDN1), Occludin (OCLN), SR-BI, and low-density lipoprotein receptor (LDLR), function mainly at postattachment steps and are considered postattachment receptors. The underlying molecular mechanisms of different receptors in HCV cell-free and cell-to-cell transmission remain elusive...
July 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28382278/removal-of-integrated-hepatitis-b-virus-dna-using-crispr-cas9
#19
Hao Li, Chunyu Sheng, Shan Wang, Lang Yang, Yuan Liang, Yong Huang, Hongbo Liu, Peng Li, Chaojie Yang, Xiaoxia Yang, Leili Jia, Jing Xie, Ligui Wang, Rongzhang Hao, Xinying Du, Dongping Xu, Jianjun Zhou, Mingzhen Li, Yansong Sun, Yigang Tong, Qiao Li, Shaofu Qiu, Hongbin Song
The presence of hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) and the permanent integration of HBV DNA into the host genome confers the risk of viral reactivation and hepatocellular carcinoma. Nucleoside/nucleotide analogs alone have little or no capacity to eliminate replicative HBV templates consisting of cccDNA or integrated HBV DNA. Recently, CRISPR/Cas9 technology has been widely applied as a promising genome-editing tool, and HBV-specific CRISPR-Cas9 systems were shown to effectively mediate HBV cccDNA disruption...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/28300165/somatic-genome-editing-with-crispr-cas9-generates-and-corrects-a-metabolic-disease
#20
Kelsey E Jarrett, Ciaran M Lee, Yi-Hsien Yeh, Rachel H Hsu, Rajat Gupta, Min Zhang, Perla J Rodriguez, Chang Seok Lee, Baiba K Gillard, Karl-Dimiter Bissig, Henry J Pownall, James F Martin, Gang Bao, William R Lagor
Germline manipulation using CRISPR/Cas9 genome editing has dramatically accelerated the generation of new mouse models. Nonetheless, many metabolic disease models still depend upon laborious germline targeting, and are further complicated by the need to avoid developmental phenotypes. We sought to address these experimental limitations by generating somatic mutations in the adult liver using CRISPR/Cas9, as a new strategy to model metabolic disorders. As proof-of-principle, we targeted the low-density lipoprotein receptor (Ldlr), which when deleted, leads to severe hypercholesterolemia and atherosclerosis...
March 16, 2017: Scientific Reports
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