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3 results on '"Tgfbr1, transforming growth factor beta receptor 1"'

1. Sestrin Proteins Protect Against Lipotoxicity-Induced Oxidative Stress in the Liver via Suppression of C-Jun N-Terminal KinasesSummary

Author

Menghao Huang, Kushan Chowdhury, Zhigang Fang, X. Charlie Dong, Ming O. Li, Suthat Liangpunsakul, and Hyeong-Geug Kim

Subjects
0301 basic medicine, Sestrins, MPO, myeloperoxidase, Mitogen-Activated Protein Kinase Kinase 7, RC799-869, DMSO, dimethyl sulfoxide, FoxO, forkhead box O, Sesn1/2/3, sestrin1/2/3, medicine.disease_cause, TKO, triple knockout, Mice, PCR, polymerase chain reaction, 0302 clinical medicine, GSH, glutathione, Phosphorylation, NF-κB, nuclear factor kappa B, Original Research, Cat, catalase, Mice, Knockout, Sestrin, Gpx3, glutathione peroxidase 3, Il6, interleukin 6, WD, Western diet, biology, Chemistry, Kinase, Fatty liver, Tgfbr1, transforming growth factor beta receptor 1, Gastroenterology, Col1a1, collagen type 1 alpha 1, Nox1, NADPH oxidase 1, Diseases of the digestive system. Gastroenterology, Dgat2, diacylglycerol O-acyltransferase 2, Cell biology, Keap1, Kelch-like ECH-associated protein 1, C-Jun N-Terminal Kinase, Liver, Lipotoxicity, c-Jun N-terminal kinases, JNK, c-Jun N-terminal kinase, 030211 gastroenterology & hepatology, Disease Susceptibility, Signal transduction, NASH, nonalcoholic steatohepatitis, Gss, glutathione synthetase, Pdgfrb, platelet-derived growth factor receptor beta, Timp1, tissue inhibitor of metalloproteinase 1, Fasn, fatty acid synthase, Fatty Liver Disease, Sod, superoxide dismutase, Acta2, smooth muscle actin alpha 2, ER, endoplasmic reticulum, PA, palmitic acid, 03 medical and health sciences, 4-HNE, 4-hydroxynonenal, MKK, mitogen-activated protein kinase kinase, medicine, Animals, Humans, Srebp, sterol regulatory element-binding protein, Protein kinase A, KD, knockdown, MDA, malondialdehyde, Inflammation, KO, knockout, Hepatology, NRF2, nuclear factor erythroid 2-related like 2, JNK Mitogen-Activated Protein Kinases, Lipid Metabolism, medicine.disease, Tgfb1, transforming growth factor beta 1, WT, wild-type, mTORC, mechanistic target of rapamycin complex, Fatty Liver, AMPK, AMP-activated protein kinase, Disease Models, Animal, Oxidative Stress, Scd1, stearoyl-CoA desaturase 1, 030104 developmental biology, Gene Expression Regulation, Cytoprotection, Hepatocytes, biology.protein, BSA, bovine serum albumin, SD, standard deviation, DHE, dihydroethidium, PERK, protein kinase R-like endoplasmic reticulum kinase, Tnf, tumor necrosis factor, Biomarkers, Oxidative stress
Abstract

Background & Aims Sestrin 1/2/3 (Sesn1/2/3) belong to a small family of proteins that have been implicated in the regulation of metabolic homeostasis and oxidative stress. However, the underlying mechanisms remain incompletely understood. The aim of this work was to illustrate the collective function of Sesn1/2/3 in the protection against hepatic lipotoxicity. Methods We used Sesn1/2/3 triple knockout (TKO) mouse and cell models to characterize oxidative stress and signal transduction under lipotoxic conditions. Biochemical, histologic, and physiological approaches were applied to illustrate the related processes. Results After feeding with a Western diet for 8 weeks, TKO mice developed remarkable metabolic associated fatty liver disease that was manifested by exacerbated hepatic steatosis, inflammation, and fibrosis compared with wild-type counterparts. Moreover, TKO mice exhibited higher levels of hepatic lipotoxicity and oxidative stress. Our biochemical data revealed a critical signaling node from sestrins to c-Jun N-terminal kinases (JNKs) in that sestrins interact with JNKs and mitogen-activated protein kinase kinase 7 and suppress the JNK phosphorylation and activity. In doing so, sestrins markedly reduced palmitate-induced lipotoxicity and oxidative stress in both mouse and human hepatocytes. Conclusions The data from this study suggest that Sesn1/2/3 play an important role in the protection against lipotoxicity-associated oxidative stress and related pathology in the liver., Graphical abstract

Published
2021

2. Computationally predicted SARS-COV-2 encoded microRNAs target NFKB, JAK/STAT and TGFB signaling pathways

Author

Ergun Pinarbasi, Merve Nur Aydemir, Mahir Budak, Nilgun Cekin, Ertan Mahir Korkmaz, Habes Bilal Aydemir, and Gaziosmanpaşa Üniversitesi, Fakülteler, Fen Edebiyat Fakültesi

Subjects
STAT5B, HDAC2, histone deacetylase 2, SOCS4, suppressor of cytokine signaling 4, AKT1, AKT serine/threonine kinase 1, 0302 clinical medicine, RB1, RB transcriptional corepressor 1, JAK2, Janus kinase 2, Coronavirus, STAT6, IL17A, interleukin 17 A, MAPK3, mitogen-activated protein kinase 3, NOS3, nitric oxide synthase 3, HDAC1, histone deacetylase 1, CTNNB1, catenin beta 1, 030220 oncology & carcinogenesis, SUMO1, small ubiquitin like modifier 1, IL7, interleukin 7, TGFB, TNFRSF21, TNF receptor superfamily member 21, STAT4, signal transducer and activator of transcription 4, CXCL16, C-X-C motif chemokine ligand 16, CXCL11, C-X-C motif chemokine ligand 11, MAPK4, mitogen-activated protein kinase 4, TGFBR2, transforming growth factor beta receptor 2, KEGG, Kyoto Encyclopedia of Genes and Genomes, stat, Article, WHO, World Health Organization, JARID1A, lysine demethylase 5A, 03 medical and health sciences, SOS1, SOS Ras/Rac guanine nucleotide exchange factor 1, microRNA, Genetics, E2F1, E2F transcription factor 1, IL33, interleukin 33, SOCS6, suppressor of cytokine signaling 6, COVID19, new type corona virus disease, SOCS5, suppressor of cytokine signaling 5, SP1, Sp1 transcription factor, TGFBR1, transforming growth factor beta receptor 1, PANTHER, protein analysis through evolutionary relationships, ICTV, International Committee on Taxonomy of Viruses, BCL2, BCL2 apoptosis regulator, 030104 developmental biology, SUMO2, small ubiquitin like modifier 2, NFKB1, nuclear factor kappa B subunit 1, 0301 basic medicine, STAT3, signal transducer and activator of transcription 3, viruses, IKBKE, inhibitor of nuclear factor kappa B kinase subunit epsilon, STAT5B, signal transducer and activator of transcription 5B, SARS-CoV-2, severe acute respiratory disease coronavirus type 2, NFKBIE, NFKB inhibitor epsilon, medicine.disease_cause, SMAD4, SMAD family member 4, IL2, interleukin 2, JARID1B, lysine demethylase 5B, SOCS1, suppressor of cytokine signaling 1, IL5, interleukin 5, SMAD3, SMAD family member 3, MAPK6, mitogen-activated protein kinase 6, IL10, interleukin 10, IL21, interleukin 21, SMAD2, SMAD family member 2, JAK-STAT signaling pathway, EIF4A1, eukaryotic translation initiation factor 4A1, STAT6, signal transducer and activator of transcription 6, JARID1C, lysine demethylase 5C, IL16, interleukin 16, IL24, interleukin 24, IL8, interleukin 8, IL13, interleukin 13, ACE-2, angiotensin-converting enzyme 2, IL22, interleukin 22, JAK1, Janus kinase 1, JARID2, Jumonji and AT-rich interaction domain containing 2, IL25, interleukin 25, Computational biology, Biology, MAPK7, mitogen-activated protein kinase 7, CXCL10, C-X-C motif chemokine ligand 10, CXCL9, C-X-C motif chemokine ligand 9, MAPK1, mitogen-activated protein kinase 1, medicine, HIF1A, hypoxia inducible factor 1 subunit alpha, TBP, TATA-box binding protein, GRB2, growth factor receptor bound protein 2, Epigenetics, CDK1, cyclin dependent kinase 1, CDKL2, cyclin dependent kinase like 2, PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, SOCS3, suppressor of cytokine signaling 3, miRNA, SARS-CoV-2, IL15, interleukin 15, HDAC3, histone deacetylase 3, IFNGR2, interferon gamma receptor 2, CXCL1, C-X-C motif chemokine ligand 1, NFKBIE, JAK/STAT, PTEN, phosphatase and tensin homolog, NFKB, RHOA, ras homolog family member A, TMPRSS4, transmembrane serine protease 4, TMPRSS11A, transmembrane serine protease 11A
Abstract

Recently an outbreak that emerged in Wuhan, China in December 2019, spread to the whole world in a short time and killed >1,410,000 people. It was determined that a new type of beta coronavirus called severe acute respiratory disease coronavirus type 2 (SARS-CoV-2) was causative agent of this outbreak and the disease caused by the virus was named as coronavirus disease 19 (COVID19). Despite the information obtained from the viral genome structure, many aspects of the virus-host interactions during infection is still unknown. In this study we aimed to identify SARS-CoV-2 encoded microRNAs and their cellular targets. We applied a computational method to predict miRNAs encoded by SARS-CoV-2 along with their putative targets in humans. Targets of predicted miRNAs were clustered into groups based on their biological processes, molecular function, and cellular compartments using GO and PANTHER. By using KEGG pathway enrichment analysis top pathways were identified. Finally, we have constructed an integrative pathway network analysis with target genes. We identified 40 SARS-CoV-2 miRNAs and their regulated targets. Our analysis showed that targeted genes including NFKB1, NFKBIE, JAK1–2, STAT3–4, STAT5B, STAT6, SOCS1–6, IL2, IL8, IL10, IL17, TGFBR1–2, SMAD2–4, HDAC1–6 and JARID1A-C, JARID2 play important roles in NFKB, JAK/STAT and TGFB signaling pathways as well as cells' epigenetic regulation pathways. Our results may help to understand virus-host interaction and the role of viral miRNAs during SARS-CoV-2 infection. As there is no current drug and effective treatment available for COVID19, it may also help to develop new treatment strategies., Highlights • The COVID-19 outbreak caused by SARS-CoV-2, spread all over the world. More than 78 Mn people were infected and 1,7 Mn people were killed. • We identified 40 SARS-CoV-2 miRNAs with using computational methods. • These miRNAs play important roles in NFKB, JAK/STAT and TGFB signaling pathways and cells’ epigenetic regulation pathways. • Our results may help to understand virus-host interaction and the role of viral miRNAs during SARS-CoV-2 infection.

Published
2020

3. Computationally predicted SARS-COV-2 encoded microRNAs target NFKB, JAK/STAT and TGFB signaling pathways.

Author

Aydemir MN, Aydemir HB, Korkmaz EM, Budak M, Cekin N, and Pinarbasi E

Abstract

Recently an outbreak that emerged in Wuhan, China in December 2019, spread to the whole world in a short time and killed >1,410,000 people. It was determined that a new type of beta coronavirus called severe acute respiratory disease coronavirus type 2 (SARS-CoV-2) was causative agent of this outbreak and the disease caused by the virus was named as coronavirus disease 19 (COVID19). Despite the information obtained from the viral genome structure, many aspects of the virus-host interactions during infection is still unknown. In this study we aimed to identify SARS-CoV-2 encoded microRNAs and their cellular targets. We applied a computational method to predict miRNAs encoded by SARS-CoV-2 along with their putative targets in humans. Targets of predicted miRNAs were clustered into groups based on their biological processes, molecular function, and cellular compartments using GO and PANTHER. By using KEGG pathway enrichment analysis top pathways were identified. Finally, we have constructed an integrative pathway network analysis with target genes. We identified 40 SARS-CoV-2 miRNAs and their regulated targets. Our analysis showed that targeted genes including NFKB1, NFKBIE, JAK1-2, STAT3-4, STAT5B, STAT6, SOCS1-6, IL2, IL8, IL10, IL17, TGFBR1-2, SMAD2-4, HDAC1-6 and JARID1A-C, JARID2 play important roles in NFKB, JAK/STAT and TGFB signaling pathways as well as cells' epigenetic regulation pathways. Our results may help to understand virus-host interaction and the role of viral miRNAs during SARS-CoV-2 infection. As there is no current drug and effective treatment available for COVID19, it may also help to develop new treatment strategies., Competing Interests: There is no conflict of interest., (© 2020 Elsevier Inc. All rights reserved.)

Published
2021
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