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Pesquisa : C06.130.120.135.250 [Categoria DeCS]
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[PMID]:29419378
[Au] Autor:Chappell LC; Chambers J; Thornton JG; Williamson C
[Ad] Endereço:Women's Health Academic Centre, King's College London, London, UK lucy.chappell@kcl.ac.uk.
[Ti] Título:Does ursodeoxycholic acid improve perinatal outcomes in women with intrahepatic cholestasis of pregnancy?
[So] Source:BMJ;360:k104, 2018 02 01.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Colagogos e Coleréticos/efeitos adversos
Colestase Intra-Hepática/tratamento farmacológico
Feto/efeitos dos fármacos
Complicações na Gravidez/tratamento farmacológico
Ácido Ursodesoxicólico/efeitos adversos
[Mh] Termos MeSH secundário: Colagogos e Coleréticos/administração & dosagem
Colagogos e Coleréticos/uso terapêutico
Colestase Intra-Hepática/epidemiologia
Feminino
Seres Humanos
Gravidez
Complicações na Gravidez/epidemiologia
Resultado da Gravidez/epidemiologia
Ácido Ursodesoxicólico/administração & dosagem
Ácido Ursodesoxicólico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholagogues and Choleretics); 724L30Y2QR (Ursodeoxycholic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k104


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[PMID]:27775690
[Au] Autor:Kennedy LL; Meng F; Venter JK; Zhou T; Karstens WA; Hargrove LA; Wu N; Kyritsi K; Greene J; Invernizzi P; Bernuzzi F; Glaser SS; Francis HL; Alpini G
[Ad] Endereço:Research, Central Texas Veterans Health Care System, Temple, TX, USA.
[Ti] Título:Knockout of microRNA-21 reduces biliary hyperplasia and liver fibrosis in cholestatic bile duct ligated mice.
[So] Source:Lab Invest;96(12):1256-1267, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cholestasis is a condition that leads to chronic hepatobiliary inflammation, fibrosis, and eventually cirrhosis. Many microRNAs (miRs) are known to have a role in fibrosis progression; however, the role of miR-21 during cholestasis remains unknown. Therefore, the aim of this study was to elucidate the role of miR-21 during cholestasis-induced biliary hyperplasia and hepatic fibrosis. Wild-type (WT) and miR-21 mice underwent Sham or bile duct ligation (BDL) for 1 week, before evaluating liver histology, biliary proliferation, hepatic stellate cell (HSC) activation, fibrotic response, and small mothers against decapentaplegic 7 (Smad-7) expression. In vitro, immortalized murine biliary cell lines (IMCLs) and human hepatic stellate cell line (hHSC) were treated with either miR-21 inhibitor or control before analyzing proliferation, apoptosis, and fibrotic responses. In vivo, the levels of miR-21 were increased in total liver and cholangiocytes after BDL, and loss of miR-21 decreased the amount of BDL-induced biliary proliferation and intrahepatic biliary mass. In addition, loss of miR-21 decreased BDL-induced HSC activation, collagen deposition, and expression of the fibrotic markers transforming growth factor-ß1 and α-smooth muscle actin. In vitro, IMCL and hHSCs treated with miR-21 inhibitor displayed decreased proliferation and expression of fibrotic markers and enhanced apoptosis when compared with control treated cells. Furthermore, mice lacking miR-21 show increased Smad-7 expression, which may be driving the decrease in biliary hyperplasia and hepatic fibrosis. During cholestatic injury, miR-21 is increased and leads to increased biliary proliferation and hepatic fibrosis. Local modulation of miR-21 may be a therapeutic option for patients with cholestasis.
[Mh] Termos MeSH primário: Ductos Biliares Intra-Hepáticos/metabolismo
Colestase Intra-Hepática/metabolismo
Modelos Animais de Doenças
Células Estreladas do Fígado/metabolismo
MicroRNAs/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Apoptose
Ductos Biliares Intra-Hepáticos/patologia
Biomarcadores/metabolismo
Linhagem Celular
Proliferação Celular
Células Cultivadas
Colestase Intra-Hepática/patologia
Colestase Intra-Hepática/fisiopatologia
Progressão da Doença
Regulação da Expressão Gênica
Células Estreladas do Fígado/patologia
Seres Humanos
Hiperplasia
Cirrose Hepática/etiologia
Masculino
Camundongos
Camundongos Knockout
MicroRNAs/antagonistas & inibidores
MicroRNAs/biossíntese
Interferência de RNA
Proteína Smad7/genética
Proteína Smad7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Biomarkers); 0 (MIRN21 microRNA, human); 0 (MIRN21 microRNA, mouse); 0 (MicroRNAs); 0 (Smad7 Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.112


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[PMID]:29390323
[Au] Autor:Xiang D; He J; Wang H; Xiong F; Cheng H; Ai J; Shan R; Wan R; Zhang L; Shi J
[Ad] Endereço:Department of General Surgery, The First Affiliated Hospital of Nanchang University.
[Ti] Título:Liver transplantation for decompensated liver cirrhosis caused by progressive familial intrahepatic cholestasis type 3: A case report.
[So] Source:Medicine (Baltimore);96(50):e9158, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Progressive familial intrahepatic cholestasis (PFIC) type 3, characterized by high gamma glutamyl transferase (GGT), is an autosomal recessive genetic disease. It often occurs in patients' first years of age. However, high GGT type PFIC is still rare. PATIENT CONCERNS: The present study reports a case of liver transplantation for decompensated liver cirrhosis caused by PFIC type 3. An 18-year-old male presented with a history of abdominal distension and jaundice for 2 months. He had abdominal tenderness but no rebounding pain. Moreover, his dullness was felt over the liver and the spleen was palpable 8 cm below the ribs. DIAGNOSES: Computed tomography and magnetic resonance cholangiopancreato graphy of the upper abdomen revealed cirrhosis, portal hypertension, collateral circulation formation, large spleen, and ascites. Blood biochemistry showed high alanine transaminase, aspartate transaminase, and GGT. The diagnosis of decompensated liver cirrhosis caused by PFIC-3 was finally confirmed by plasma gene detecting. INTERVENTIONS: The patient received an open surgery named allogeneic liver transplantation after successful matching of immune types between the recipient and donor. Peritoneal puncture and catheter drainage under B-ultrasound was performed when an encapsulated effusion between the liver and stomach arose. OUTCOMES: The patient was discharged without specific discomfort and was almost free of fluid accumulation 51 days after the surgery. At the 6-month follow-up, he had no discomfort and the blood routine, liver functions showed no abnormalities. LESSONS: We found a new mutant fragment of ABCB4 gene in the process of diagnosis. Liver transplantation remains the most definitive treatment for PFIC. Current medical therapies and surgical interventions such as biliary diversion have potentially created a synergistic outcome.
[Mh] Termos MeSH primário: Subfamília B de Transportador de Cassetes de Ligação de ATP/deficiência
Colestase Intra-Hepática/complicações
Cirrose Hepática/etiologia
Cirrose Hepática/cirurgia
Transplante de Fígado
[Mh] Termos MeSH secundário: Adolescente
Seres Humanos
Cirrose Hepática/diagnóstico por imagem
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009158


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[PMID]:29384912
[Au] Autor:Han B; Sheng Y; Wang L; Feng H; Hou X; Li Y
[Ad] Endereço:Centre for Reproductive Medicine.
[Ti] Título:Intrahepatic cholestasis of pregnancy or azithromycin-induced intrahepatic cholestasis: A case report.
[So] Source:Medicine (Baltimore);96(52):e9346, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Azithromycin-induced liver injury has been rarely reported in adult individuals, let alone in a pregnant woman. Here, we describe the clinical features and outcomes of azithromycin-induced liver injury in a pregnant woman. PATIENT CONCERNS: A 30-year-old pregnant woman presented with generalized pruritus and elevated serum bile acid level (123.6 µmol/L) on day 4 of azithromycin administration. A diagnosis of intrahepatic cholestasis of pregnancy was made, and cesarean section was performed immediately. Interestingly, the alanine aminotransferase level (ALT) reached 211.2 U/L on day 9 after azithromycin administration. DIAGNOSIS: Therefore, drug-induced intrahepatic cholestasis was considered. INTERVENTIONS: (1) Azithromycin withdrawal after the patient hospitalized. (2) Termination of pregnancy by cesarean section was performed inmmediately to protect the fetus. (3) Silymarin capsules and bifendate are used to protect the liver after liver enzymes elevation was discovered. OUTCOMES: The liver enzymes recovered within 4 weeks without any symptoms after treatment with silymarin capsules and bifendate, which helps reduce ALT level and protects the liver from further injury. LESSIONS: A pregnant woman developed azithromycin-induced intrahepatic cholestasis. Physicians should be aware of this side effect of azithromycin, which is widely prescribed.
[Mh] Termos MeSH primário: Antibacterianos/efeitos adversos
Azitromicina/efeitos adversos
Colestase Intra-Hepática/induzido quimicamente
Colestase Intra-Hepática/diagnóstico
Complicações na Gravidez/induzido quimicamente
Complicações na Gravidez/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Cesárea
Colestase Intra-Hepática/terapia
Feminino
Seres Humanos
Gravidez
Complicações na Gravidez/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 83905-01-5 (Azithromycin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009346


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[PMID]:29310368
[Au] Autor:Hong JB; Kang DH; Nam HS; Choi CW; Kim HW; Park SB; Kim SJ; Choi WH
[Ad] Endereço:Department of Internal Medicine, Pusan National University School of Medicine and Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan, Korea.
[Ti] Título:Endoscopic reintervention for stent malfunction after stent-in-stent deployment for malignant hilar obstruction.
[So] Source:Medicine (Baltimore);96(48):e8867, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endoscopic bilateral stenting has been increasingly performed for advanced hilar obstruction. As disease progresses, stent malfunction eventually occurs. However, endoscopic reintervention is difficult in these patients. We aimed to evaluate a suitable reintervention procedure for stent malfunction after stent-in-stent (SIS) deployment for malignant hilar obstruction.Among 52 patients with bilateral stenting performed using the SIS method between September 2009 and June 2016, 20 patients with stent malfunction were enrolled in this study. Reintervention was performed endoscopically or percutaneously. Technical and functional success rates were evaluated retrospectively.Technical and functional success rates of endoscopic reintervention were 83% (10/12) and 80% (8/10), respectively. Endoscopic bilateral and unilateral reintervention success rates were 75% (6/8) and 100% (4/4), respectively. For bilateral reintervention, either plastic or plastic and metal stents were used.Endoscopic reintervention could be considered for in-stent malfunction if patients are in fair condition after SIS placement for malignant hilar obstruction. Decisions regarding whether to use bilateral or unilateral drainage and the type of stent to use should depend on the conditions of the disease and the patient.
[Mh] Termos MeSH primário: Neoplasias dos Ductos Biliares/cirurgia
Colestase Intra-Hepática/cirurgia
Endoscopia/métodos
Stents
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Neoplasias dos Ductos Biliares/diagnóstico por imagem
Colestase Intra-Hepática/diagnóstico por imagem
Progressão da Doença
Falha de Equipamento
Feminino
Seres Humanos
Masculino
Meia-Idade
Reoperação
Tomografia Computadorizada por Raios X
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180115
[Lr] Data última revisão:
180115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008867


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[PMID]:28784620
[Au] Autor:Sohail MI; Schmid D; Wlcek K; Spork M; Szakács G; Trauner M; Stockner T; Chiba P
[Ad] Endereço:Institute of Medical Chemistry, Center for Pathobiochemistry and Genetics (M.I.S., M.S., P.C.), Institute of Physiology, Center for Physiology and Pharmacology (D.S.), Institute of Cancer Research (G.S.), Hans Popper Laboratory of Molecular Hepatology, Division of Gastroenterology and Hepatology, De
[Ti] Título:Molecular Mechanism of Taurocholate Transport by the Bile Salt Export Pump, an ABC Transporter Associated with Intrahepatic Cholestasis.
[So] Source:Mol Pharmacol;92(4):401-413, 2017 Oct.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The bile salt export pump (BSEP/ABCB11) transports bile salts from hepatocytes into bile canaliculi. Its malfunction is associated with severe liver disease. One reason for functional impairment of BSEP is systemic administration of drugs, which as a side effect inhibit the transporter. Therefore, drug candidates are routinely screened for potential interaction with this transporter. Hence, understanding the functional biology of BSEP is of key importance. In this study, we engineered the transporter to dissect interdomain communication paths. We introduced mutations in noncanonical and in conserved residues of either of the two nucleotide binding domains and determined the effect on BSEP basal and substrate-stimulated ATPase activity as well as on taurocholate transport. Replacement of the noncanonical methionine residue M584 (Walker B sequence of nucleotide binding site 1) by glutamate imparted hydrolysis competency to this site. Importantly, this mutation was able to sustain 15% of wild-type transport activity, when the catalytic glutamate of the canonical nucleotide binding site 2 was mutated to glutamine. Kinetic modeling of experimental results for the ensuing M584E/E1244Q mutant suggests that a transfer of hydrolytic capacity from the canonical to the noncanonical nucleotide binding site results in loss of active and adoption of facilitative characteristics. This facilitative transport is ATP-gated. To the best of our knowledge, this result is unprecedented in ATP-binding cassette proteins with one noncanonical nucleotide binding site. Our study promotes an understanding of the domain interplay in BSEP as a basis for exploration of drug interactions with this transporter.
[Mh] Termos MeSH primário: Transportadores de Cassetes de Ligação de ATP/metabolismo
Ácidos e Sais Biliares/metabolismo
Colestase Intra-Hepática/metabolismo
Ácido Taurocólico/metabolismo
[Mh] Termos MeSH secundário: Membro 11 da Subfamília B de Transportadores de Cassetes de Ligação de ATP
Transportadores de Cassetes de Ligação de ATP/química
Sítios de Ligação/fisiologia
Transporte Biológico/fisiologia
Células HEK293
Seres Humanos
Estrutura Secundária de Proteína
Estrutura Terciária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABCB11 protein, human); 0 (ATP Binding Cassette Subfamily B Member 11); 0 (Bile Acids and Salts); 5E090O0G3Z (Taurocholic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1124/mol.117.108688


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[PMID]:28759700
[Au] Autor:Martí-Carvajal AJ; Martí-Amarista CE
[Ad] Endereço:Iberoamerican Cochrane Network, Valencia, Venezuela.
[Ti] Título:Interventions for treating intrahepatic cholestasis in people with sickle cell disease.
[So] Source:Cochrane Database Syst Rev;7:CD010985, 2017 07 31.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sickle cell disease is the most common hemoglobinopathy occurring worldwide and sickle cell intrahepatic cholestasis is a complication long recognized in this population. Cholestatic liver diseases are characterized by impaired formation or excretion (or both) of bile from the liver. There is a need to assess the clinical benefits and harms of the interventions used to treat intrahepatic cholestasis in people with sickle cell disease. This is an update of a previously published Cochrane Review. OBJECTIVES: To assess the benefits and harms of the interventions for treating intrahepatic cholestasis in people with sickle cell disease. SEARCH METHODS: We searched the Cystic Fibrosis and Genetic Disorders Group's Haemoglobinopathies Trials Register, which comprises references identified from comprehensive electronic database searches and handsearching of relevant journals and abstract books of conference proceedings. We also searched the LILACS database (1982 to 23 May 2017), the WHO International Clinical Trials Registry Platform Search Portal (23 May 2017) and ClinicalTrials.gov.Date of last search of the Cochrane Cystic Fibrosis and Genetic Disorders Group's Haemoglobinopathies Trials Register: 12 April 2017. SELECTION CRITERIA: We searched for published or unpublished randomised controlled trials. DATA COLLECTION AND ANALYSIS: Each author intended to independently extract data and assess the risk of bias of the trials by standard Cochrane methodologies; however, no trials were included in the review. MAIN RESULTS: There were no randomised controlled trials identified. AUTHORS' CONCLUSIONS: This updated Cochrane Review did not identify any randomised controlled trials assessing interventions for treating intrahepatic cholestasis in people with sickle cell disease. Randomised controlled trials are needed to establish the optimum treatment for this condition.
[Mh] Termos MeSH primário: Anemia Falciforme/complicações
Colestase Intra-Hepática/terapia
[Mh] Termos MeSH secundário: Colestase Intra-Hepática/etiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD010985.pub3


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[PMID]:28697498
[Au] Autor:Shao Y; Chen J; Zheng J; Liu CR
[Ad] Endereço:Department of Obstetrics and Gynecology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Título:Effect of Histone Deacetylase HDAC3 on Cytokines IL-18, IL-12 and TNF-α in Patients with Intrahepatic Cholestasis of Pregnancy.
[So] Source:Cell Physiol Biochem;42(4):1294-1302, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The pathogenesis of intrahepatic cholestasis of pregnancy (ICP) is poorly understood. OBJECTIVE: This study aimed to explore the possible effect of HDAC3 (histone deacetylase) on cytokines IL-18, IL-12 and TNF-α in ICP. METHODS: Serum levels of cytokines IL-18, IL-12 and TNF-α, bile acids and hepatic function parameters were measured. The expression of HDAC3 in the placenta was determined by immunohistochemistry (IHC), western blotting and RT-PCR. RESULTS: IL-18, IL-12 and TNF-α serum levels were significantly higher in the severe ICP group than in the mild ICP group and the control group, and the difference between the mild ICP group and control group was not significant. HDAC3 protein expression was identified in the nucleus of the placental trophoblast by IHC. HDAC3 mRNA and protein expression were significantly lower in the ICP groups (mild ICP and severe ICP groups) than in the control groups, and no significant difference was found between the mild ICP and severe ICP groups. CONCLUSIONS: The low expression of HDAC3 and overexpession of inflammatory cytokines (IL-18, IL-12 and TNF-α) in ICP may be involved in liver cell apoptosis. We suspect that HDAC3 may play an important role in the pathophysiology of ICP.
[Mh] Termos MeSH primário: Colestase Intra-Hepática/genética
Histona Desacetilases/genética
Interleucina-12/genética
Interleucina-18/genética
Placenta/metabolismo
Complicações na Gravidez/genética
Fator de Necrose Tumoral alfa/genética
[Mh] Termos MeSH secundário: Adulto
Alanina Transaminase/sangue
Aspartato Aminotransferases/sangue
Ácidos e Sais Biliares/metabolismo
Estudos de Casos e Controles
Colestase Intra-Hepática/diagnóstico
Colestase Intra-Hepática/metabolismo
Colestase Intra-Hepática/patologia
Feminino
Regulação da Expressão Gênica
Histona Desacetilases/metabolismo
Seres Humanos
Interleucina-12/metabolismo
Interleucina-18/metabolismo
Testes de Função Hepática
Gravidez
Complicações na Gravidez/diagnóstico
Complicações na Gravidez/metabolismo
Complicações na Gravidez/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Índice de Gravidade de Doença
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Interleukin-18); 0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 0 (interleukin 18 protein, human); 187348-17-0 (Interleukin-12); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 3.5.1.98 (Histone Deacetylases); EC 3.5.1.98 (histone deacetylase 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1159/000478958


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[PMID]:28647962
[Au] Autor:Yu Y; Zhou CL; Yu TT; Han XJ; Shi HY; Wang HZ; Shen JJ; He J
[Ad] Endereço:Department of Obstetrics, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China.
[Ti] Título:[Effect of endoplasmic reticulum stress in trophocytes on the pathogenesis of intrahepatic cholestasis of pregnancy].
[So] Source:Zhonghua Fu Chan Ke Za Zhi;52(6):392-397, 2017 Jun 25.
[Is] ISSN:0529-567X
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To evaluate the effect of endoplasmic reticulum stress in trophocytes, in patients with intrahepatic cholestasis of pregnancy (ICP). Sixty-one pregnant women who were hospitalized in Women's Hospital, School of Medicine, Zhejiang University from January to December 2015 were recruited. Thirty-one women who were diagnosed as ICP were defined as the ICP group and 30 healthy pregnant women were defined as the control group. The localization and expression intensity of glucose regulated protein 78 (GRP-78) in placental tissues were detected by immunohistochemistry technique. Electronic microscope was used to observe ultra-microstructure change of the endoplasmic reticulum in trophocytes and cell line Swan71. Reverse transcription (RT)-PCR and western blot were used to investigate the expression of GRP-78 mRNA and protein in Swan 71 cell. (1) GRP-78 protein was mainly expressed in the cytoplasm of cytotrophoblasts and syncytiotrophoblasts. The protein expression of GRP-78 in placentas of the ICP group (13.2±2.4) was significantly higher than that in the control group (7.8±1.3, 0.01). (2) The volume of endoplasmie reticulum did not increase and the microvilli developed well, with no swelling and no expansion of endoplasmic reticulum in the control group.In the ICP group, microvilli injury, endoplasmic reticulum edema were found; the volume of endoplasmic reticulum increased, with dilation, vacuolation and significant degranulation. After treated with 100 µmol/L cholyglycine for 24 hours, universal dilatation of the endoplasmic reticulum were seen in the Swan71 cells. (3) In Swan71 cells, cholylglycine displayed a concentration-dependent up-regulation on the expression of GRP-78. The expressions of GRP-78 mRNA in 0, 25, 50, 100 µmol/L cholylglycine experimental group were 1.01±0.17, 2.17±0.16, 5.47±0.36, 5.65±0.82, respectively. The expression of GRP-78 protein in 0, 25, 50, 100 µmol/L cholylglycine experimental group were 1.01±0.04, 1.17±0.15, 1.33±0.13, 1.73±0.13, respectively. The expression of GRP-78 mRNA and protein in 100 and 50 µmol/L cholylglycine experimental group were significantly higher than 0 µmol/L (all 0.01). The obvious expansion of endoplasmic reticulum and the increased expression of GRP-78 in trophocytes indicated that endoplasmic reticulum stress of trophocytes may be involved in the pathogenesis of ICP.
[Mh] Termos MeSH primário: Colestase Intra-Hepática/patologia
Estresse do Retículo Endoplasmático
Retículo Endoplasmático/metabolismo
Proteínas de Choque Térmico/genética
Placenta/metabolismo
Complicações na Gravidez/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Estudos de Casos e Controles
Feminino
Ácido Glicocólico
Proteínas de Choque Térmico/metabolismo
Seres Humanos
Gravidez
Terceiro Trimestre da Gravidez
RNA Mensageiro/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Trofoblastos
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heat-Shock Proteins); 0 (RNA, Messenger); 0 (molecular chaperone GRP78); G59NX3I3RT (Glycocholic Acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-567X.2017.06.007


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[PMID]:28575098
[Au] Autor:Rao ZZ; Zhang XW; Ding YL; Yang MY
[Ad] Endereço:Department of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, China.
[Ti] Título:miR-148a-mediated estrogen-induced cholestasis in intrahepatic cholestasis of pregnancy: Role of PXR/MRP3.
[So] Source:PLoS One;12(6):e0178702, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intrahepatic cholestasis of pregnancy (ICP) is an idiopathic liver disease while the biochemical characteristic is the elevated level of total bile acid (TBA). The present study investigated whether miR-148a mediates the induced effect of estrogen on the development of ICP and the proper mechanism: PXR/MRP3 signal pathway. mRNA expression was detected by qPCR, protein expression was detected by western blotting, the concentration of estrogen and TBA were detected by reagent kit respectively. In the cinical research, it was found that miR-148a expression was positive related with the concentration of TBA in the serum of ICP patients. In in vitro research, estradiol (500 nmol/L, 12 h) significantly upregulated miR-148a expression and LV-148a-siRNA inhibited the function of estradiol (500 nmol/L, 48 h) on TBA secretion. In addition, gene silence of miR-148a upregulated PXR expression which was inhibited by estradiol in LO2 cells. Pretreatment of rifampin (10 µmol/L), the agonist of PXR alleviated the TBA secretion induced by estradiol (500 nmol/L, 48 h). miR-148a-siRNA and PXR had a synergistic action on TBA secretion of LO2. Both of miR-148a-siRNA and rifampin (10 µmol/L) inhibited the upregulated effect of estradiol on MRP3 expression. This research has demonstrated that miR-148a may be involved in the induction of estrogen on ICP via PXR signal pathway, and MRP3 may be involved.
[Mh] Termos MeSH primário: Colestase Intra-Hepática/metabolismo
Estradiol/fisiologia
MicroRNAs/fisiologia
Proteínas Associadas à Resistência a Múltiplos Medicamentos/fisiologia
Complicações na Gravidez/metabolismo
Receptores de Esteroides/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Ácidos e Sais Biliares/sangue
Ácidos e Sais Biliares/secreção
Linhagem Celular
Colestase Intra-Hepática/genética
Estradiol/farmacologia
Estradiol/secreção
Feminino
Regulação da Expressão Gênica
Genes Reporter
Hepatócitos/efeitos dos fármacos
Hepatócitos/secreção
Seres Humanos
MicroRNAs/genética
Gravidez
Complicações na Gravidez/genética
Interferência de RNA
RNA Interferente Pequeno/genética
Reação em Cadeia da Polimerase em Tempo Real
Transdução Genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (MIRN148 microRNA, human); 0 (MicroRNAs); 0 (Multidrug Resistance-Associated Proteins); 0 (RNA, Small Interfering); 0 (Receptors, Steroid); 0 (pregnane X receptor); 1YV0492L5Z (multidrug resistance-associated protein 3); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178702



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