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[PMID]:28453726
[Au] Autor:Li J; Yousefi K; Ding W; Singh J; Shehadeh LA
[Ad] Endereço:Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, FL 33136, USA.
[Ti] Título:Osteopontin RNA aptamer can prevent and reverse pressure overload-induced heart failure.
[So] Source:Cardiovasc Res;113(6):633-643, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Cardiac myocyte hypertrophy, the main compensatory response to chronic stress in the heart often progresses to a state of decompensation that can lead to heart failure. Osteopontin (OPN) is an effector for extracellular signalling that induces myocyte growth and fibrosis. Although increased OPN activity has been observed in stressed myocytes and fibroblasts, the detailed and long term effects of blocking OPN signalling on the heart remain poorly defined. Targeting cardiac OPN protein by an RNA aptamer may be beneficial for tuning down OPN pathologic signalling. We aimed to demonstrate the therapeutic effects of an OPN RNA aptamer on cardiac dysfunction. Methods and results: In vivo, we show that in a mouse model of pressure overload, treating at the time of surgeries with an OPN aptamer prevented cardiomyocyte hypertrophy and cardiac fibrosis, blocked OPN downstream signalling (PI3K and Akt phosphorylation), reduced expression of extracellular matrix (Lum, Col3a1, Fn1) and hypertrophy (Nppa, Nppb) genes, and prevented cardiac dysfunction. Treating at two months post-surgeries with the OPN aptamer reversed cardiac dysfunction and fibrosis and myocyte hypertrophy. While genetic homozygous deletion of OPN reduced myocardial wall thickness, surprisingly cardiac function and myocardial fibrosis, specifically collagen deposition and myofibroblast infiltration, were worse compared with wild type mice at three months of pressure overload. Conclusion: Taken together, these data demonstrate that tuning down cardiac OPN signalling by an OPN RNA aptamer is a novel and effective approach for preventing cardiac hypertrophy and fibrosis, improving cardiac function, and reversing pressure overload-induced heart failure.
[Mh] Termos MeSH primário: Aorta/fisiopatologia
Aptâmeros de Nucleotídeos/metabolismo
Pressão Arterial
Insuficiência Cardíaca/prevenção & controle
Hipertrofia Ventricular Esquerda/prevenção & controle
Miocárdio/metabolismo
Osteopontina/metabolismo
Disfunção Ventricular Esquerda/prevenção & controle
Função Ventricular Esquerda
Remodelação Ventricular
[Mh] Termos MeSH secundário: Animais
Aorta/cirurgia
Aptâmeros de Nucleotídeos/genética
Colágeno Tipo III/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Fibrose
Regulação da Expressão Gênica
Predisposição Genética para Doença
Insuficiência Cardíaca/genética
Insuficiência Cardíaca/metabolismo
Insuficiência Cardíaca/fisiopatologia
Hipertrofia Ventricular Esquerda/genética
Hipertrofia Ventricular Esquerda/metabolismo
Hipertrofia Ventricular Esquerda/fisiopatologia
Ligadura
Lumicana/metabolismo
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocárdio/patologia
Osteopontina/deficiência
Osteopontina/genética
Fenótipo
Fosfatidilinositol 3-Quinase/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Fatores de Tempo
Disfunção Ventricular Esquerda/genética
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aptamers, Nucleotide); 0 (COL3A1 protein, mouse); 0 (Collagen Type III); 0 (Cytokines); 0 (Lum protein, mouse); 0 (Lumican); 0 (Spp1 protein, mouse); 106441-73-0 (Osteopontin); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx016


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[PMID]:29408431
[Au] Autor:Li Y; Hu W; Han G; Lu W; Jia D; Hu M; Wang D
[Ad] Endereço:Department of Orthodontics, School and Hospital of Stomatology, Jilin University, Changchun 130021, China; Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Changchun 130021, China. Electronic address: m18643107595@163.com.
[Ti] Título:Involvement of bone morphogenetic protein-related pathways in the effect of aucubin on the promotion of osteoblast differentiation in MG63 cells.
[So] Source:Chem Biol Interact;283:51-58, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Aucubin, an iridoid glycoside found in several plants, such as Eucommia ulmoide and Rehmannia, has various pharmacological effects. Bone formation is a complex process in which osteoblast differentiation plays an important role. This study aimed to investigate the promotion effects of aucubin on osteoblast differentiation in MG63 cells, a human osteoblast-like cell line. Aucubin not only improved osteoblast differentiation, as shown by enhanced ALP (alkaline phosphatase) concentration and mineralization in cells, but increased the expression of various cytokines, including collagen I, osteocalcin, osteopontin, integrin ß1, and Osterix. Aucubin strongly enhanced the levels of BMP2 (bone morphogenetic proteins-2) in MG63 cells, which play a central role during osteoblast differentiation. Further data show that aucubin exposure after 1 day, 7 days, and 14 days enhanced the expression of Smad1, 5, and 8, and the phosphoresced levels of MAPKs (mitogen-activated protein kinases) family Erk (extracellular signal-regulated kinases), JNK (c-Jun-NH2-terminal kinases), P38, and Akt (serine/threonine protein kinase)/mTOR (mammalian target of rapamycin)/p70s6k in MG63 cells. This study shows the improved effects of aucubin on osteoblast differentiation in MG63 cells, related to the signaling of BMP2-mediated Smads (drosophila mothers against decapentaplegic proteins), MAPKs, and Akt/mTOR/p70S6K. This study indicates the potential of aucubin for osteoporosis treatment.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/metabolismo
Diferenciação Celular/efeitos dos fármacos
Glucosídeos Iridoides/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Colágeno Tipo I/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Glucosídeos Iridoides/química
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Osteoblastos/citologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteocalcina/metabolismo
Osteopontina/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteína Smad1/metabolismo
Proteína Smad5/metabolismo
Proteína Smad8/metabolismo
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (Collagen Type I); 0 (Iridoid Glucosides); 0 (Smad1 Protein); 0 (Smad5 Protein); 0 (Smad8 Protein); 104982-03-8 (Osteocalcin); 106441-73-0 (Osteopontin); 2G52GS8UML (aucubin); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:29332262
[Au] Autor:Karpinsky G; Krawczyk MA; Izycka-Swieszewska E; Fatyga A; Budka A; Balwierz W; Sobol G; Zalewska-Szewczyk B; Rychlowska-Pruszynska M; Klepacka T; Dembowska-Baginska B; Kazanowska B; Gabrych A; Bien E
[Ad] Endereço:Children's Hospital of Michigan, 3901 Beaubien St, Detroit, MI, USA.
[Ti] Título:Tumor expression of survivin, p53, cyclin D1, osteopontin and fibronectin in predicting the response to neo-adjuvant chemotherapy in children with advanced malignant peripheral nerve sheath tumor.
[So] Source:J Cancer Res Clin Oncol;144(3):519-529, 2018 Mar.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Selected cell-cycle regulators and extracellular matrix proteins were found to play roles in malignant peripheral nerve sheath tumor (MPNST) biology. We aimed to analyze whether initial tumor tissue expressions of survivin, p53, cyclin D1, osteopontin (OPN) and fibronectin (FN) correlate with the response to neo-adjuvant CHT (naCHT) in children with advanced inoperable MPNST. METHODS: The study included 26 children with MPNST (M/F 14/12, median age 130 months) treated in Polish centers of pediatric oncology between 1992 and 2013. Tissue expression of markers was studied immunohistochemically in the manually performed tissue microarrays and assessed semi-quantitatively as low and high, based on the rate of positive cells and staining intensity. RESULTS: Good response to naCHT was noted in 47.6%, while poor-in 52.4% of patients. The response to naCHT was influenced negatively by the presence of neurofibromatosis NF1 and high initial tumor tissue expression of OPN, survivin, p53 and cyclin D1. Patients with high tumor expression of either OPN, survivin or p53 and those with simultaneous high expression of ≥ 3 of the markers, responded significantly worse to naCHT, than patients, in whom expression of ≤ 2 markers were detected at diagnosis. Nearly, 85% of patients expressing ≥ 3 markers, responded poor to CHT; while 87.5% of children, expressing ≤ 2 markers, were good responders. CONCLUSION: The initial tumor tissue expression of OPN, survivin, p53 and cyclin D1 may serve as markers to predict response to naCHT in pediatric advanced MPNST. Future studies in more numerous group of patients are needed to confirm these preliminary results.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/metabolismo
Ciclina D1/metabolismo
Citocinas/metabolismo
Proteínas Inibidoras de Apoptose/metabolismo
Neoplasias da Bainha Neural/diagnóstico
Neoplasias da Bainha Neural/tratamento farmacológico
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores Farmacológicos/metabolismo
Criança
Pré-Escolar
Progressão da Doença
Feminino
Seres Humanos
Lactente
Masculino
Terapia Neoadjuvante
Neoplasias da Bainha Neural/metabolismo
Neoplasias da Bainha Neural/patologia
Neurilemoma/tratamento farmacológico
Neurilemoma/metabolismo
Neurilemoma/patologia
Prognóstico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BIRC5 protein, human); 0 (Biomarkers, Pharmacological); 0 (Biomarkers, Tumor); 0 (CCND1 protein, human); 0 (Cytokines); 0 (Inhibitor of Apoptosis Proteins); 0 (SPP1 protein, human); 0 (migration stimulating factor, human); 106441-73-0 (Osteopontin); 136601-57-5 (Cyclin D1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-018-2580-1


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[PMID]:28456769
[Au] Autor:Al Dera H
[Ad] Endereço:Department of Basic Medical Sciences, College of Medicine at King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Riyadh, Kingdom of Saudi Arabia. derah@ksau-hs.edu.sa.
[Ti] Título:Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta.
[So] Source:J Physiol Pharmacol;68(1):47-56, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:This study was carried out to investigate the expression pattern and role of osteopontin (OPN) in late global ischemia-reperfusion (I/R) injury with or without resveratrol (RES) pre-treatment. Young male rats were divided into 3 groups (n = 12) of I) sham, II) I/R model group and III) I/R + RES. Vehicle and RES (20 mg/kg) were administered to designed groups intraperitoneally 30 days prior global I/R injury (2-VO) induction and continued for 7 days, later. Then, percentages of infarct areas, mRNA levels of OPN, inducible nitric oxide synthase (iNOS) and other biochemical parameter related to endogenous antioxidants activities and inflammation were measured in the cerebral cortices of all groups. Significant elevations in the levels of malondialdehyde (MDA), the inflammatory mediator interleukin 1ß (IL-1ß), chemokines (KC and MIP-2) and adhesive molecules (ICAM-1) as well as parallel reductions in enzymes activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and chloramphenicol acetyltransferase (CAT) were observed in the cerebral homogenates of rats with late I/R injury. Associated with these changes, mRNA levels of OPN were significantly downregulated and those of iNOS and Bax were upregulated. All these changes were reversed by in 2-VO I/R induced rats pre-administered RES. These findings suggest that inhibition of sustained inflammatory response driven by IL-1ß, decreased activities of endogenous antioxidants and downregulation of OPN induced upregulation of iNOS play important roles in the pathogenesis of neurodegeneration during late cerebral I/R injury, effects that can be modulated by RES which might explain its neuroprotection effect during late global ischemia.
[Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo
Fármacos Neuroprotetores/farmacologia
Traumatismo por Reperfusão/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/tratamento farmacológico
Catalase/metabolismo
Córtex Cerebral/metabolismo
Quimiocina CXCL2/metabolismo
Quimiocinas/metabolismo
Glutationa Peroxidase/metabolismo
Molécula 1 de Adesão Intercelular/metabolismo
Interleucina-1beta/antagonistas & inibidores
Interleucina-1beta/metabolismo
Masculino
Fármacos Neuroprotetores/uso terapêutico
Óxido Nítrico Sintase Tipo II/genética
Osteopontina/genética
Estresse Oxidativo/efeitos dos fármacos
Ratos Wistar
Traumatismo por Reperfusão/tratamento farmacológico
Estilbenos/uso terapêutico
Superóxido Dismutase/metabolismo
Regulação para Cima
Proteína X Associada a bcl-2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Chemokine CXCL2); 0 (Chemokines); 0 (Cxcl2 protein, rat); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Neuroprotective Agents); 0 (Spp1 protein, rat); 0 (Stilbenes); 0 (bcl-2-Associated X Protein); 106441-73-0 (Osteopontin); 126547-89-5 (Intercellular Adhesion Molecule-1); 147037-79-4 (keratinocyte-derived chemokines); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.15.1.1 (Superoxide Dismutase); Q369O8926L (resveratrol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29346446
[Au] Autor:Agah E; Zardoui A; Saghazadeh A; Ahmadi M; Tafakhori A; Rezaei N
[Ad] Endereço:Students' Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Título:Osteopontin (OPN) as a CSF and blood biomarker for multiple sclerosis: A systematic review and meta-analysis.
[So] Source:PLoS One;13(1):e0190252, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Identifying a reliable biomarker may accelerate diagnosis of multiple sclerosis (MS) and lead to early management of the disease. Accumulating evidence suggest that cerebrospinal fluid (CSF) and peripheral blood concentration of osteopontin (OPN) may have diagnostic and prognostic value in MS. We conducted a systematic review and meta-analysis of studies that measured peripheral blood and CSF levels of OPN in MS patients and controls to evaluate the diagnostic potential of this biomarker better. We searched PubMed, Web of Science and Scopus databases to find articles that measured OPN concentration in peripheral blood and CSF samples from MS patients up to October 19, 2016. Q statistic tests and the I2 index were applied for heterogeneity assessment. If the I2 index was less than 40%, the fixed-effects model was used for meta-analysis. Random-effects meta-analysis was chosen if the I2 value was greater than 40%. After removal of duplicates, 918 articles were identified, and 27 of them fulfilled the inclusion criteria. We included 22 eligible studies in the final meta-analysis. MS patients, in general, had considerably higher levels of OPN in their CSF and blood when compared to all types of controls (p<0.05). When the comparisons were made between different subtypes of MS patients and controls, the results pointed to significantly higher levels of OPN in CSF of MS subgroups (p<0.05). All subtypes of MS patients, except CIS patients, had increased blood levels of OPN compared to controls (p<0.05). In the second set of meta-analyses, we compared the peripheral blood and CSF concentrations of OPN between MS patient subtypes. CIS patients had significantly lower levels of OPN both in their peripheral blood and CSF compared to patients with progressive subtypes of MS (p<0.05). CSF concentration of OPN was significantly higher among RRMS patients compared to the CIS patients and SPMS patients (P<0.05). Finally, patients with active MS had significantly higher OPN levels in their CSF compared to patients with stable disease (P = 0.007). The result of this study confirms that increased levels of OPN exist in CSF and peripheral blood of MS patients and strengthens the evidence regarding the clinical utility of OPN as a promising and validated biomarker for MS.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Esclerose Múltipla/metabolismo
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Biomarcadores/líquido cefalorraquidiano
Estudos de Casos e Controles
Seres Humanos
Esclerose Múltipla/sangue
Esclerose Múltipla/líquido cefalorraquidiano
Osteopontina/sangue
Osteopontina/líquido cefalorraquidiano
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 106441-73-0 (Osteopontin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190252


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[PMID]:28471397
[Au] Autor:Xu D; Gao Y; Hu N; Wu L; Chen Q
[Ad] Endereço:Department of Pharmacology, Guangdong Medical University, Dongguan 523808, China. daohuaxu@gdmu.edu.com.
[Ti] Título:miR-365 Ameliorates Dexamethasone-Induced Suppression of Osteogenesis in MC3T3-E1 Cells by Targeting HDAC4.
[So] Source:Int J Mol Sci;18(5), 2017 May 04.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Glucocorticoid administration is the leading cause of secondary osteoporosis. In this study, we tested the hypotheses that histone deacetylase 4 (HDAC4) is associated with glucocorticoid-induced bone loss and that HDAC4 dependent bone loss can be ameliorated by miRNA-365. Our previous studies showed that miR-365 mediates mechanical stimulation of chondrocyte proliferation and differentiation by targeting HDAC4. However, it is not clear whether miR-365 has an effect on glucocorticoid-induced osteoporosis. We have shown that, in MC3T3-E1 osteoblasts, dexamethasone (DEX) treatment decreased the expression of miR-365, which is accompanied by the decrease of cell viability in a dose-dependent manner. Transfection of miR-365 ameliorated DEX-induced inhibition of MC3T3-E1 cell viability and alkaline phosphatase activity, and attenuated the suppressive effect of DEX on runt-related transcription factor 2 (Runx2), osteopontin (OPN), and collagen 1a1 (Col1a1) osteogenic gene expression. In addition, miR-365 decreased the expression of HDAC4 mRNA and protein by direct targeting the 3'-untranslated regions (3'-UTR) of HDAC4 mRNA in osteoblasts. MiR-365 increased Runx2 expression and such stimulatory effect could be reversed by HDAC4 over-expression in osteoblasts. Collectively, our findings indicate that miR-365 ameliorates DEX-induced suppression of cell viability and osteogenesis by regulating the expression of HDAC4 in osteoblasts, suggesting miR-365 might be a novel therapeutic agent for treatment of glucocorticoid-induced osteoporosis.
[Mh] Termos MeSH primário: Histona Desacetilases/genética
MicroRNAs/genética
Osteogênese
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Linhagem Celular
Colágeno Tipo I/genética
Colágeno Tipo I/metabolismo
Subunidade alfa 1 de Fator de Ligação ao Core/genética
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Dexametasona/farmacologia
Histona Desacetilases/metabolismo
Camundongos
MicroRNAs/metabolismo
Osteoblastos/citologia
Osteoblastos/efeitos dos fármacos
Osteoblastos/metabolismo
Osteopontina/genética
Osteopontina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Collagen Type I); 0 (Core Binding Factor Alpha 1 Subunit); 0 (MIRN365 microRNA, mouse); 0 (MicroRNAs); 0 (Runx2 protein, mouse); 106441-73-0 (Osteopontin); 7S5I7G3JQL (Dexamethasone); EC 3.5.1.98 (Hdac5 protein, mouse); EC 3.5.1.98 (Histone Deacetylases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:29180017
[Au] Autor:Cai M; Bompada P; Salehi A; Acosta JR; Prasad RB; Atac D; Laakso M; Groop L; De Marinis Y
[Ad] Endereço:Diabetes and Endocrinology, Department of Clinical Sciences, University Hospital Malmö, Lund University, Malmö, Sweden; Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
[Ti] Título:Role of osteopontin and its regulation in pancreatic islet.
[So] Source:Biochem Biophys Res Commun;495(1):1426-1431, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteopontin (OPN) is involved in various physiological processes and also implicated in multiple pathological states. It has been suggested that OPN may have a role in type 2 diabetes (T2D) by protecting pancreatic islets and interaction with incretins. However, the regulation and function of OPN in islets, especially in humans, remains largely unexplored. In this study, we performed our investigations on both diabetic mouse model SUR1-E1506K+/+ and islets from human donors. We demonstrated that OPN protein, secretion and gene expression was elevated in the diabetic SUR1-E1506K+/+ islets. We also showed that high glucose and incretins simultaneously stimulated islet OPN secretion. In islets from human cadaver donors, OPN gene expression was elevated in diabetic islets, and externally added OPN significantly increased glucose-stimulated insulin secretion (GSIS) from diabetic but not normal glycemic donors. The increase in GSIS by OPN in diabetic human islets was Ca dependent, which was abolished by Ca -channel inhibitor isradipine. Furthermore, we also confirmed that OPN promoted cell metabolic activity when challenged by high glucose. These observations provided evidence on the protective role of OPN in pancreatic islets under diabetic condition, and may point to novel therapeutic targets for islet protection in T2D.
[Mh] Termos MeSH primário: Diabetes Mellitus/metabolismo
Glucose/metabolismo
Ilhotas Pancreáticas/metabolismo
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Regulação da Expressão Gênica
Técnicas de Introdução de Genes
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SPP1 protein, human); 0 (Spp1 protein, mouse); 106441-73-0 (Osteopontin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


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[PMID]:29244844
[Au] Autor:Gschwantler-Kaulich D; Weingartshofer S; Rappaport-Fürhauser C; Zeilinger R; Pils D; Muhr D; Braicu EI; Kastner MT; Tan YY; Semmler L; Sehouli J; Singer CF
[Ad] Endereço:Department of Obstetrics and Gynecology, Cancer Comprehensive Center, Medical University Vienna, Vienna, Austria.
[Ti] Título:Diagnostic markers for the detection of ovarian cancer in BRCA1 mutation carriers.
[So] Source:PLoS One;12(12):e0189641, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Screening for ovarian cancer (OC) in women at high risk consists of a combination of carbohydrate antigen 125 (CA125) and transvaginal ultrasound, despite their low sensitivity and specificity. This could be improved by the combination of several biomarkers, which has been shown in average risk patients but has not been investigated until now in female BRCA mutation carriers. METHODS: Using a multiplex, bead-based, immunoassay system, we analyzed the concentrations of leptin, prolactin, osteopontin, insulin-like growth factor II, macrophage inhibitory factor, CA125 and human epididymis antigen 4 in 26 healthy wild type women, 26 healthy BRCA1 mutation carriers, 28 wildtype OC patients and 26 OC patients with BRCA1 mutation. RESULTS: Using the ROC analysis, we found a high overall sensitivity of 94.3% in differentiating healthy controls from OC patients with comparable results in the wildtype subgroup (sensitivity 92.8%, AUC = 0.988; p = 5.2e-14) as well as in BRCA1 mutation carriers (sensitivity 95.2%, AUC = 0.978; p = 1.7e-15) at an overall specificity of 92.3%. The used algorithm also allowed to identify healthy BRCA1 mutation carriers when compared to healthy wildtype women (sensitivity 88.4%, specificity 80.7%, AUC = 0.895; p = 6e-08), while this was less pronounced in patients with OC (sensitivity 66.7%, specificity 67.8%, AUC = 0.724; p = 0.00065). CONCLUSION: We have developed an algorithm, which can differentiate between healthy women and OC patients and have for the first time shown, that such an algorithm can also be used in BRCA mutation carriers. To clarify a suggested benefit to the existing early detection program, large prospective trials with mainly early stage OC cases are warranted.
[Mh] Termos MeSH primário: Proteína BRCA1/genética
Biomarcadores Tumorais/sangue
Detecção Precoce de Câncer
Neoplasias Ovarianas/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/genética
Antígeno Ca-125/sangue
Feminino
Seres Humanos
Fator de Crescimento Insulin-Like II/genética
Leptina/sangue
Meia-Idade
Mutação
Osteopontina/sangue
Neoplasias Ovarianas/sangue
Neoplasias Ovarianas/patologia
Prolactina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BRCA1 Protein); 0 (BRCA1 protein, human); 0 (Biomarkers, Tumor); 0 (CA-125 Antigen); 0 (Leptin); 0 (SPP1 protein, human); 0 (human epithelial antigen-125); 106441-73-0 (Osteopontin); 67763-97-7 (Insulin-Like Growth Factor II); 9002-62-4 (Prolactin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180102
[Lr] Data última revisão:
180102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189641


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[PMID]:28745831
[Au] Autor:Nghiem PP; Kornegay JN; Uaesoontrachoon K; Bello L; Yin Y; Kesari A; Mittal P; Schatzberg SJ; Many GM; Lee NH; Hoffman EP
[Ad] Endereço:Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, 4458 TAMU, Texas A&M University, College Station, Texas, 77843-4458, USA.
[Ti] Título:Osteopontin is linked with AKT, FoxO1, and myostatin in skeletal muscle cells.
[So] Source:Muscle Nerve;56(6):1119-1127, 2017 Dec.
[Is] ISSN:1097-4598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Osteopontin (OPN) polymorphisms are associated with muscle size and modify disease progression in Duchenne muscular dystrophy (DMD). We hypothesized that OPN may share a molecular network with myostatin (MSTN). METHODS: Studies were conducted in the golden retriever (GRMD) and mdx mouse models of DMD. Follow-up in-vitro studies were employed in myogenic cells and the mdx mouse treated with recombinant mouse (rm) or human (Hu) OPN protein. RESULTS: OPN was increased and MSTN was decreased and levels correlated inversely in GRMD hypertrophied muscle. RM-OPN treatment led to induced AKT1 and FoxO1 phosphorylation, microRNA-486 modulation, and decreased MSTN. An AKT1 inhibitor blocked these effects, whereas an RGD-mutant OPN protein and an RGDS blocking peptide showed similar effects to the AKT inhibitor. RMOPN induced myotube hypertrophy and minimal Feret diameter in mdx muscle. DISCUSSION: OPN may interact with AKT1/MSTN/FoxO1 to modify normal and dystrophic muscle. Muscle Nerve 56: 1119-1127, 2017.
[Mh] Termos MeSH primário: Proteína Forkhead Box O1/metabolismo
Fibras Musculares Esqueléticas/metabolismo
Mioblastos/metabolismo
Miostatina/metabolismo
Osteopontina/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Transformada
Cães
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos mdx
Fibras Musculares Esqueléticas/efeitos dos fármacos
Mioblastos/efeitos dos fármacos
Osteopontina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXO1 protein, human); 0 (Forkhead Box Protein O1); 0 (MSTN protein, human); 0 (Myostatin); 0 (SPP1 protein, human); 106441-73-0 (Osteopontin); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1002/mus.25752


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[PMID]:28962925
[Au] Autor:Chen LZ; He CY; Su X; Peng JL; Chen DL; Ye Z; Yang DD; Wang ZX; Wang F; Shao JY; Xu RH
[Ad] Endereço:Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China; Department of Medical Oncology, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
[Ti] Título:SPP1 rs4754 and its epistatic interactions with SPARC polymorphisms in gastric cancer susceptibility.
[So] Source:Gene;640:43-50, 2018 Jan 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The matricellular glycoprotein products of the SPP1 and SPARC genes play critical roles in many aggressive tumor phenotypes including gastric cancer. We sought to test whether the polymorphisms of these two genes, individually or jointly, influence gastric cancer susceptibility. Nine potentially functional, tagging single nucleotide polymorphisms (tagSNPs) of SPP1 and SPARC were selected and detected using the Kompetitive Allele Specific PCR method in 301 gastric cancer cases and 1441 healthy control subjects. We found that the genotype frequencies of SPP1 rs4754 in gastric cancer were significantly different from those in controls. The rs4754 TT genotype conferred an increased risk of gastric cancer, with unadjusted and adjusted ORs ranging from 1.75 to 1.95 (all P<0.05). The assessment of the effect modifications of sex and age on the genetic effects also confirmed the statistically significant association of the rs4754 TT genotype with increased gastric cancer risk. Epistatic interactions were found between SPP1 rs4754 and SPARC rs1054204, rs3210714 and rs3549 (all P values for interaction<0.05). During the assessment of the epistatic effects between pairs of interacting factors, increased gastric cancer risk was observed in the combined presence of the SPP1 rs4754 TT genotype and the common genotypes of interacting SPARC SNPs, with ORs ranging from 3.94 to 4.41. When the genetic influence of SPP1 rs4754 TT was excluded, the genetic effects of the SPARC rs1054204, rs3210714 and rs3549 common genotypes on gastric cancer susceptibility switched from being risky to beneficial. These data reveal an association between the SPP1 rs4754 polymorphism and altered risk of gastric cancer and highlight an important role of the epistatic effects of SPP rs4754 with SPARC polymorphisms in gastric carcinogenesis. Additional functional experiments and independent large-scale studies, especially in other ethnic populations, are needed to confirm our results.
[Mh] Termos MeSH primário: Epistasia Genética
Osteonectina/genética
Osteopontina/genética
Polimorfismo de Nucleotídeo Único
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Feminino
Predisposição Genética para Doença
Seres Humanos
Masculino
Meia-Idade
Fatores de Risco
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Osteonectin); 0 (SPARC protein, human); 0 (SPP1 protein, human); 106441-73-0 (Osteopontin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE



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