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[PMID]:29254292
[Au] Autor:Cantore S; Ballini A; De Vito D; Martelli FS; Georgakopoulos I; Almasri M; Dibello V; Altini V; Farronato G; Dipalma G; Farronato D; Inchingolo F
[Ad] Endereço:Department of Interdisciplinary Medicine, School of Medicine, University of Bari Aldo Moro, Bari, Italy.
[Ti] Título:Characterization of human apical papilla-derived stem cells.
[So] Source:J Biol Regul Homeost Agents;31(4):901-910, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Dental tissues represent an alternative and promising source of post-natal Mesenchymal stem cells (MSCs) for tissue engineering. Furthermore, dental stem cells from apical papilla (SCAPs) cells can be obtained from the wisdom tooth which is unnecessary for human masticatory function and frequently extracted for orthodontic reasons or dysodontiasis. More precisely, apical papilla is the immature, mostly uncalcified, precursor of the tooth root, therefore is composed of more undifferentiated cells than dental pulp. In addition, tooth extraction, especially by piezosurgery technique, can be considered less invasive in comparison to bone marrow or other tissues biopsy. Our work is aimed to investigate the safety of and predictable procedure on surgical immature third molar extraction and to provide new insight on SCAP research for future biomedical applications. The isolated cells were examined for stem cell properties by analyzing their colony-forming efficiency, differentiation characteristics and the expression of MSC markers.
[Mh] Termos MeSH primário: Polpa Dentária/citologia
Células Mesenquimais Estromais/citologia
Osteogênese/genética
Raiz Dentária/citologia
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores/metabolismo
Diferenciação Celular
Proliferação Celular
Separação Celular
Criança
Ensaio de Unidades Formadoras de Colônias
Polpa Dentária/metabolismo
Feminino
Expressão Gênica
Seres Humanos
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Masculino
Células Mesenquimais Estromais/metabolismo
Dente Molar/cirurgia
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/genética
Membro 2 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Engenharia Tecidual
Extração Dentária
Raiz Dentária/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (JunB protein, human); 0 (NR4A2 protein, human); 0 (Nuclear Receptor Subfamily 4, Group A, Member 2); 0 (Transcription Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29235329
[Au] Autor:Minchenko OH; Kharkova AP; Minchenko DO; Karbovskyi LL
[Ti] Título:Expression of IGFBP6, IGFBP7, NOV, CYR61, WISP1 and WISP2 genes in U87 glioma cells in glutamine deprivation condition.
[So] Source:Ukr Biochem J;88(3):66-77, 2016 May-Jun.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:We have studied gene expression of insulin-like growth factor binding proteins in U87 glioma cells upon glutamine deprivation depending on the inhibition of IRE1 (inositol requiring enzyme-1), a central mediator of endoplasmic reticulum stress. We have shown that exposure of control glioma cells upon glutamine deprivation leads to down-regulation of NOV/IGFBP9, WISP1 and WISP2 gene expressions and up-regulation of CYR61/IGFBP10 gene expression at the mRNA level. At the same time, the expression of IGFBP6 and IGFBP7 genes in control glioma cells was resistant to glutamine deprivation. It was also shown that the inhibition of IRE1 modifies the effect of glutamine deprivation on the expression of all studied genes. Thus, the inhibition of IRE1 signaling enzyme enhances the effect of glutamine deprivation on the expression of CYR61 and WISP1 genes and suppresses effect of the deprivation on WISP2 gene expression in glioma cells. Moreover, the inhibition of IRE1 introduces sensitivity of the expression of IGFBP6 and IGFBP7 genes to glutamine deprivation and removes this sensitivity to NOV gene. We have also demonstrated that the expression of all studied genes in glioma cells growing with glutamine is regulated by IRE1 signaling enzyme, because the inhibition of IRE1 significantly down-regulates IGFBP6 and NOV genes and up-regulates IGFBP7, CYR61, WISP1, and WISP2 genes as compared to control glioma cells. The present study demonstrates that glutamine deprivation condition affects most studied IGFBP and WISP gene expressions in relation to IRE1 signaling enzyme function and possibly contributes to slower glioma cell proliferation upon inhibition of IRE1.
[Mh] Termos MeSH primário: Proteínas de Sinalização Intercelular CCN/genética
Endorribonucleases/genética
Regulação Neoplásica da Expressão Gênica
Glutamina/deficiência
Proteína 6 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
Neuroglia/enzimologia
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
[Mh] Termos MeSH secundário: Proteínas de Sinalização Intercelular CCN/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Proteína Rica em Cisteína 61/genética
Proteína Rica em Cisteína 61/metabolismo
Endorribonucleases/deficiência
Seres Humanos
Proteína 6 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Proteína Sobre-Expressa em Nefroblastoma/genética
Proteína Sobre-Expressa em Nefroblastoma/metabolismo
Neuroglia/patologia
Proteínas Serina-Treonina Quinases/deficiência
Proteínas Proto-Oncogênicas/metabolismo
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCN Intercellular Signaling Proteins); 0 (CYR61 protein, human); 0 (Cysteine-Rich Protein 61); 0 (Insulin-Like Growth Factor Binding Protein 6); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (NOV protein, human); 0 (Nephroblastoma Overexpressed Protein); 0 (Proto-Oncogene Proteins); 0 (Repressor Proteins); 0 (WISP1 protein, human); 0 (WISP2 protein, human); 0 (insulin-like growth factor binding protein-related protein 1); 0RH81L854J (Glutamine); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.1.- (Endoribonucleases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.03.066


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[PMID]:28939196
[Au] Autor:Zhang H; Shi Y; He M
[Ad] Endereço:CAS Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China; University of Chinese Academy of Sciences, Beijing 100049, China.
[Ti] Título:Molecular identification of an insulin growth factor binding protein (IGFBP) and its potential role in an insulin-like peptide system of the pearl oyster, Pinctada fucata.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;214:27-35, 2017 Dec.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Insulin-like growth factors (IGFs) play critical roles in regulating metabolism, growth, and reproduction in invertebrates. IGF binding proteins (IGFBPs) serve as major regulators of IGF activity and regulate endocrine system. In the present study, the full-length cDNA of an igfbp was identified from the pearl oyster, Pinctada fucata, using expressed sequence tag (EST) sequence. The 1124bp Pfigfbp cDNA contains a 465bp open reading frame (ORF) encoding a putative protein of 154 amino acids, a 5'-untranslated region (UTR) of 238bp, and a 3'-UTR of 394bp (not including polyA+). Multiple sequence alignment of the deduced IB domain sequences revealed that twelve conserved Cys and ILP binding site in PfIGFBP were well aligned with human IGFBPs1-7, Mizuhopecten yessoensis IGFBP5 and Eriocheir sinensis IGFBP7. Gene expression analysis indicated that Pfigfbp mRNA was expressed in all the tissues and developmental stages examined, with a higher level in the foot than in other tissues and a higher level in the polar body stage and 32-cell stage than in the other stages. Pfigfbp and PfILP (insulin-like peptide) mRNA levels significantly increased in the digestive gland after feeding, while levels were dramatically reduced during a week of food deprivation and increased upon refeeding. In vitro experiments indicated that Pfigfbp mRNA expression in mantle cells was affected by insulin/IGFs (IGF-I, IGF-II). Our data suggests that Pfigfbp may be involved in endocrine signaling in P. fucata via the regulation of insulin-like peptide signaling.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Insulina/genética
Fases de Leitura Aberta
Pinctada/genética
Somatomedinas/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação
Clonagem Molecular
Ingestão de Alimentos/genética
Escherichia coli/genética
Escherichia coli/metabolismo
Etiquetas de Sequências Expressas/química
Seres Humanos
Insulina/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Especificidade de Órgãos
Pectinidae
Filogenia
Pinctada/classificação
Pinctada/crescimento & desenvolvimento
Pinctada/metabolismo
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Transdução de Sinais
Somatomedinas/metabolismo
Inanição/genética
Inanição/metabolismo
Regiões não Traduzidas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (Recombinant Proteins); 0 (Somatomedins); 0 (Untranslated Regions)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE


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[PMID]:28911141
[Au] Autor:Sarem Z; Bumke-Vogt C; Mahmoud AM; Assefa B; Weickert MO; Adamidou A; Bähr V; Frystyk J; Möhlig M; Spranger J; Lieske S; Birkenfeld AL; Pfeiffer AFH; Arafat AM
[Ad] Endereço:Department of Endocrinology, Diabetes, and Nutrition, Charité-University Medicine Berlin, Berlin 10117, Germany.
[Ti] Título:Glucagon Decreases IGF-1 Bioactivity in Humans, Independently of Insulin, by Modulating Its Binding Proteins.
[So] Source:J Clin Endocrinol Metab;102(9):3480-3490, 2017 Sep 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Depending on its lipolytic activity, glucagon plays a promising role in obesity treatment. Glucagon-induced growth hormone (GH) release can promote its effect on lipid metabolism, although the underlying mechanisms have not been well-defined. Objective: The present study highlights the glucagon effect on the GH/insulinlike growth factor 1 (IGF-1)/IGF-binding protein (IGFBP) axis in vivo and in vitro, taking into consideration insulin as a confounding factor. Materials and Methods: In a double-blind, placebo-controlled study, we investigated changes in GH, IGFBP, and IGF-1 bioactivity after intramuscular glucagon administration in 13 lean controls, 11 obese participants, and 13 patients with type 1 diabetes mellitus (T1DM). The effect of glucagon on the transcription factor forkhead box protein O1 (FOXO1) translocation, the transcription of GH/IGF-1 system members, and phosphorylation of protein kinase B (Akt) was further investigated in vitro. Results: Despite unchanged total IGF-1 and IGFBP-3 levels, glucagon decreased IGF-1 bioactivity in all study groups by increasing IGFBP-1 and IGFBP-2. The reduction in IGF-1 bioactivity occurred before the glucagon-induced surge in GH. In contrast to the transient increase in circulating insulin in obese and lean participants, no change was observed in those with T1DM. In vitro, glucagon dose dependently induced a substantial nuclear translocation of FOXO1 in human osteosarcoma cells and tended to increase IGFBP-1 and IGFBP-2 gene expression in mouse primary hepatocytes, despite absent Akt phosphorylation. Conclusions: Our data point to the glucagon-induced decrease in bioactive IGF-1 levels as a mechanism through which glucagon induces GH secretion. This insulin-independent reduction is related to increased IGFBP-1 and IGFBP-2 levels, which are most likely mediated via activation of the FOXO/mTOR (mechanistic target of rapamycin) pathway.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/metabolismo
Glucagon/administração & dosagem
Hormônio do Crescimento/efeitos dos fármacos
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Western Blotting
Diabetes Mellitus Tipo 1/diagnóstico
Diabetes Mellitus Tipo 1/tratamento farmacológico
Relação Dose-Resposta a Droga
Método Duplo-Cego
Esquema de Medicação
Ensaio de Imunoadsorção Enzimática
Feminino
Proteína Forkhead Box O1/efeitos dos fármacos
Proteína Forkhead Box O1/metabolismo
Hormônio do Crescimento/secreção
Seres Humanos
Injeções Intramusculares
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/secreção
Fator de Crescimento Insulin-Like I/secreção
Masculino
Obesidade/metabolismo
Obesidade/fisiopatologia
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Forkhead Box Protein O1); 0 (Insulin-Like Growth Factor Binding Proteins); 67763-96-6 (Insulin-Like Growth Factor I); 9002-72-6 (Growth Hormone); 9007-92-5 (Glucagon)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00558


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[PMID]:28886098
[Au] Autor:Rahman MS; Thomas P
[Ad] Endereço:School of Earth, Environmental and Marine Sciences, University of Texas Rio Grande Valley, Brownsville, Texas, United States of America.
[Ti] Título:Molecular and biochemical responses of hypoxia exposure in Atlantic croaker collected from hypoxic regions in the northern Gulf of Mexico.
[So] Source:PLoS One;12(9):e0184341, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major impact of global climate change has been the marked increase worldwide in the incidence of coastal hypoxia (dissolved oxygen, DO<2.0 mg l-1). However, the extent of hypoxia exposure to motile animals such as fish collected from hypoxic waters as well as their molecular and physiological responses to environmental hypoxia exposure are largely unknown. A suite of potential hypoxia exposure biomarkers was evaluated in Atlantic croaker collected from hypoxic and normoxic regions in the northern Gulf of Mexico (nGOM), and in croaker after laboratory exposure to hypoxia (DO: 1.7 mg l-1). Expression of hypoxia-inducible factor-α, hif-α; neuronal nitric oxide synthase, nNOS; and insulin-like growth factor binding protein, igfbp mRNAs and protein carbonyl (PC, an oxidative stress indicator) content were elevated several-fold in brain and liver tissues of croaker collected from nGOM hypoxic sites. All of these molecular and biochemical biomarkers were also upregulated ~3-10-fold in croaker brain and liver tissues within 1-2 days of hypoxia exposure in controlled laboratory experiments. These results suggest that hif-αs, nNOS and igfbp-1 transcripts and PC contents are useful biomarkers of environmental hypoxia exposure and some of its physiological effects, making them important components for improved assessments of long-term impacts of environmental hypoxia on fish populations.
[Mh] Termos MeSH primário: Hipóxia/genética
Hipóxia/metabolismo
Perciformes/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Análise por Conglomerados
Perfilação da Expressão Gênica
Golfo do México
Fator 1 Induzível por Hipóxia/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Fígado/metabolismo
Óxido Nítrico/sangue
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo I/genética
Óxido Nítrico Sintase Tipo I/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoxia-Inducible Factor 1); 0 (Insulin-Like Growth Factor Binding Proteins); 31C4KY9ESH (Nitric Oxide); EC 1.14.13.39 (Nitric Oxide Synthase Type I)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184341


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[PMID]:28799580
[Au] Autor:Kimmel M; Schanz M; Alscher MD
[Ad] Endereço:Department of Internal Medicine, Division of General Internal Medicine and Nephrology, Robert-Bosch Hospital Stuttgart, Germany. martin.kimmel@rbk.de.
[Ti] Título:Risk prediction of acute kidney injury by [TIMP-2]•[IGFBP7].
[So] Source:Drugs Today (Barc);53(6):349-356, 2017 Jun.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Acute kidney injury (AKI) is a common syndrome with increased mortality, a heavy burden of illness and high cost. The Kidney Disease Improving Global Outcomes (KDIGO) criteria for staging of AKI have been validated in large patient cohorts and classify AKI into three stages. In order to achieve prevention or early therapy, the focus of scientific interest is early detection and risk prediction of AKI. The combination of the two cell cycle arrest markers [TIMP-2]·[IGFBP7] in the urine shows good results in the risk prediction of AKI in different clinical settings (intensive care medicine, sepsis, cardiac surgery, emergency department). Clinical use is currently being tested in different randomized intervention studies.
[Mh] Termos MeSH primário: Lesão Renal Aguda/urina
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/urina
Inibidor Tecidual de Metaloproteinase-2/urina
[Mh] Termos MeSH secundário: Lesão Renal Aguda/sangue
Biomarcadores
Procedimentos Cirúrgicos Cardíacos
Ensaios Clínicos como Assunto
Creatinina/sangue
Emergências
Seres Humanos
Complicações Pós-Operatórias/urina
Valor Preditivo dos Testes
Medição de Risco
Sepse/urina
Urinálise/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (TIMP2 protein, human); 0 (insulin-like growth factor binding protein-related protein 1); 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.6.2604170


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[PMID]:28682920
[Au] Autor:Liu C; Lu X; Mao Z; Kang H; Liu H; Pan L; Hu J; Wang L; Zhou F
[Ad] Endereço:aDepartment of Critical Care Medicine, Chinese People's Liberation Army General Hospital bDepartment of Cardiology, Division of Southbuilding, Chinese People's Liberation Army General Hospital, Beijing, China.
[Ti] Título:The diagnostic accuracy of urinary [TIMP-2]·[IGFBP7] for acute kidney injury in adults: A PRISMA-compliant meta-analysis.
[So] Source:Medicine (Baltimore);96(27):e7484, 2017 Jul.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Early diagnosis of acute kidney injury (AKI) remains a challenge. Recently, [TIMP-2]·[IGFBP7], which is a combination of urine tissue inhibitor of metalloproteinase 2 (TIMP-2) and insulin-like growth factor (IGF) binding protein 7 (IGFBP7), has been identified as a potential biomarker of AKI. We performed this meta-analysis to assess the diagnostic accuracy of urinary [TIMP-2]·[IGFBP7] for AKI in adult patients. METHODS: We searched the PubMed, Embase, and Cochrane Library databases from database inception to March 2017. Two authors independently screened articles based on inclusion and exclusion criteria and assessed the methodological quality of each included study using the Quality Assessment of Diagnostic Accuracy Studies 2 criteria. Review Manager and STATA were used for all statistical analyses. RESULTS: Nine studies (n = 1886) satisfied the inclusion criteria. Pooled analyses demonstrated that urinary [TIMP-2]·[IGFBP7] exhibited fair diagnostic accuracy for AKI (sensitivity [SEN] 0.83 [95% CI 0.75-0.89], specificity [SPE] 0.72 [95% CI 0.56-0.84], and area under the summary receiver operating characteristic [SROC] curve 0.86 [95% CI 0.82-0.88]) and AKI stage ≥ 2 (according to the 2012 Kidney Disease: Improving Global Outcomes [KDIGO] 2012 classification system; SEN 0.92 [95% CI 0.81-0.96], SPE 0.63 [95% CI 0.49-0.74], and area under the SROC curve 0.88 [95% CI 0.85-0.91]) in adult patients. CONCLUSION: Our findings indicate that urinary [TIMP-2]·[IGFBP7] may be a reliable biomarker for the early detection of AKI. However, given the significant heterogeneity among the included studies, clinicians should be aware of the utility and limitations of this biomarker in clinical practice. Additional high-quality studies examining a larger sample of patients are required.
[Mh] Termos MeSH primário: Lesão Renal Aguda/urina
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/urina
Inibidor Tecidual de Metaloproteinase-2/urina
[Mh] Termos MeSH secundário: Biomarcadores/urina
Diagnóstico Precoce
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (TIMP2 protein, human); 0 (insulin-like growth factor binding protein-related protein 1); 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007484


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[PMID]:28679590
[Au] Autor:Boddu R; Fan C; Rangarajan S; Sunil B; Bolisetty S; Curtis LM
[Ad] Endereço:Division of Nephrology, Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and.
[Ti] Título:Unique sex- and age-dependent effects in protective pathways in acute kidney injury.
[So] Source:Am J Physiol Renal Physiol;313(3):F740-F755, 2017 Sep 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sex and age influence susceptibility to acute kidney injury (AKI), with young females exhibiting lowest incidence. In these studies, we investigated mechanisms which may underlie the sex/age-based dissimilarities. Cisplatin (Cp)-induced AKI resulted in morphological evidence of injury in all groups. A minimal rise in plasma creatinine (PCr) was seen in Young Females, whereas in Aged Females, PCr rose precipitously. Relative to Young Males, Aged Males showed significantly, but temporally, comparably elevated PCr. Notably, Aged Females showed significantly greater mortality, whereas Young Females exhibited none. Tissue KIM-1 and plasma NGAL were significantly lower in Young Females than all others. IGFBP7 levels were modestly increased in both Young groups. IGFBP7 levels in Aged Females were significantly elevated at baseline relative to Aged Males, and increased linearly through , when these levels were comparable in both Aged groups. Plasma cytokine levels similarly showed a pattern of protective effects preferentially in Young Females. Expression of the drug transporter MATE2 did not explain the sex/age distinctions. Heme oxygenase-1 (HO-1) levels (~28-kDa species) showed elevation at in all groups with highest levels seen in Young Males. Exclusively in Young Females, these levels returned to baseline on , suggestive of a more efficient recovery. In aggregate, we demonstrate, for the first time, a distinctive pattern of response to AKI in Young Females relative to males which appears to be significantly altered in aging. These distinctions may offer novel targets to exploit therapeutically in both females and males in the treatment of AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Envelhecimento/metabolismo
Rim/metabolismo
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/metabolismo
Lesão Renal Aguda/patologia
Fatores Etários
Envelhecimento/patologia
Animais
Autofagia
Proliferação Celular
Cisplatino
Creatinina/sangue
Citocinas/sangue
Modelos Animais de Doenças
Feminino
Heme Oxigenase-1/metabolismo
Receptor Celular 1 do Vírus da Hepatite A/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Rim/patologia
Lipocalina-2/sangue
Masculino
Proteínas de Membrana/metabolismo
Metionina Adenosiltransferase/metabolismo
Camundongos Endogâmicos C57BL
Fatores Sexuais
Transdução de Sinais
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Havcr1 protein, mouse); 0 (Hepatitis A Virus Cellular Receptor 1); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (Lipocalin-2); 0 (Membrane Proteins); 0 (insulin-like growth factor binding protein-related protein 1); 126469-30-5 (Lcn2 protein, mouse); AYI8EX34EU (Creatinine); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); EC 2.5.1.6 (Methionine Adenosyltransferase); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00049.2017


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[PMID]:28619711
[Au] Autor:Akiel M; Guo C; Li X; Rajasekaran D; Mendoza RG; Robertson CL; Jariwala N; Yuan F; Subler MA; Windle J; Garcia DK; Lai Z; Chen HH; Chen Y; Giashuddin S; Fisher PB; Wang XY; Sarkar D
[Ad] Endereço:Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia.
[Ti] Título:IGFBP7 Deletion Promotes Hepatocellular Carcinoma.
[So] Source:Cancer Res;77(15):4014-4025, 2017 Aug 01.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activation of IGF signaling is a major oncogenic event in diverse cancers, including hepatocellular carcinoma (HCC). In this setting, the insulin-like growth factor binding protein IGFBP7 inhibits IGF signaling by binding the IGF1 receptor (IGF1R), functioning as a candidate tumor suppressor. IGFBP7 abrogates tumors by inhibiting angiogenesis and inducing cancer-specific senescence and apoptosis. Here, we report that Igfbp7-deficient mice exhibit constitutively active IGF signaling, presenting with proinflammatory and immunosuppressive microenvironments and spontaneous liver and lung tumors occurring with increased incidence in carcinogen-treated subjects. Igfbp7 deletion increased proliferation and decreased senescence of hepatocytes and mouse embryonic fibroblasts, effects that were blocked by treatment with IGF1 receptor inhibitor. Significant inhibition of genes regulating immune surveillance was observed in Igfbp7 murine livers, which was associated with a marked inhibition in antigen cross-presentation by Igfbp7 dendritic cells. Conversely, IGFBP7 overexpression inhibited growth of HCC cells in syngeneic immunocompetent mice. Depletion of CD4 or CD8 T lymphocytes abolished this growth inhibition, identifying it as an immune-mediated response. Our findings define an immune component of the pleiotropic mechanisms through which IGFBP7 suppresses HCC. Furthermore, they offer a genetically based preclinical proof of concept for IGFBP7 as a therapeutic target for immune management of HCC. .
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/patologia
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/deficiência
Neoplasias Hepáticas/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/imunologia
Modelos Animais de Doenças
Citometria de Fluxo
Imunofluorescência
Imuno-Histoquímica
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/imunologia
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos SCID
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin-Like Growth Factor Binding Proteins); 0 (insulin-like growth factor binding protein-related protein 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-2885


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[PMID]:28537976
[Au] Autor:Finge T; Bertran S; Roger C; Candela D; Pereira B; Scott C; Muller L; Louart B; Lefrant JY
[Ad] Endereço:From the *Service of Anesthesia and Intensive Care, Hôpital Privé Les Franciscaines, 3 Rue Jean Bouin 30032 NÎMES Cedex 1, France; †Division of Anaesthesiology, Critical Care, Pain and Emergency Medicine, Nimes University Hospital, Place du Professeur Robert Debré, 30 029 Nîmes Cedex 9, France; and ‡Department of Clinical Research and Innovation (DRCI), Clermont-Ferrand, France.
[Ti] Título:Interest of Urinary [TIMP-2] × [IGFBP-7] for Predicting the Occurrence of Acute Kidney Injury After Cardiac Surgery: A Gray Zone Approach.
[So] Source:Anesth Analg;125(3):762-769, 2017 Sep.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This study assessed the ability of 3-hour postoperative urinary tissue inhibitor of metalloproteinases-2 × insulin-like growth factor binding protein-7 ([TIMP-2] × [IGFBP-7]) to predict postoperative acute kidney injury (AKI) in patients undergoing cardiopulmonary bypass during cardiac surgery. METHODS: Patients undergoing cardiac surgery with cardiopulmonary bypass were eligible for this study. Patients with initial chronic renal insufficiency requiring renal replacement therapy, patients <18 years of age, and parturients were not included. Anesthesia and hemodynamic management followed current practices. Urinary [TIMP2] × [IGFBP-7] was measured in 3-hour postoperative period. The primary objective was the occurrence of AKI (Kidney Disease: Improving Global Outcome [KDIGO] stage >0) within the first 48 hours postoperatively. The ability of urinary [TIMP-2] × [IGFBP-7] to predict postoperative AKI was assessed by building a receiver operating characteristic curve (with 95% confidence interval [CI] and by a gray zone approach that allowed either the prediction or the exclusion of postoperative AKI with a sensitivity >0.90 and a specificity >0.90). RESULTS: AKI occurred in 34 of 93 patients included (37%). The area under the receiver operating characteristic curve of urinary [TIMP-2] × [IGFBP-7] was 0.73 (95% CI, 0.62-0.83). The best cutoff value for urinary [TIMP-2] × [IGFBP-7] in predicting AKI was 0.3 ng/mL/1000 [0.09-1.40] (sensitivity = 76%; 95% CI, 73-97, specificity = 64%; 95% CI, 42-69). Urinary [TIMP-2] × [IGFBP-7] of <0.09 ng/mL/1000 and >1.40 ng/mL/1000 had a sensitivity and specificity >90% in predicting postoperative AKI. Fifty-nine patients (63%) were within the gray zone. CONCLUSIONS: In patients undergoing cardiopulmonary bypass during cardiac surgery, urinary [TIMP-2] × [IGFBP-7] could not accurately predict the occurrence of postoperative AKI.
[Mh] Termos MeSH primário: Lesão Renal Aguda/urina
Procedimentos Cirúrgicos Cardíacos/efeitos adversos
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/urina
Complicações Pós-Operatórias/urina
Inibidor Tecidual de Metaloproteinase-2/urina
[Mh] Termos MeSH secundário: Lesão Renal Aguda/diagnóstico
Lesão Renal Aguda/epidemiologia
Idoso
Idoso de 80 Anos ou mais
Biomarcadores/urina
Procedimentos Cirúrgicos Cardíacos/tendências
Feminino
Seres Humanos
Masculino
Meia-Idade
Complicações Pós-Operatórias/diagnóstico
Complicações Pós-Operatórias/epidemiologia
Valor Preditivo dos Testes
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (TIMP2 protein, human); 0 (insulin-like growth factor binding protein-related protein 1); 127497-59-0 (Tissue Inhibitor of Metalloproteinase-2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002116



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