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[PMID]:29040309
[Au] Autor:Suarez-Bregua P; Saxena A; Bronner ME; Rotllant J
[Ad] Endereço:Aquatic Molecular Pathobiology Group, Institute of Marine Research (IIM-CSIC), Vigo, Spain.
[Ti] Título:Targeted Pth4-expressing cell ablation impairs skeletal mineralization in zebrafish.
[So] Source:PLoS One;12(10):e0186444, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Skeletal development and mineralization are essential processes driven by the coordinated action of neural signals, circulating molecules and local factors. Our previous studies revealed that the novel neuropeptide Pth4, synthesized by hypothalamic cells, was involved in bone metabolism via phosphate regulation in adult zebrafish. Here, we investigate the role of pth4 during skeletal development using single-cell resolution, two-photon laser ablation of Pth4:eGFP-expressing cells and confocal imaging in vivo. Using a stable transgenic Pth4:eGFP zebrafish line, we identify Pth4:eGFP-expressing cells as post-mitotic neurons. After targeted ablation of eGFP-expressing cells in the hypothalamus, the experimental larvae exhibited impaired mineralization of the craniofacial bones whereas cartilage development was normal. In addition to a decrease in pth4 transcript levels, we noted altered expression of phex and entpd5, genes associated with phosphate homeostasis and mineralization, as well as a delay in the expression of osteoblast differentiation markers such as sp7 and sparc. Taken together, these results suggest that Pth4-expressing hypothalamic neurons participate in the regulation of bone metabolism, possibly through regulating phosphate balance during zebrafish development.
[Mh] Termos MeSH primário: Calcificação Fisiológica/genética
Calcinose/genética
Hipotálamo/metabolismo
Neurônios/metabolismo
Osteoblastos/metabolismo
Proteína Relacionada ao Hormônio Paratireóideo/genética
Proteínas de Xenopus/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Densidade Óssea
Osso e Ossos/metabolismo
Osso e Ossos/patologia
Calcinose/patologia
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Hipotálamo/crescimento & desenvolvimento
Hipotálamo/lesões
Larva
Terapia a Laser
Neurônios/patologia
Osteoblastos/patologia
Osteogênese/genética
Osteonectina/genética
Osteonectina/metabolismo
Endopeptidase Neutra Reguladora de Fosfato PHEX/genética
Endopeptidase Neutra Reguladora de Fosfato PHEX/metabolismo
Proteína Relacionada ao Hormônio Paratireóideo/metabolismo
Fosfatos/metabolismo
Pirofosfatases/genética
Pirofosfatases/metabolismo
Transdução de Sinais
Fator de Transcrição Sp7
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Proteínas de Xenopus/metabolismo
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Osteonectin); 0 (Osterix protein, zebrafish); 0 (Parathyroid Hormone-Related Protein); 0 (Phosphates); 0 (Pth4 protein, zebrafish); 0 (Sp7 Transcription Factor); 0 (Transcription Factors); 0 (Xenopus Proteins); 0 (Zebrafish Proteins); 147336-22-9 (Green Fluorescent Proteins); EC 3.4.24.- (PHEX Phosphate Regulating Neutral Endopeptidase); EC 3.6.1.- (Entpd5 protein, zebrafish); EC 3.6.1.- (Pyrophosphatases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186444


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[PMID]:28836858
[Au] Autor:Dede AD; Makras P; Anastasilakis AD
[Ad] Endereço:a Department of Endocrinology and Diabetes , Chelsea and Westminster Hospital , London , UK.
[Ti] Título:Investigational anabolic agents for the treatment of osteoporosis: an update on recent developments.
[So] Source:Expert Opin Investig Drugs;26(10):1137-1144, 2017 Oct.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Teriparatide, a PTH analogue, was the first anabolic agent to be approved for the treatment of osteoporosis in 2002. Abaloparatide was also recently approved by the FDA. The need for other anabolic agents is still unmet. Areas covered: In this review, we discuss target molecules and recent advances in the field of anabolic therapy for osteoporosis. PTH and PTHrP analogues binding to the PTH receptor and different routes of administration of teriparatide to avoid the burden of daily subcutaneous injections are discussed. We also review antibodies targeting suppressors of the Wnt pathway such as sclerostin and Dickopff-1. Expert opinion: The development of alternative ways of administering PTH receptor ligands is a promising field, especially via the transdermal route. Other more promising molecules are still at very early stages of development. FDA recently requested more data on Romosozumab.
[Mh] Termos MeSH primário: Anabolizantes/uso terapêutico
Drogas em Investigação/uso terapêutico
Osteoporose/tratamento farmacológico
[Mh] Termos MeSH secundário: Anabolizantes/administração & dosagem
Anabolizantes/farmacologia
Animais
Desenho de Drogas
Drogas em Investigação/administração & dosagem
Drogas em Investigação/farmacologia
Seres Humanos
Terapia de Alvo Molecular
Osteoporose/fisiopatologia
Proteína Relacionada ao Hormônio Paratireóideo/administração & dosagem
Proteína Relacionada ao Hormônio Paratireóideo/uso terapêutico
Receptores de Hormônios Paratireóideos/metabolismo
Teriparatida/administração & dosagem
Teriparatida/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anabolic Agents); 0 (Drugs, Investigational); 0 (Parathyroid Hormone-Related Protein); 0 (Receptors, Parathyroid Hormone); 10T9CSU89I (Teriparatide); AVK0I6HY2U (abaloparatide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2017.1371136


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[PMID]:28756709
[Au] Autor:Lovato C; Lewiecki EM
[Ad] Endereço:a Division of Endocrinology, Diabetes and Metabolism , University of New Mexico Health Sciences Center , Albuquerque , NM , USA.
[Ti] Título:Emerging anabolic agents in the treatment of osteoporosis.
[So] Source:Expert Opin Emerg Drugs;22(3):247-257, 2017 Sep.
[Is] ISSN:1744-7623
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Osteoporosis is a common skeletal disease with serious consequences due to osteoporotic fractures and high costs to society for post-fracture care. Most patients at high risk for fracture are not receiving care to reduce fracture risk. The osteoporosis treatment gap has reached crisis proportions. Strategies to reduce the treatment gap include systematic methods for identifying and treating high risk patients, better education of patients and healthcare providers, better use of currently available drugs, and development of new drugs to treat osteoporosis. Areas covered: Two osteoanabolic agents with novel mechanisms of action have recently completed phase 3 clinical trials. The efficacy and safety findings of these studies are reviewed. Abaloparatide, a synthetic analog of parathyroid hormone-related protein, has received regulatory approval for the treatment of postmenopausal women with osteoporosis at high risk for fracture. Romosozumab, a humanized monoclonal antibody to sclerostin, an endogenous inhibitor of bone formation, is under regulatory review. Expert opinion: Osteoanabolic therapy for osteoporosis can restore, at least in part, the degradation of bone microarchitecture that is a hallmark of this disease. The emergence of new osteoanabolic compounds expands the treatment options for patients at high risk for fracture.
[Mh] Termos MeSH primário: Anabolizantes/uso terapêutico
Osteoporose/tratamento farmacológico
Fraturas por Osteoporose/prevenção & controle
[Mh] Termos MeSH secundário: Anabolizantes/efeitos adversos
Anabolizantes/farmacologia
Animais
Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/farmacologia
Anticorpos Monoclonais/uso terapêutico
Desenho de Drogas
Seres Humanos
Osteoporose/complicações
Osteoporose/patologia
Proteína Relacionada ao Hormônio Paratireóideo/efeitos adversos
Proteína Relacionada ao Hormônio Paratireóideo/farmacologia
Proteína Relacionada ao Hormônio Paratireóideo/uso terapêutico
Educação de Pacientes como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anabolic Agents); 0 (Antibodies, Monoclonal); 0 (Parathyroid Hormone-Related Protein); 3VHF2ZD92J (AMG 785); AVK0I6HY2U (abaloparatide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1080/14728214.2017.1362389


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[PMID]:28739257
[Au] Autor:Kim JH; Yamaori S; Tanabe T; Takagi M; Matsubara T; Okamoto M; Kimura S; Gonzalez FJ
[Ad] Endereço:Department of Pharmacology, School of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Republic of Korea; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: j
[Ti] Título:Lack of epithelial PPARγ causes cystic adenomatoid malformations in mouse fetal lung.
[So] Source:Biochem Biophys Res Commun;491(2):271-276, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptor-γ (PPARγ) plays an important role in lipid and glucose metabolism. In this study, the function of PPARγ on lung development was investigated. Lung-specific Pparg conditional knockout mice (Pparg ) were developed using Cre-Lox system. Pparg mice showed abnormal lung development with enlarged airspaces and followed by increase of apoptotic cells at E14.5 to E18.5. Gene analysis revealed that expression of Pmaip1, a gene related to apoptosis, was significantly increased while expression of Retnla, a gene related to anti-apoptosis, was dramatically decreased in the fetal lung (E14.5) of Pparg mice. In addition, expression of Pthlh, a gene phenotypically expressed in the congenital cystic adenomatoid malformation (CCAM), was increased at E14.5 to E18.5 in the lung of Pparg mice. Cell culture studies revealed that PPARγ could bind to promoter region of Pthlh gene as a repressor in the immortalized mouse lung epithelial cell line MLE-15. Surprisingly, phenotypic changes in MLE-15-shPparg cells, stably transfected with shPparg plasmid, were similar to the Pparg mice model. In addition, MLE-15-shPparg cells were easily detached from the cultured plate when cold phosphate buffered saline was applied. Furthermore, expression of Cdh1, a gene related to cell adhesion, was significantly reduced in the MLE-15-shPparg cells. Taken together, PPARγ may play an important role in fetal lung development via alveolar cell-to-cell adhesion system.
[Mh] Termos MeSH primário: Malformação Adenomatoide Cística Congênita do Pulmão/genética
Células Epiteliais/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Peptídeos e Proteínas de Sinalização Intercelular/genética
PPAR gama/genética
Proteínas Proto-Oncogênicas c-bcl-2/genética
[Mh] Termos MeSH secundário: Animais
Apoptose
Sítios de Ligação
Proteínas Cdh1/genética
Proteínas Cdh1/metabolismo
Adesão Celular
Linhagem Celular Transformada
Malformação Adenomatoide Cística Congênita do Pulmão/metabolismo
Malformação Adenomatoide Cística Congênita do Pulmão/patologia
Embrião de Mamíferos
Células Epiteliais/patologia
Feto
Genes Reporter
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Luciferases/genética
Luciferases/metabolismo
Pulmão/metabolismo
Pulmão/patologia
Camundongos
Camundongos Knockout
PPAR gama/deficiência
Proteína Relacionada ao Hormônio Paratireóideo/genética
Proteína Relacionada ao Hormônio Paratireóideo/metabolismo
Cultura Primária de Células
Regiões Promotoras Genéticas
Ligação Proteica
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Mucosa Respiratória/metabolismo
Mucosa Respiratória/patologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cdh1 Proteins); 0 (Fzr1 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (PPAR gamma); 0 (Parathyroid Hormone-Related Protein); 0 (Pmaip1 protein, mouse); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Retnla protein, mouse); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28679985
[Au] Autor:Ozawa N; Doi S; Tsujikawa T; Mabuchi M; Kajiyama Y; Sato K; Kikuchi K; Takahashi M; Kawamoto M; Yasuda I
[Ad] Endereço:Department of Gastroenterology, Teikyo University Mizonoguchi Hospital.
[Ti] Título:Intrahepatic cholangiocarcinoma producing granulocyte colony-stimulating factor and parathyroid hormone-related protein.
[So] Source:Nihon Shokakibyo Gakkai Zasshi;114(7):1285-1292, 2017.
[Is] ISSN:0446-6586
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 78-year-old man was referred to our hospital with suspected liver abscess. Fever and inflammatory reaction resolved after percutaneous drainage and administration of antibiotics. However, leukocyte count was remarkably increased, and hypercalcemia was noted. The liver mass was also enlarged, as observed in the follow-up abdominal CT scans. Therefore, a percutaneous needle biopsy was performed, and the histopathological findings indicated the presence of adenocarcinoma. Additional blood examination revealed high serum levels of granulocyte colony-stimulating factor (G-CSF) and parathyroid hormone-related protein (PTHrP). Lastly, the patient was diagnosed with cholangiocarcinoma producing G-CSF and PTHrP. Chemoradiotherapy with S-1 was initiated, which was partially effective. However, the patient died 134 days after initiating the therapy. Only two cases of cholangiocarcinoma producing G-CSF and PTHrP have been reported to date. Here we reported an additional case of cholangiocarcinoma producing G-CSF and PTHrP.
[Mh] Termos MeSH primário: Adenocarcinoma/diagnóstico por imagem
Neoplasias dos Ductos Biliares/diagnóstico por imagem
Colangiocarcinoma/diagnóstico por imagem
Fator Estimulador de Colônias de Granulócitos/biossíntese
Proteína Relacionada ao Hormônio Paratireóideo/biossíntese
[Mh] Termos MeSH secundário: Adenocarcinoma/complicações
Adenocarcinoma/metabolismo
Idoso
Neoplasias dos Ductos Biliares/complicações
Neoplasias dos Ductos Biliares/metabolismo
Neoplasias dos Ductos Biliares/patologia
Colangiocarcinoma/complicações
Colangiocarcinoma/metabolismo
Seres Humanos
Hipercalcemia/etiologia
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Parathyroid Hormone-Related Protein); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.11405/nisshoshi.114.1285


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[PMID]:28445262
[Au] Autor:Wang J; Li J; Yang L; Zhou Y; Wang Y
[Ad] Endereço:aDepartment of Orthopedics, Zhongnan Hospital of Wuhan University bDepartment of Orthopedics, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
[Ti] Título:Dose-dependence of PTH-related peptide-1 on the osteogenic induction of MC3T3-E1 cells in vitro.
[So] Source:Medicine (Baltimore);96(17):e6637, 2017 Apr.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parathyroid hormone (PTH), an 84-amino acid peptide, is an endocrine hormone that is secreted by parathyroid glands. PTH performs important functions in calcium regulation and bone remodeling. The PTH (1-34) named teriparatide, a 34-amino acid peptide derived from the N-terminus of PTH, conserves most of the functions of PTH, specifically the osteogenic capability. However, teriparatide is only used by injection and exhibits short duration. In addition, this PTH could not thoroughly expose active sites. In this study, a novel PTH-related peptide (designated PTHrP-1) derived from the N-terminus of PTH was added into the complete medium at different concentrations of PTHrP-1 (0, 50, 100, and 200 ng/mL) to induce the MC3T3-E1 cells. PTHrP-1 was detected by high-performance liquid chromatography and matrix-assisted laser desorption/ionization-time-of-flight mass spectroscopy. Cell morphology, cell proliferation, alkaline phosphatase (ALP), and ALP activity, osteocalcin concentration, and collagen type I (Col-I), osteopontin (OPN), and osteocalcin (OCN) mRNA expression by RT-PCR and protein expression by western blotting were observed and detected. The purity of the PTHrP-1 was 95.14%, and the PTHrP-1 can induce MC3T3-E1 cells into osteoblasts, thus improving ALP activity and OCN concentration, and increasing Col-I, OPN, and OCN mRNA expression and protein expression in MC3T3-E1 cell cultures. The PTHrP-1 proved to be an ideal active peptide. In addition, the osteogenic ability of PTHrP-1 at 200 and 100 ng/mL concentrations was not significantly different but significantly higher than 50 and 0 ng/mL groups. Results indicate that PTHrP-1 is a kind of active peptides that exhibits good biocompatibility with MC3T3-E1 cells and could improve cell proliferation and osteogenic differentiation. Moreover, PTHrP-1, at the preferable concentration of 100 ng/mL, could effectively promote MC3T3-E1 cells into osteoblasts.
[Mh] Termos MeSH primário: Proliferação Celular
Osteoblastos/metabolismo
Proteína Relacionada ao Hormônio Paratireóideo/farmacologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cromatografia Líquida de Alta Pressão
Colágeno Tipo I/metabolismo
Espectrometria de Massas
Camundongos Endogâmicos C57BL
Osteoblastos/citologia
Osteocalcina/metabolismo
Osteogênese
Osteopontina/metabolismo
Proteína Relacionada ao Hormônio Paratireóideo/administração & dosagem
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Collagen Type I); 0 (PTH-related peptide-1 PTHrP-1); 0 (Parathyroid Hormone-Related Protein); 0 (RNA, Messenger); 0 (Spp1 protein, mouse); 104982-03-8 (Osteocalcin); 106441-73-0 (Osteopontin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170602
[Lr] Data última revisão:
170602
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006637


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[PMID]:28408643
[Au] Autor:Al Menhali A; Keeley TM; Demitrack ES; Samuelson LC
[Ad] Endereço:Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan.
[Ti] Título:Gastrin induces parathyroid hormone-like hormone expression in gastric parietal cells.
[So] Source:Am J Physiol Gastrointest Liver Physiol;312(6):G649-G657, 2017 Jun 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parietal cells play a fundamental role in stomach maintenance, not only by creating a pathogen-free environment through the production of gastric acid, but also by secreting growth factors important for homeostasis of the gastric epithelium. The gastrointestinal hormone gastrin is known to be a central regulator of both parietal cell function and gastric epithelial cell proliferation and differentiation. Our previous gene expression profiling studies of mouse stomach identified parathyroid hormone-like hormone (PTHLH) as a potential gastrin-regulated gastric growth factor. Although PTHLH is commonly overexpressed in gastric tumors, its normal expression, function, and regulation in the stomach are poorly understood. In this study we used pharmacologic and genetic mouse models as well as human gastric cancer cell lines to determine the cellular localization and regulation of this growth factor by the hormone gastrin. Analysis of knock-in reporter mice localized expression to parietal cells in the gastric corpus. Regulation by gastrin was demonstrated by increased mRNA abundance after acute gastrin treatment in wild-type mice and reduced expression in gastrin-deficient mice. transcripts were also observed in normal human stomach as well as in human gastric cancer cell lines. Gastrin treatment of AGS-E gastric cancer cells induced a rapid and robust increase in numerous mRNA isoforms. This induction was largely due to increased transcriptional initiation, although analysis of mRNA half-life showed that gastrin treatment also extended the half-life of mRNA, suggesting that gastrin regulates expression by both transcriptional and posttranscriptional mechanisms. We show that the growth factor parathyroid hormone-like hormone (PTHLH) is expressed in acid-secreting parietal cells of the mouse stomach. We define the specific PTHLH mRNA isoforms expressed in human stomach and in human gastric cancer cell lines and show that gastrin induces PTHLH expression via transcription activation and mRNA stabilization. Our findings suggest that PTHLH is a gastrin-regulated growth factor that might contribute to gastric epithelial cell homeostasis.
[Mh] Termos MeSH primário: Gastrinas/metabolismo
Proteína Relacionada ao Hormônio Paratireóideo/metabolismo
Células Parietais Gástricas/efeitos dos fármacos
Neoplasias Gástricas/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Gastrinas/deficiência
Gastrinas/genética
Gastrinas/farmacologia
Regulação Neoplásica da Expressão Gênica
Genótipo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Proteína Relacionada ao Hormônio Paratireóideo/genética
Células Parietais Gástricas/metabolismo
Fenótipo
Processamento Pós-Transcricional do RNA
Estabilidade de RNA
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Neoplasias Gástricas/genética
Fatores de Tempo
Ativação Transcricional
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gastrins); 0 (PTHLH protein, human); 0 (Parathyroid Hormone-Related Protein); 0 (RNA, Messenger); 9045-90-3 (gastrin I)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00366.2016


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[PMID]:28408247
[Au] Autor:Jia KZ; Jin SL; Yao C; Rong R; Wang C; Du P; Jiang WH; Huang XF; Hu QG; Miao DS; Hua ZC
[Ad] Endereço:The State Key Laboratory of Pharmaceutical Biotechnology, School of Stomatology, Affiliated Stomatological Hospital, Nanjing University, Nanjing 210093, PR China.
[Ti] Título:Absence of PTHrP nuclear localization and C-terminus sequences leads to abnormal development of T cells.
[So] Source:Biochimie;138:13-19, 2017 Jul.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Parathyroid hormone-related protein (PTHrP), a ubiquitously expressed protein, is composed of four functional domains including N-terminus, mid region, nuclear localization signal (NLS) and C-terminus. Under the direction of NLS, PTHrP can enter cell nucleus from cytoplasm and stimulate mitogenesis. Although PTHrP is considered to have important developmental roles, the role of PTHrP NLS and C-terminus in developmental process remains unknown, especially in T-cell development. Here, we used a knock-in mouse model, which expresses a truncated form of PTHrP missing the NLS (87-107) and C-terminus (108-139) of the protein, to examine the role of PTHrP NLS and C-terminus in T-cell development. Our results showed that the truncated PTHrP (1-84) led to abnormal subpopulations, impaired proliferation and increased apoptosis in the thymus, indicating that PTHrP is involved in the development of T cells, and the NLS and C-terminus part is necessary for the normal role of PTHrP in T-cell development.
[Mh] Termos MeSH primário: Sequência de Aminoácidos
Sinais de Localização Nuclear
Proteína Relacionada ao Hormônio Paratireóideo/genética
Deleção de Sequência
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Proliferação Celular
Camundongos
Modelos Animais
Proteína Relacionada ao Hormônio Paratireóideo/metabolismo
Proteína Relacionada ao Hormônio Paratireóideo/fisiologia
Linfócitos T/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nuclear Localization Signals); 0 (PTHLH protein, human); 0 (Parathyroid Hormone-Related Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE


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[PMID]:28368420
[Au] Autor:Frieling JS; Shay G; Izumi V; Aherne ST; Saul RG; Budzevich M; Koomen J; Lynch CC
[Ad] Endereço:Departments of Tumor Biology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
[Ti] Título:Matrix metalloproteinase processing of PTHrP yields a selective regulator of osteogenesis, PTHrP .
[So] Source:Oncogene;36(31):4498-4507, 2017 Aug.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Parathyroid hormone-related protein (PTHrP) is a critical regulator of bone resorption and augments osteolysis in skeletal malignancies. Here we report that the mature PTHrP hormone is processed by matrix metalloproteinases to yield a stable product, PTHrP . PTHrP retains the ability to signal through PTH1R to induce calcium flux and ERK phosphorylation but not cyclic AMP production or CREB phosphorylation. Notably, PTHrP promotes osteoblast migration and mineralization in vitro, and systemic administration of PTHrP augments ectopic bone formation in vivo. Further, in contrast to PTHrP , PTHrP does not affect osteoclast formation/function in vitro or in vivo. Finally, immunoprecipitation-mass spectrometry analyses using PTHrP -specific antibodies establish that PTHrP is indeed generated by cancer cells. Thus, matrix metalloproteinase-directed processing of PTHrP disables the osteolytic functions of the mature hormone to promote osteogenesis, indicating important roles for this circuit in bone remodelling in normal and disease contexts.
[Mh] Termos MeSH primário: Metaloproteinases da Matriz/fisiologia
Osteogênese
Proteína Relacionada ao Hormônio Paratireóideo/fisiologia
[Mh] Termos MeSH secundário: Animais
Reabsorção Óssea/etiologia
Diferenciação Celular
Linhagem Celular
Movimento Celular
Feminino
Seres Humanos
Camundongos
Osteoblastos/citologia
Osteoblastos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Parathyroid Hormone-Related Protein); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.70


  10 / 3084 MEDLINE  
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[PMID]:28342003
[Au] Autor:Hastings RH; Montgrain PR; Quintana RA; Chobrutskiy B; Davani A; Miyanohara A; Mahooti S
[Ad] Endereço:Anesthesiology Service, VA Medical Center (125), VA San Diego Healthcare System, 3350 La Jolla Village Dr., San Diego, CA, 92161, USA. rhhastings@ucsd.edu.
[Ti] Título:Lung carcinoma progression and survival versus amino- and carboxyl-parathyroid hormone-related protein expression.
[So] Source:J Cancer Res Clin Oncol;143(8):1395-1407, 2017 Aug.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Expression of the carboxyl PTHrP region of parathyroid hormone-related protein (PTHrP) is a positive prognostic indicator in women with lung cancer, but amino PTHrP is a negative indicator in other lung cancer patients. This project investigated whether PTHrP could be expressed as predominantly amino PTHrP or carboxyl PTHrP in individual lung carcinomas. It also assessed domain-specific effects on cancer progression and patient survival. METHODS: PTHrP immunoreactivities were analyzed versus survival in a human lung cancer tissue microarray (TMA). Growth was compared in athymic mice for isogenic lung carcinoma xenografts differing in expression of amino and carboxyl PTHrP domains. RESULTS: In the TMA, 33 of 99 patient tumors expressed only one PTHrP domain, while 54 expressed both. By Cox regression, the hazard ratio for cancer-specific mortality (95% confidence interval) was 2.6 (1.28-5.44) for amino PTHrP (P = 0.008) and 0.6 (0-2.58) for carboxyl PTHrP (P = 0.092). Xenografts of H358 lung adenocarcinoma cells that overexpressed amino PTHrP grew twice as fast as isogenic low PTHrP tumors in athymic mice, but growth of tumors expressing amino plus carboxyl PTHrP was not significantly different than growth of the control tumors. In summary, the presence of amino PTHrP signifies worse prognosis in lung cancer patients. In mouse xenografts, this effect was abrogated if carboxyl PTHrP was also present. CONCLUSION: Amino PTHrP and carboxyl PTHrP can vary independently in different lung carcinomas. Carboxyl PTHrP may temper the stimulatory effect of amino PTHrP on cancer progression.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Biomarcadores Tumorais/genética
Carcinoma Pulmonar de Células não Pequenas/genética
Neoplasias Pulmonares/genética
Proteína Relacionada ao Hormônio Paratireóideo/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adulto
Idoso
Animais
Biomarcadores Tumorais/biossíntese
Carcinoma Pulmonar de Células não Pequenas/patologia
Progressão da Doença
Intervalo Livre de Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias Pulmonares/patologia
Masculino
Camundongos
Meia-Idade
Proteína Relacionada ao Hormônio Paratireóideo/biossíntese
Domínios Proteicos/genética
Análise Serial de Tecidos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (PTHLH protein, human); 0 (Parathyroid Hormone-Related Protein)
[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:170326
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2396-4



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