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[PMID]:27776448
[Au] Autor:Ye C; Zhang W; Jiang S; Yu Y; Zhou X; Zhu L; Xue D; He R
[Ad] Endereço:a Department of Orthopedic Surgery , the Second Affiliated Hospital, School of Medicine, Zhejiang University , Hangzhou , Zhejiang , China.
[Ti] Título:Platelet-derived growth factor-BB attenuates titanium-particle-induced osteolysis in vivo.
[So] Source:Growth Factors;34(5-6):177-186, 2016 12.
[Is] ISSN:1029-2292
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inflammation and osteoclastogenesis play critical roles in wear-particle-induced periprosthetic osteolysis (WPO). Platelet-derived growth factor-BB (PDGF-BB) could promote osteogenesis and inhibit inflammatory response. The aim of this study was to investigate the impact of PDGF-BB on WPO. Mice were divided into four groups, namely, sham, vehicle, low-, and high-dose PDGF-BB groups. Mice in the rhPDGF-BB groups were treated with PDGF-BB at 0.25 or 1 mg/ml/kg/day. Mice in the sham and vehicle groups received PBS daily. Two weeks after surgery, calvariae were harvested. Immunohistochemical analysis and µ-CT showed that PDGF-BB significantly reduced osteoclast formation and bone resorption. ELISA showed that rhPDGF-BB decreased the secretion of TNF-α, IL-1ß, and IL-6. Western blotting revealed that rhPDGF-BB stimulated the expression of osteocalcin and osteoprotegerin. Furthermore, more VEGF and CD31 proteins were observed due to PDGF-BB by immunofluorescence. In conclusion, these findings suggest that rhPDGF-BB represents a potential treatment for WPO.
[Mh] Termos MeSH primário: Interface Osso-Implante/patologia
Osteólise/tratamento farmacológico
Proteínas Proto-Oncogênicas c-sis/uso terapêutico
Titânio/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Interleucina-1beta/genética
Interleucina-1beta/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Osteólise/etiologia
Molécula-1 de Adesão Celular Endotelial de Plaquetas/genética
Molécula-1 de Adesão Celular Endotelial de Plaquetas/metabolismo
Proteínas Proto-Oncogênicas c-sis/administração & dosagem
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Platelet Endothelial Cell Adhesion Molecule-1); 0 (Proto-Oncogene Proteins c-sis); 0 (Tumor Necrosis Factor-alpha); 0 (Vascular Endothelial Growth Factor A); 1B56C968OA (becaplermin); D1JT611TNE (Titanium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1080/08977194.2016.1240680


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[PMID]:29214007
[Au] Autor:Masi A; Breen EJ; Alvares GA; Glozier N; Hickie IB; Hunt A; Hui J; Beilby J; Ravine D; Wray J; Whitehouse AJO; Guastella AJ
[Ad] Endereço:Autism Clinic for Translational Research, Brain and Mind Centre, Central Clinical School, Sydney Medical School, University of Sydney, 100 Mallett Street, Camperdown, New South Wales 2050 Australia.
[Ti] Título:Cytokine levels and associations with symptom severity in male and female children with autism spectrum disorder.
[So] Source:Mol Autism;8:63, 2017.
[Is] ISSN:2040-2392
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Autism spectrum disorders (ASDs) are complex, pervasive, and heterogeneous neurodevelopmental conditions with varying trajectories, significant male bias and largely unknown etiology. However, an understanding of the biological mechanisms driving pathophysiology is evolving. Immune system aberrations, as identified through cytokine profiles, are believed to have a role in ASD. Altered cytokine levels may facilitate identification of ASD subtypes as well as provide biological markers of response to effective treatments. Research exploring the relationship between cytokine profiles and ASD symptoms is, however, in its infancy. The objective of this study was to explore relationships between cytokine levels and the severity of ASD and other clinical traits. Methods: Multiplex assay techniques were used to measure levels of 27 cytokines in plasma samples from a cohort of 144 children diagnosed with ASD. Results: Overall, results showed a significant negative association between platelet-derived growth factor (PDGF)-BB, and the severity of ASD symptoms. Furthermore, a significant interaction with sex suggested a different immune profile for females compared to males. ASD symptom severity was negatively associated with levels of 4 cytokines, IL-1ß, IL-8, MIP-1ß, and VEGF, in females, but not in males. Conclusions: Results of the present study suggest that an altered cytokine response or profile is associated with the severity of ASD-related symptoms, with sex a potential modifier of this relationship. Further research in larger populations which recognizes the importance of sex comparisons and longitudinal assessments are now required to extend and further describe the role of the immune system in ASD.
[Mh] Termos MeSH primário: Transtorno do Espectro Autista/diagnóstico
Citocinas/sangue
[Mh] Termos MeSH secundário: Adolescente
Transtorno do Espectro Autista/metabolismo
Transtorno do Espectro Autista/patologia
Comportamento/fisiologia
Criança
Pré-Escolar
Feminino
Seres Humanos
Masculino
Proteínas Proto-Oncogênicas c-sis/sangue
Índice de Gravidade de Doença
Fatores Sexuais
Inquéritos e Questionários
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Proto-Oncogene Proteins c-sis); 1B56C968OA (becaplermin)
[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:171208
[St] Status:MEDLINE
[do] DOI:10.1186/s13229-017-0176-2


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[PMID]:29242904
[Au] Autor:Takahashi K; Shimazawa M; Izawa H; Inoue Y; Kuse Y; Hara H
[Ad] Endereço:Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan.
[Ti] Título:Platelet-Derived Growth Factor-BB Lessens Light-Induced Rod Photoreceptor Damage in Mice.
[So] Source:Invest Ophthalmol Vis Sci;58(14):6299-6307, 2017 Dec 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Platelet-derived growth factor (PDGF)-BB is known to have neuroprotective effects against various neurodegenerative disorders. The purpose of this study was to determine whether PDGF-BB can be neuroprotective against light-induced photoreceptor damage in mice. Methods: Mice were exposed to 8000-lux luminance for 3 hours to induce phototoxicity. Two hours before light exposure, the experimental mice were injected with PDGF-BB intravitreally, and the control mice were injected with phosphate-buffered saline. The light-exposed PDGF-BB-injected mice and saline-injected mice were evaluated electroretinographically and histologically. The site and expression levels of PDGFR-ß and PDGF-BB were determined by immunostaining and Western blotting, respectively. The effect of PDGF-BB on light-induced cone and rod photoreceptor damage was also evaluated in vitro in 661W cells, a murine cone photoreceptor cell line, and in primary retinal cell cultures. Results: An intravitreal injection of PDGF-BB significantly reduced the decrease in the amplitudes of the electroretinograms (ERGs) and the thinning of the outer nuclear layer (ONL) induced by the light exposure. It also reduced the number of TUNEL-positive cells in the ONL. PDGFR-ß was expressed in the rod outer segments (OSs) but not the cone OSs. The levels of PDGF-BB and PDGFR-ß were decreased after light irradiation. In addition, PDGF-BB had protective effects against light-induced damage to cells of rod photoreceptors but had no effect on the 661W cells in vitro. Conclusions: These findings indicate that PDGF-BB reduces the degree of light-induced retinal damage by activating PDGFR-ß in rod photoreceptors. These findings suggest that PDGF-BB could play a role in the prevention of degeneration in eyes susceptible to phototoxicity.
[Mh] Termos MeSH primário: Luz/efeitos adversos
Células Fotorreceptoras de Vertebrados/efeitos dos fármacos
Prenhez
Proteínas Proto-Oncogênicas c-sis/administração & dosagem
Lesões Experimentais por Radiação/prevenção & controle
Doenças Retinianas/prevenção & controle
[Mh] Termos MeSH secundário: Indutores da Angiogênese/administração & dosagem
Animais
Animais Recém-Nascidos
Western Blotting
Morte Celular/efeitos dos fármacos
Morte Celular/efeitos da radiação
Linhagem Celular
Eletrorretinografia
Feminino
Imuno-Histoquímica
Marcação In Situ das Extremidades Cortadas
Injeções Intravítreas
Masculino
Camundongos
Células Fotorreceptoras de Vertebrados/patologia
Células Fotorreceptoras de Vertebrados/efeitos da radiação
Fator de Crescimento Derivado de Plaquetas/administração & dosagem
Gravidez
Lesões Experimentais por Radiação/etiologia
Lesões Experimentais por Radiação/fisiopatologia
Proteínas Recombinantes
Doenças Retinianas/etiologia
Doenças Retinianas/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inducing Agents); 0 (Platelet-Derived Growth Factor); 0 (Proto-Oncogene Proteins c-sis); 0 (Recombinant Proteins); 0 (platelet-derived growth factor A); 1B56C968OA (becaplermin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22556


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[PMID]:29016699
[Au] Autor:Pan J; Li K; Huang W; Zhang X
[Ad] Endereço:Clinical Medical College, Xi'an Medical University, Xi'an City, Shaanxi Province, China.
[Ti] Título:MiR-137 inhibited cell proliferation and migration of vascular smooth muscle cells via targeting IGFBP-5 and modulating the mTOR/STAT3 signaling.
[So] Source:PLoS One;12(10):e0186245, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abnormal proliferation of vascular smooth muscle cells (VSMCs) contributes to the development of cardiovascular diseases. Studies have shown the great impact of microRNAs (miRNAs) on the cell proliferation of VSMCs. This study examined the effects of miR-137 on the cell proliferation and migration of VSMCs and also explored the underlying molecular mechanisms. The mRNA and protein expression levels were determined by qRT-PCR and western blot assays, respectively. The CCK-8 assay, wound healing assay and transwell migration assay were performed to measure cell proliferation and migration of VSMCs. The miR-137-targeted 3'untranslated region of insulin-like growth factor-binding protein-5 (IGFBP-5) was confirmed by luciferase reporter assay. Platelet-derived growth factor-bb (PDGF-bb) treatment enhanced cell proliferation and suppressed the expression of miR-137 in VSMCs. The gain-of-function and loss-of-function assays showed that overexpression of miR-137 suppressed the cell proliferation and migration, and also inhibited the expression of matrix genes of VSMCs; down-regulation of miR-137 had the opposite effects on VSMCs. Bioinformatics analysis and luciferase report assay results showed that IGFBP-5 was a direct target of miR-137, and miR-137 overexpression suppressed the IGFBP-5 expression and down-regulation of miR-137 increased the IGFBP-5 expression in VSMCs. PDGF-bb treatment also increased the IGFBP-5 mRNA expression. In addition, enforced expression of IGFBP-5 reversed the inhibitory effects of miR-137 on cell proliferation and migration of VSMCs. More importantly, overexpression of miR-137 also suppressed the activity of mTOR/STAT3 signaling in VSMCs. Taken together, the results suggest that miR-137 may suppress cell proliferation and migration of VSMCs via targeting IGFBP-5 and modulating mTOR/STAT3 signaling pathway.
[Mh] Termos MeSH primário: Proteína 5 de Ligação a Fator de Crescimento Semelhante à Insulina/genética
MicroRNAs/genética
Miócitos de Músculo Liso/metabolismo
Fator de Transcrição STAT3/genética
Transdução de Sinais
Serina-Treonina Quinases TOR/genética
[Mh] Termos MeSH secundário: Aorta/citologia
Aorta/efeitos dos fármacos
Aorta/metabolismo
Sequência de Bases
Sítios de Ligação
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Biologia Computacional
Cultura em Câmaras de Difusão
Regulação da Expressão Gênica
Genes Reporter
Seres Humanos
Proteína 5 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Luciferases/genética
Luciferases/metabolismo
MicroRNAs/metabolismo
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-sis/farmacologia
Fator de Transcrição STAT3/metabolismo
Serina-Treonina Quinases TOR/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin-Like Growth Factor Binding Protein 5); 0 (MIRN137 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-sis); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 1B56C968OA (becaplermin); EC 1.13.12.- (Luciferases); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186245


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[PMID]:28977029
[Au] Autor:Oh E; Jeong HM; Kwon MJ; Ha SY; Park HK; Song JY; Kim YJ; Choi JS; Lee EH; Lee J; Choi YL; Shin YK
[Ad] Endereço:Laboratory of Cancer Genomics and Molecular Pathology, Samsung Medical Center, Seoul, Korea.
[Ti] Título:Unforeseen clonal evolution of tumor cell population in recurrent and metastatic dermatofibrosarcoma protuberans.
[So] Source:PLoS One;12(10):e0185826, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dermatofibrosarcoma protuberans (DFSP) is a very rare soft tissue sarcoma, generally of low-grade malignancy. DFSP is locally aggressive with a high recurrence rate, but metastasis occurs rarely. To investigate the mechanism of metastasis in DFSP, we analyzed the whole exome sequencing data of serial tumor samples obtained from a patient who had a 10-year history of recurrent and metastatic DFSP. Tracking various genomic alterations, namely somatic mutations, copy number variations, and chromosomal rearrangements, we observed a dramatic change in tumor cell population during the occurrence of metastasis in this DFSP case. The new subclone that emerged in metastatic DFSP harbored a completely different set of somatic mutations and new focal amplifications, which had not been observed in the primary clone before metastasis. The COL1A1-PDGFB fusion, characteristic of DFSP, was found in all of the serial samples. Moreover, the break position on the fusion gene was identical in all samples. Based on these observations, we suggest a clonal evolution model to explain the mechanism underlying metastasis in DFSP and identified several candidate target genes responsible for metastatic DFSP by utilizing The Cancer Genome Atlas database. This is the first study to observe clonal evolution in metastatic DFSP and provide insight for a possible therapeutic strategy for imatinib-resistant or metastatic DFSP.
[Mh] Termos MeSH primário: Evolução Clonal
Dermatofibrossarcoma/patologia
Metástase Neoplásica
[Mh] Termos MeSH secundário: Colágeno Tipo I/genética
Dermatofibrossarcoma/genética
Fusão Gênica
Seres Humanos
Masculino
Meia-Idade
Proteínas Proto-Oncogênicas c-sis/genética
Recidiva
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Proto-Oncogene Proteins c-sis); 0 (collagen type I, alpha 1 chain)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185826


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[PMID]:28882648
[Au] Autor:Liu K; Sun X; Zhang Y; Liu L; Yuan Q
[Ad] Endereço:Department of Orthopedics, the First Affiliated Hospital of Xi'an Jiao Tong University, Xi'an 710061, China. Electronic address: kailiuxjtu@mail.xjtu.edu.cn.
[Ti] Título:MiR-598: A tumor suppressor with biomarker significance in osteosarcoma.
[So] Source:Life Sci;188:141-148, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Osteosarcoma is the most frequent primary malignant bone tumor in children and adolescents. Identifying specific and sensitive biomarkers is beneficial to early detection and improvement of life qualities and overall survival rates of osteosarcoma patients. MATERIALS AND METHODS: Realtime PCR was used to detect the expression of miR-598. CCK-8 assay was employed to detect the proliferation of osteosarcoma cells, while transwell assays were used to examine the migration and invasion. Tumor xenograft experiments were performed to test the in vivo malignancy of osteosarcoma cells. Co-culture experiment was used to study the relationship between osteosarcoma cells and osteoblast. Realtime PCR, Western Blotting and luciferase report assays were conducted for the target genes analysis. KEY FINDINGS: Using a cohort of 20 cases of osteosarcoma and paired adjacent tissue samples, we found that miR-598 expression was decreased in osteosarcoma tissues and serum, as well as the osteosarcoma cell lines. Over expression of miR-598 suppressed the proliferation, migration, and invasion of osteosarcoma cells, while inhibition of miR-598 expression stimulated the proliferation, migration, and invasion. However, MiR-598 had no effect on osteosarcoma cell apoptosis. Data from nude mice further demonstrated the inhibitory role of miR-598 in osteosarcoma progression in vivo. Mechanically, miR-598 played its role by modulating osteoblastic differentiation in the microenvironment and targeting PDGFB and MET. SIGNIFICANCE: Our findings enrich the knowledge of miR-598 in osteosarcoma progression, and reveal miR-598 as a promising diagnostic, prognostic, therapeutic biomarker for osteosarcoma.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Genes Supressores de Tumor
MicroRNAs/genética
MicroRNAs/fisiologia
Osteossarcoma/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/metabolismo
Neoplasias Ósseas/sangue
Neoplasias Ósseas/metabolismo
Estudos de Casos e Controles
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Técnicas de Cocultura
Regulação para Baixo
Seres Humanos
Camundongos
MicroRNAs/biossíntese
MicroRNAs/sangue
Invasividade Neoplásica/fisiopatologia
Osteoblastos/fisiologia
Osteossarcoma/sangue
Proteínas Proto-Oncogênicas c-met/biossíntese
Proteínas Proto-Oncogênicas c-sis/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (MIRN-598 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-sis); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28851707
[Au] Autor:Wang Y; Jin Y; Mäe MA; Zhang Y; Ortsäter H; Betsholtz C; Mäkinen T; Jakobsson L
[Ad] Endereço:Karolinska Institutet, Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Scheeles Väg 2, SE171 77 Stockholm, Sweden.
[Ti] Título:Smooth muscle cell recruitment to lymphatic vessels requires PDGFB and impacts vessel size but not identity.
[So] Source:Development;144(19):3590-3601, 2017 10 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tissue fluid drains through blind-ended lymphatic capillaries, via smooth muscle cell (SMC)-covered collecting vessels into venous circulation. Both defective SMC recruitment to collecting vessels and ectopic recruitment to lymphatic capillaries are thought to contribute to vessel failure, leading to lymphedema. However, mechanisms controlling lymphatic SMC recruitment and its role in vessel maturation are unknown. Here, we demonstrate that platelet-derived growth factor B (PDGFB) regulates lymphatic SMC recruitment in multiple vascular beds. PDGFB is selectively expressed by lymphatic endothelial cells (LECs) of collecting vessels. LEC-specific deletion of prevented SMC recruitment causing dilation and failure of pulsatile contraction of collecting vessels. However, vessel remodelling and identity were unaffected. Unexpectedly, overexpression in LECs did not induce SMC recruitment to capillaries. This was explained by the demonstrated requirement of PDGFB extracellular matrix (ECM) retention for lymphatic SMC recruitment, and the low presence of PDGFB-binding ECM components around lymphatic capillaries. These results demonstrate the requirement of LEC-autonomous PDGFB expression and retention for SMC recruitment to lymphatic vessels, and suggest an ECM-controlled checkpoint that prevents SMC investment of capillaries, which is a common feature in lymphedematous skin.
[Mh] Termos MeSH primário: Células Endoteliais/metabolismo
Vasos Linfáticos/anatomia & histologia
Vasos Linfáticos/metabolismo
Miócitos de Músculo Liso/metabolismo
Proteínas Proto-Oncogênicas c-sis/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Capilares/metabolismo
Comunicação Celular
Derme/metabolismo
Matriz Extracelular/metabolismo
Feminino
Membro Posterior/metabolismo
Masculino
Mesentério/metabolismo
Morfogênese
Tamanho do Órgão
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-sis)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1242/dev.147967


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[PMID]:28825469
[Au] Autor:Vu CQ; Rotkrua P; Tantirungrotechai Y; Soontornworajit B
[Ad] Endereço:Division of Chemistry, Faculty of Science and Technology, Thammasat University , Pathumthani 12120, Thailand.
[Ti] Título:Oligonucleotide Hybridization Combined with Competitive Antibody Binding for the Truncation of a High-Affinity Aptamer.
[So] Source:ACS Comb Sci;19(10):609-617, 2017 Oct 09.
[Is] ISSN:2156-8944
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Truncation can enhance the affinity of aptamers for their targets by limiting nonessential segments and therefore limiting the molecular degrees of freedom that must be overcome in the binding process. This study demonstrated a truncation protocol relying on competitive antibody binding and the hybridization of complementary oligonucleotides, using platelet derived growth factor BB (PDGF-BB) as the model target. On the basis of the immunoassay results, an initial long aptamer was truncated to a number of sequences with lengths of 36-40 nucleotides (nt). These sequences showed apparent K values in the picomolar range, with the best case being a 36-nt truncated aptamer with a 150-fold increase in affinity over the full-length aptamer. The observed binding energies correlated well with relative energies calculated by molecular dynamics simulations. The effect of the truncated aptamer on PDGF-BB-stimulated fibroblasts was found to be equivalent to that of the full-length aptamer.
[Mh] Termos MeSH primário: Anticorpos/química
Aptâmeros de Nucleotídeos/química
Proteínas Proto-Oncogênicas c-sis/química
[Mh] Termos MeSH secundário: Aptâmeros de Nucleotídeos/farmacologia
Sítios de Ligação
Proliferação Celular
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Seres Humanos
Hibridização Genética
Simulação de Dinâmica Molecular
Ligação Proteica
Proteínas Proto-Oncogênicas c-sis/farmacologia
Ressonância de Plasmônio de Superfície/métodos
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Aptamers, Nucleotide); 0 (Proto-Oncogene Proteins c-sis); 1B56C968OA (becaplermin)
[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:170822
[St] Status:MEDLINE
[do] DOI:10.1021/acscombsci.6b00163


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[PMID]:28759044
[Au] Autor:Yan D; Kowal J; Akkari L; Schuhmacher AJ; Huse JT; West BL; Joyce JA
[Ad] Endereço:Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
[Ti] Título:Inhibition of colony stimulating factor-1 receptor abrogates microenvironment-mediated therapeutic resistance in gliomas.
[So] Source:Oncogene;36(43):6049-6058, 2017 Oct 26.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glioblastomas represent the most aggressive glioma grade and are associated with a poor patient prognosis. The current standard of care, consisting of surgery, radiation and chemotherapy, only results in a median survival of 14 months, underscoring the importance of developing effective new therapeutic strategies. Among the challenges in treating glioblastomas are primary resistance and the rapid emergence of recurrent disease, which can result from tumor cell-intrinsic mechanisms in addition to tumor microenvironment (TME)-mediated extrinsic resistance. Using a PDGF-B-driven proneural glioma mouse model, we assessed a panel of tyrosine kinase inhibitors with different selectivity profiles. We found that PLX3397, an inhibitor of colony stimulating factor-1 receptor (CSF-1R), blocks glioma progression, markedly suppresses tumor cell proliferation and reduces tumor grade. By contrast, the multi-targeted tyrosine kinase inhibitors dovitinib and vatalanib, which directly target tumor cells, exert minimal anti-tumoral effects in vivo, despite killing glioma cells in vitro, suggesting a TME-mediated resistance mechanism may be involved. Interestingly, PLX3397 interferes with tumor-mediated education of macrophages and consequently restores the sensitivity of glioma cells to tyrosine kinase inhibitors in vivo in preclinical combination trials. Our findings thus demonstrate that microenvironmental alteration by CSF-1R blockade renders tumor cells more susceptible to receptor tyrosine kinase inhibition in a preclinical glioblastoma model, which may have important translational relevance.
[Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos/genética
Glioma/tratamento farmacológico
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/genética
[Mh] Termos MeSH secundário: Aminopiridinas/administração & dosagem
Animais
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Modelos Animais de Doenças
Glioma/genética
Glioma/patologia
Seres Humanos
Camundongos
Inibidores de Proteínas Quinases/administração & dosagem
Proteínas Proto-Oncogênicas c-sis/genética
Pirróis/administração & dosagem
Microambiente Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-((5-chloro-1H-pyrrolo(2,3-b)pyridin-3-yl)methyl)-N-((6-(trifluoromethyl)pyridin-3-yl)methyl)pyridin-2-amine); 0 (Aminopyridines); 0 (Csf1r protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-sis); 0 (Pyrroles); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 1B56C968OA (becaplermin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.261


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[PMID]:28701355
[Au] Autor:Qian Z; Li Y; Chen J; Li X; Gou D
[Ad] Endereço:Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, Guangdong China; zj.qian@siat.ac.cn.
[Ti] Título:miR-4632 mediates PDGF-BB-induced proliferation and antiapoptosis of human pulmonary artery smooth muscle cells via targeting cJUN.
[So] Source:Am J Physiol Cell Physiol;313(4):C380-C391, 2017 Oct 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) can regulate the proliferative status of pulmonary artery smooth muscle cells (PASMCs), which is a core factor modulating pulmonary vascular remodeling diseases, such as atherosclerosis and pulmonary arterial hypertension (PAH). Our previous work has shown that miR-4632, a rarely reported miRNA, is significantly downregulated in platelet-derived growth factor (PDGF)-BB-stimulated human pulmonary artery smooth muscle cells (HPASMCs), yet its cell function and the underlying molecular mechanisms remain to be elucidated. Here, we find that miR-4632 is highly expressed in HPASMCs and its expression significantly decreased in response to different stimuli. Functional studies revealed that miR-4632 inhibited proliferation and promoted apoptosis of HPASMCs but had no effects on cell contraction and migration. Furthermore, the cJUN was identified as a direct target gene of miR-4632, while knockdown of cJUN was necessary for miR-4632-mediated HPASMC proliferation and apoptosis. In addition, the downregulation of miR-4632 by PDGF-BB was found to associate with histone deacetylation through the activation of PDGF receptor/phosphatidylinositol 3'-kinase/histone deacetylase 4 signaling. Finally, the expression of miR-4632 was reduced in the serum of patients with PAH. Overall, our results suggest that miR-4632 plays an important role in regulating HPASMC proliferation and apoptosis by suppression of cJUN, providing a novel therapeutic miRNA candidate for the treatment of pulmonary vascular remodeling diseases. It also implies that serum miR-4632 has the potential to serve as a circulating biomarker for PAH diagnosis.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Proliferação Celular/fisiologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
MicroRNAs/metabolismo
Músculo Liso Vascular/fisiologia
Miócitos de Músculo Liso/fisiologia
Proteínas Proto-Oncogênicas c-sis/metabolismo
Artéria Pulmonar/fisiologia
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Sobrevivência Celular/fisiologia
Células Cultivadas
Seres Humanos
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Artéria Pulmonar/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (MIRN4632 microRNA, human); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-sis); 1B56C968OA (becaplermin); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00061.2017



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