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Pesquisa : D08.811.913.400.450.480.500 [Categoria DeCS]
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[PMID]:28460475
[Au] Autor:Song JM; Molla K; Anandharaj A; Cornax I; O Sullivan MG; Kirtane AR; Panyam J; Kassie F
[Ad] Endereço:Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
[Ti] Título:Triptolide suppresses the in vitro and in vivo growth of lung cancer cells by targeting hyaluronan-CD44/RHAMM signaling.
[So] Source:Oncotarget;8(16):26927-26940, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Higher levels of hyaluronan (HA) and its receptors CD44 and RHAMM have been associated with poor prognosis and metastasis in NSCLC. In the current study, our goal was to define, using cellular and orthotopic lung tumor models, the role of HA-CD44/RHAMM signaling in lung carcinogenesis and to assess the potential of triptolide to block HA-CD44/RHAMM signaling and thereby suppress the development and progression of lung cancer. Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP. Silencing of HAS2, CD44 or RHAMM induced similar effects. Addition of excess HA to the culture media completely abrogated the effects of triptolide and siRNAs targeting HAS2, CD44, or RHAMM. In an orthotopic lung cancer model in nude rats, intranasal administration of liposomal triptolide (400 µg/kg) for 8 weeks significantly reduced lung tumor growth as determined by bioluminescence imaging, lung weight measurements and gross and histopathological analysis of tumor burden. Also, triptolide suppressed expressions of Ki-67, a marker for cell proliferation, HAS2, HAS3, HA, CD44, and RHAMM in lung tumors. Overall, our results provide a strong rationale for mitigating lung cancer by targeting the HA-CD44/RHAMM signaling axis.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/farmacologia
Diterpenos/farmacologia
Proteínas da Matriz Extracelular/metabolismo
Receptores de Hialuronatos/antagonistas & inibidores
Receptores de Hialuronatos/metabolismo
Neoplasias Pulmonares/metabolismo
Fenantrenos/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Modelos Animais de Doenças
Compostos de Epóxi/farmacologia
Inativação Gênica
Seres Humanos
Receptores de Hialuronatos/genética
Hialuronan Sintases/genética
Hialuronan Sintases/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Masculino
RNA Interferente Pequeno/genética
Ratos
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (CD44 protein, human); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (Extracellular Matrix Proteins); 0 (Hyaluronan Receptors); 0 (Phenanthrenes); 0 (RNA, Small Interfering); 0 (hyaluronan-mediated motility receptor); 19ALD1S53J (triptolide); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15879


  2 / 779 MEDLINE  
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[PMID]:28863216
[Au] Autor:Gesteira TF; Sun M; Coulson-Thomas YM; Yamaguchi Y; Yeh LK; Hascall V; Coulson-Thomas VJ
[Ad] Endereço:Universidade Federal de Sao Paulo, Sao Paulo, Brazil.
[Ti] Título:Hyaluronan Rich Microenvironment in the Limbal Stem Cell Niche Regulates Limbal Stem Cell Differentiation.
[So] Source:Invest Ophthalmol Vis Sci;58(11):4407-4421, 2017 Sep 01.
[Is] ISSN:1552-5783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: Limbal epithelial stem cells (LSCs), located in the basal layer of the corneal epithelium in the corneal limbus, are vital for maintaining the corneal epithelium. LSCs have a high capacity of self-renewal with increased potential for error-free proliferation and poor differentiation. To date, limited research has focused on unveiling the composition of the limbal stem cell niche, and, more important, on the role the specific stem cell niche may have in LSC differentiation and function. Our work investigates the composition of the extracellular matrix in the LSC niche and how it regulates LSC differentiation and function. Methods: Hyaluronan (HA) is naturally synthesized by hyaluronan synthases (HASs), and vertebrates have the following three types: HAS1, HAS2, and HAS3. Wild-type and HAS and TSG-6 knockout mice-HAS1-/-;HAS3-/-, HAS2Δ/ΔCorEpi, TSG-6-/--were used to determine the importance of the HA niche in LSC differentiation and specification. Results: Our data demonstrate that the LSC niche is composed of a HA rich extracellular matrix. HAS1-/-;HAS3-/-, HAS2Δ/ΔCorEpi, and TSG-6-/- mice have delayed wound healing and increased inflammation after injury. Interestingly, upon insult the HAS knock-out mice up-regulate HA throughout the cornea through a compensatory mechanism, and in turn this alters LSC and epithelial cell specification. Conclusions: The LSC niche is composed of a specialized HA matrix that differs from that present in the rest of the corneal epithelium, and the disruption of this specific HA matrix within the LSC niche leads to compromised corneal epithelial regeneration. Finally, our findings suggest that HA has a major role in maintaining the LSC phenotype.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Microambiente Celular/fisiologia
Epitélio Anterior/metabolismo
Ácido Hialurônico/metabolismo
Limbo da Córnea/citologia
Nicho de Células-Tronco/fisiologia
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Queimaduras Químicas/metabolismo
Modelos Animais de Doenças
Queimaduras Oculares/induzido quimicamente
Glucuronosiltransferase/metabolismo
Hialuronan Sintases
Ácido Hialurônico/genética
Imuno-Histoquímica
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Microscopia Confocal
Microscopia Eletrônica de Transmissão
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Hidróxido de Sódio
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 55X04QC32I (Sodium Hydroxide); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1167/iovs.17-22326


  3 / 779 MEDLINE  
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[PMID]:28533273
[Au] Autor:Liu S; Cheng C
[Ad] Endereço:Lester & Sue Smith Breast Center, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.
[Ti] Título:Akt Signaling Is Sustained by a CD44 Splice Isoform-Mediated Positive Feedback Loop.
[So] Source:Cancer Res;77(14):3791-3801, 2017 Jul 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor cells nearly invariably evolve sustained PI3K/Akt signaling as an effective means to circumvent apoptosis and maintain survival. However, for those tumor cells that do not acquire PI3K/Akt mutations to achieve this end, the underlying mechanisms have remained obscure. Here, we describe the discovery of a splice isoform-dependent positive feedback loop that is essential to sustain PI3K/Akt signaling in breast cancer. Splice isoform CD44s promoted expression of the hyaluronan synthase HAS2 by activating the Akt signaling cascade. The HAS2 product hyaluronan further stimulated CD44s-mediated Akt signaling, creating a feed-forward signaling circuit that promoted tumor cell survival. Mechanistically, we identified FOXO1 as a bona fide transcriptional repressor of HAS2. Akt-mediated phosphorylation of FOXO1 relieved its suppression of HAS2 transcription, with FOXO1 phosphorylation status maintained by operation of the positive feedback loop. In clinical specimens of breast cancer, we established that the expression of CD44s and HAS2 was positively correlated. Our results establish a positive feedback mechanism that sustains PI3K/Akt signaling in tumor cells, further illuminating the nearly universal role of this pathway in cancer cell survival. .
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Receptores de Hialuronatos/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
[Mh] Termos MeSH secundário: Neoplasias da Mama/enzimologia
Neoplasias da Mama/genética
Linhagem Celular Tumoral
Sobrevivência Celular/fisiologia
Retroalimentação Fisiológica
Feminino
Proteína Forkhead Box O1/genética
Proteína Forkhead Box O1/metabolismo
Glucuronosiltransferase/genética
Glucuronosiltransferase/metabolismo
Células HEK293
Seres Humanos
Receptores de Hialuronatos/genética
Hialuronan Sintases
Isoformas de Proteínas
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD44 protein, human); 0 (FOXO1 protein, human); 0 (Forkhead Box Protein O1); 0 (Hyaluronan Receptors); 0 (Protein Isoforms); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (HAS2 protein, human); EC 2.4.1.212 (Hyaluronan Synthases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-2545


  4 / 779 MEDLINE  
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[PMID]:28496038
[Au] Autor:Hirooka T; Yoshida E; Eto K; Kaji T
[Ad] Endereço:Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science.
[Ti] Título:Methylmercury induces hyaluronan synthesis in cultured human brain microvascular endothelial cells and pericytes via different mechanisms.
[So] Source:J Toxicol Sci;42(3):329-333, 2017.
[Is] ISSN:1880-3989
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:In a cerebrum damaged by methylmercury, where neuropathological lesions tend to localize along deep sulci and fissures, edematous changes in white matter have been proposed as the cause of such localization. Since hyaluronan has a high water-retention capability and can contribute to the progression of edematous changes, we hypothesize that methylmercury increases hyaluronan in brain microvascular cells. Our experimental results indicate that methylmercury induces the expression of hyaluronan in cultured human microvascular endothelial cells and pericytes through the induction of expressed UDP-glucose dehydrogenase and hyaluronan synthase 2, respectively. After exposure to methylmercury, hyaluronan largely accumulates in perivascular space, where it contributes to the progression of edematous changes.
[Mh] Termos MeSH primário: Encéfalo/irrigação sanguínea
Células Endoteliais/metabolismo
Ácido Hialurônico/biossíntese
Compostos de Metilmercúrio/toxicidade
Pericitos/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Edema
Células Endoteliais/enzimologia
Células Endoteliais/patologia
Indução Enzimática/efeitos dos fármacos
Glucuronosiltransferase/metabolismo
Seres Humanos
Hialuronan Sintases
Pericitos/enzimologia
Pericitos/patologia
Uridina Difosfato Glucose Desidrogenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Methylmercury Compounds); 9004-61-9 (Hyaluronic Acid); EC 1.1.1.22 (Uridine Diphosphate Glucose Dehydrogenase); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (HAS2 protein, human); EC 2.4.1.212 (Hyaluronan Synthases)
[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:170513
[St] Status:MEDLINE
[do] DOI:10.2131/jts.42.329


  5 / 779 MEDLINE  
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[PMID]:28485478
[Au] Autor:Zhu G; Wang S; Chen J; Wang Z; Liang X; Wang X; Jiang J; Lang J; Li L
[Ti] Título:Long noncoding RNA HAS2-AS1 mediates hypoxia-induced invasiveness of oral squamous cell carcinoma.
[So] Source:Mol Carcinog;56(10):2210-2222, 2017 Oct.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A hypoxic microenvironment plays important roles in the progression of solid tumors, including oral squamous cell carcinoma (OSCC). Long noncoding RNAs (lncRNAs) have gained much attention in the past few years. However, it is not clear whether lncRNAs can regulate hypoxia adaptation of OSCC or which lncRNAs participate in this process. Using a lncRNA microarray, we analyzed the aberrant lncRNA expression profiles in OSCC tissues compared with paired normal oral mucosa and in hypoxic OSCC cells compared with normoxic OSCC cells. The top 10 lncRNAs that had more than threefold increase with P-value <0.01 in both microarray data were validated by qRT-PCR. Among the top 10 lncRNAs, hyaluronan synthase 2 antisense 1 (HAS2-AS1) was the only one that has a hypoxia-responsive element (HRE) on its promoter region and has been validated to increase in OSCC tissues and in cells cultured under hypoxia. Tumor HAS2-AS1 levels were closely associated with lymph node metastasis and hypoxic tumor status in patients with OSCC. Moreover, the hypoxia-induced HAS2-AS1 expression is dependent on HIF-1α which directly binds to and activates the transcription of HAS2-AS1. In addition, HAS2-AS1 mediates hypoxia-induced epithelial mesenchymal transition of OSCC cells via stabilizing HAS2. In conclusion, our results suggest that hypoxia would induce an overexpression of HAS2-AS1 in an HIF-1α dependent manner. The increase of HAS2-AS1 plays important roles mediating the hypoxia-regulated EMT and invasiveness of OSCC.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
Perfilação da Expressão Gênica/métodos
Glucuronosiltransferase/genética
Neoplasias Bucais/genética
Análise de Sequência com Séries de Oligonucleotídeos/métodos
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Carcinoma de Células Escamosas/metabolismo
Hipóxia Celular
Linhagem Celular Tumoral
Transição Epitelial-Mesenquimal
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Hialuronan Sintases
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Masculino
Camundongos
Neoplasias Bucais/metabolismo
Invasividade Neoplásica
Regiões Promotoras Genéticas
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (RNA, Long Noncoding); 0 (long noncoding RNA HAS2-AS1, human); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (HAS2 protein, human); EC 2.4.1.212 (Hyaluronan Synthases)
[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:170510
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22674


  6 / 779 MEDLINE  
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[PMID]:28482035
[Au] Autor:Reed MJ; Vernon RB; Damodarasamy M; Chan CK; Wight TN; Bentov I; Banks WA
[Ad] Endereço:Department of Medicine, University of Washington, Seattle.
[Ti] Título:Microvasculature of the Mouse Cerebral Cortex Exhibits Increased Accumulation and Synthesis of Hyaluronan With Aging.
[So] Source:J Gerontol A Biol Sci Med Sci;72(6):740-746, 2017 Jun 01.
[Is] ISSN:1758-535X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The microvasculature of the aged brain is less dense and more vulnerable to dysfunction than that of the young brain. Brain microvasculature is supported by its surrounding extracellular matrix, which is comprised largely of hyaluronan (HA). HA is continually degraded into lower molecular weight forms that induce neuroinflammation. We examined HA associated with microvessels (MV) of the cerebral cortex of young (4 months), middle-aged (14 months), and aged (24-26 months) mice. We confirmed that the density of cortical MV decreased with age. Perivascular HA levels increased with age, but there was no age-associated change in HA molecular weight profile. MV isolated from aged cortex had more HA than MV from young cortex. Examination of mechanisms that might account for elevated HA levels with aging showed increased HA synthase 2 (HAS2) mRNA and protein in aged MV relative to young MV. In contrast, mRNAs for HA-degrading hyaluronidases or hyaladherins that mitigate HA degradation showed no changes with age. Corresponding to increased HAS2, aged MV synthesized significantly more HA (of all molecular weight classes) in vitro than young MV. We propose that increased HA synthesis and accumulation in brain MV contributes to neuroinflammation and reduced MV density and function in aging.
[Mh] Termos MeSH primário: Envelhecimento/metabolismo
Córtex Cerebral/metabolismo
Ácido Hialurônico/biossíntese
Microvasos/metabolismo
[Mh] Termos MeSH secundário: Animais
Córtex Cerebral/irrigação sanguínea
Ensaio de Imunoadsorção Enzimática
Imunofluorescência
Expressão Gênica
Glucuronosiltransferase/genética
Glucuronosiltransferase/metabolismo
Hialuronan Sintases
Hialuronoglucosaminidase/genética
Hialuronoglucosaminidase/metabolismo
Imuno-Histoquímica
Camundongos Endogâmicos C57BL
RNA Mensageiro
Reação em Cadeia da Polimerase em Tempo Real
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Has2 protein, mouse); EC 2.4.1.212 (Hyaluronan Synthases); EC 3.2.1.35 (Hyaluronoglucosaminidase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1093/gerona/glw213


  7 / 779 MEDLINE  
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[PMID]:28389562
[Au] Autor:Ghatak S; Markwald RR; Hascall VC; Dowling W; Lottes RG; Baatz JE; Beeson G; Beeson CC; Perrella MA; Thannickal VJ; Misra S
[Ad] Endereço:From the Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, South Carolina 29425, ghatak@musc.edu.
[Ti] Título:Transforming growth factor ß1 (TGFß1) regulates CD44V6 expression and activity through extracellular signal-regulated kinase (ERK)-induced EGR1 in pulmonary fibrogenic fibroblasts.
[So] Source:J Biol Chem;292(25):10465-10489, 2017 Jun 23.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The appearance of myofibroblasts is generally thought to be the underlying cause of the fibrotic changes that underlie idiopathic pulmonary fibrosis. However, the cellular/molecular mechanisms that account for the fibroblast-myofibroblast differentiation/activation in idiopathic pulmonary fibrosis remain poorly understood. We investigated the functional role of hyaluronan receptor CD44V6 (CD44 containing variable exon 6 (v6)) for differentiation of lung fibroblast to myofibroblast phenotype. Increased hyaluronan synthesis and CD44 expression have been detected in numerous fibrotic organs. Previously, we found that the TGFß1/CD44V6 pathway is important in lung myofibroblast collagen-1 and α-smooth-muscle actin synthesis. Because increased EGR1 (early growth response-1) expression has been shown to appear very early and nearly coincident with the expression of CD44V6 found after TGFß1 treatment, we investigated the mechanism(s) of regulation of CD44V6 expression in lung fibroblasts by TGFß1. TGFß1-mediated CD44V6 up-regulation was initiated through EGR1 via ERK-regulated transcriptional activation. We showed that TGFß1-induced CD44V6 expression is through EGR1-mediated (activator protein-1) activity and that the - and -binding sites in the promoter account for its responsiveness to TGFß1 in lung fibroblasts. We also identified a positive-feedback loop in which ERK/EGR1 signaling promotes CD44V6 splicing and found that CD44V6 then sustains ERK signaling, which is important for activity in lung fibroblasts. Furthermore, we identified that -produced hyaluronan is required for CD44V6 and TGFßRI co-localization and subsequent CD44V6/ERK1/EGR1 signaling. These results demonstrate a novel positive-feedback loop that links the myofibroblast phenotype to TGFß1-stimulated CD44V6/ERK/EGR1 signaling.
[Mh] Termos MeSH primário: Proteína 1 de Resposta de Crescimento Precoce/metabolismo
Receptores de Hialuronatos/biossíntese
Pulmão/metabolismo
Sistema de Sinalização das MAP Quinases
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Miofibroblastos/metabolismo
Fibrose Pulmonar/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica
Glucuronosiltransferase/metabolismo
Hialuronan Sintases
Ácido Hialurônico/biossíntese
Pulmão/patologia
Camundongos
Miofibroblastos/patologia
Fibrose Pulmonar/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD44v6 antigen); 0 (Early Growth Response Protein 1); 0 (Egr1 protein, mouse); 0 (Hyaluronan Receptors); 0 (Tgfb1 protein, mouse); 0 (Transforming Growth Factor beta1); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Has2 protein, mouse); EC 2.4.1.212 (Hyaluronan Synthases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170409
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.752451


  8 / 779 MEDLINE  
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[PMID]:28247017
[Au] Autor:Li WH; Wong HK; Serrano J; Randhawa M; Kaur S; Southall MD; Parsa R
[Ad] Endereço:Johnson & Johnson Skin Research Center, Johnson & Johnson Consumer Inc., 199 Grandview Road, Skillman, NJ, 08558, USA.
[Ti] Título:Topical stabilized retinol treatment induces the expression of HAS genes and HA production in human skin in vitro and in vivo.
[So] Source:Arch Dermatol Res;309(4):275-283, 2017 May.
[Is] ISSN:1432-069X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Skin Aging manifests primarily with wrinkles, dyspigmentations, texture changes, and loss of elasticity. During the skin aging process, there is a loss of moisture and elasticity in skin resulting in loss of firmness finally leading to skin sagging. The key molecule involved in skin moisture is hyaluronic acid (HA), which has a significant water-binding capacity. HA levels in skin decline with age resulting in decrease in skin moisture, which may contribute to loss of firmness. Clinical trials have shown that topically applied ROL effectively reduces wrinkles and helps retain youthful appearance. In the current study, ROL was shown to induce HA production and stimulates the gene expression of all three forms of hyaluronic acid synthases (HAS) in normal human epidermal keratinocytes monolayer cultures. Moreover, in human skin equivalent tissues and in human skin explants, topical treatment of tissues with a stabilized-ROL formulation significantly induced the gene expression of HAS mRNA concomitant with an increased HA production. Finally, in a vehicle-controlled human clinical study, histochemical analysis confirmed increased HA accumulation in the epidermis in ROL-treated human skin as compared to vehicle. These results show that ROL increases skin expression of HA, a significant contributing factor responsible for wrinkle formation and skin moisture, which decrease during aging. Taken together with the activity to increase collagen, elastin, and cell proliferation, these studies establish that retinol provides multi-functional activity for photodamaged skin.
[Mh] Termos MeSH primário: Senilidade Prematura/tratamento farmacológico
Glucuronosiltransferase/metabolismo
Queratinócitos/efeitos dos fármacos
Pele/efeitos dos fármacos
Vitamina A/uso terapêutico
[Mh] Termos MeSH secundário: Administração Tópica
Células Cultivadas
Elastina/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Glucuronosiltransferase/genética
Seres Humanos
Hialuronan Sintases
Ácido Hialurônico/metabolismo
Queratinócitos/metabolismo
Técnicas de Cultura de Órgãos
Pele/patologia
Envelhecimento da Pele/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
11103-57-4 (Vitamin A); 9004-61-9 (Hyaluronic Acid); 9007-58-3 (Elastin); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Hyaluronan Synthases)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE
[do] DOI:10.1007/s00403-017-1723-6


  9 / 779 MEDLINE  
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[PMID]:28207787
[Au] Autor:Ouyang X; Panetta NJ; Talbott MD; Payumo AY; Halluin C; Longaker MT; Chen JK
[Ad] Endereço:Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, California, United States of America.
[Ti] Título:Hyaluronic acid synthesis is required for zebrafish tail fin regeneration.
[So] Source:PLoS One;12(2):e0171898, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Using genome-wide transcriptional profiling and whole-mount expression analyses of zebrafish larvae, we have identified hyaluronan synthase 3 (has3) as an upregulated gene during caudal fin regeneration. has3 expression is induced in the wound epithelium within hours after tail amputation, and its onset and maintenance requires fibroblast growth factor, phosphoinositide 3-kinase, and transforming growth factor-ß signaling. Inhibition of hyaluronic acid (HA) synthesis by the small molecule 4-methylumbelliferone (4-MU) impairs tail regeneration in zebrafish larvae by preventing injury-induced cell proliferation. In addition, 4-MU reduces the expression of genes associated with wound epithelium and blastema function. Treatment with glycogen synthase kinase 3 inhibitors rescues 4-MU-induced defects in cell proliferation and tail regeneration, while restoring a subset of wound epithelium and blastema markers. Our findings demonstrate a role for HA biosynthesis in zebrafish tail regeneration and delineate its epistatic relationships with other regenerative processes.
[Mh] Termos MeSH primário: Nadadeiras de Animais/fisiologia
Glucuronosiltransferase/fisiologia
Ácido Hialurônico/fisiologia
Regeneração/genética
Proteínas de Peixe-Zebra/fisiologia
Peixe-Zebra/fisiologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/genética
Epistasia Genética
Regulação da Expressão Gênica/efeitos dos fármacos
Glucuronosiltransferase/genética
Glucuronosiltransferase/metabolismo
Hialuronan Sintases
Ácido Hialurônico/biossíntese
Himecromona/farmacologia
Regeneração/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Cicatrização/genética
Peixe-Zebra/metabolismo
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Zebrafish Proteins); 3T5NG4Q468 (Hymecromone); 9004-61-9 (Hyaluronic Acid); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Hyaluronan Synthases)
[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:170217
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171898


  10 / 779 MEDLINE  
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[PMID]:28192668
[Au] Autor:Yang J; Cheng F; Yu H; Wang J; Guo Z; Stephanopoulos G
[Ti] Título:Key Role of the Carboxyl Terminus of Hyaluronan Synthase in Processive Synthesis and Size Control of Hyaluronic Acid Polymers.
[So] Source:Biomacromolecules;18(4):1064-1073, 2017 Apr 10.
[Is] ISSN:1526-4602
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The essential pathophysiological roles of hyaluronic acid (HA) strongly depend on HA binding and HA size. Here we deployed the atomic vision of molecular dynamics (MD) simulation to experimentally investigate the influence of C-terminal mutations of Streptococcus equisimilis hyaluronan synthase (SeHAS) on HA product synthesis in Escherichia coli. R413 was vital for HA production, as the removal or mutation of R413 led to inactivation of SeHAS. MD simulations indicated that R406-R413 constituted an HA-binding pattern that stabilized the HA-SeHAS complex. We further increased HA product size via site-directed mutation of the SeHAS C-terminal residues 414-417 based on the hypothesis that higher binding affinity between the SeHAS C-terminus and HA would lead to larger HA size, underlying the important role of the HA-SeHAS interaction in HA size control. W410A and T412A mutations also completely deactivated SeHAS. Moreover, a catalysis-transformation-translocation model was proposed for the HA synthesis and translocation processes.
[Mh] Termos MeSH primário: Glucuronosiltransferase/metabolismo
Ácido Hialurônico/química
Polímeros/química
Streptococcus/enzimologia
[Mh] Termos MeSH secundário: Arginina/química
DNA Bacteriano/genética
Escherichia coli/genética
Escherichia coli/metabolismo
Hialuronan Sintases
Lisina/química
Simulação de Dinâmica Molecular
Peso Molecular
Mutação
Streptococcus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (Polymers); 9004-61-9 (Hyaluronic Acid); 94ZLA3W45F (Arginine); EC 2.4.1.17 (Glucuronosyltransferase); EC 2.4.1.212 (Hyaluronan Synthases); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biomac.6b01239



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