Base de dados : MEDLINE
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[PMID]:29237418
[Au] Autor:Cattaneo M; La Sala L; Rondinelli M; Errichiello E; Zuffardi O; Puca AA; Genovese S; Ceriello A
[Ad] Endereço:Cardiovascular Research Unit, IRCCS MultiMedica, Via G. Fantoli 16/15, 20138, Milan, Italy. monica.cattaneo@multimedica.it.
[Ti] Título:A donor splice site mutation in CISD2 generates multiple truncated, non-functional isoforms in Wolfram syndrome type 2 patients.
[So] Source:BMC Med Genet;18(1):147, 2017 12 13.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mutations in the gene that encodes CDGSH iron sulfur domain 2 (CISD2) are causative of Wolfram syndrome type 2 (WFS2), a rare autosomal recessive neurodegenerative disorder mainly characterized by diabetes mellitus, optic atrophy, peptic ulcer bleeding and defective platelet aggregation. Four mutations in the CISD2 gene have been reported. Among these mutations, the homozygous c.103 + 1G > A substitution was identified in the donor splice site of intron 1 in two Italian sisters and was predicted to cause a exon 1 to be skipped. METHODS: Here, we employed molecular assays to characterize the c.103 + 1G > A mutation using the patient's peripheral blood mononuclear cells (PBMCs). 5'-RACE coupled with RT-PCR were used to analyse the effect of the c.103 + 1G > A mutation on mRNA splicing. Western blot analysis was used to analyse the consequences of the CISD2 mutation on the encoded protein. RESULTS: We demonstrated that the c.103 + 1G > A mutation functionally impaired mRNA splicing, producing multiple splice variants characterized by the whole or partial absence of exon 1, which introduced amino acid changes and a premature stop. The affected mRNAs resulted in either predicted targets for nonsense mRNA decay (NMD) or non-functional isoforms. CONCLUSIONS: We concluded that the c.103 + 1G > A mutation resulted in the loss of functional CISD2 protein in the two Italian WFS2 patients.
[Mh] Termos MeSH primário: Senilidade Prematura/genética
Perda Auditiva Neurossensorial/genética
Proteínas de Membrana/genética
Doenças Mitocondriais/genética
Mutação
Atrofia Óptica/genética
Sítios de Splice de RNA/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Células Sanguíneas
Códon sem Sentido
Éxons/genética
Feminino
Seres Humanos
Íntrons/genética
Leucócitos Mononucleares
Proteínas de Membrana/química
Isoformas de Proteínas/genética
Sítios de Splice de RNA/fisiologia
Processamento de RNA
RNA Mensageiro/genética
Análise de Sequência
Deleção de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Codon, Nonsense); 0 (ERIS protein, human); 0 (Membrane Proteins); 0 (Protein Isoforms); 0 (RNA Splice Sites); 0 (RNA, Messenger)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171231
[Lr] Data última revisão:
171231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-017-0508-2


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[PMID]:28846075
[Au] Autor:Lessel D; Wu D; Trujillo C; Ramezani T; Lessel I; Alwasiyah MK; Saha B; Hisama FM; Rading K; Goebel I; Schütz P; Speit G; Högel J; Thiele H; Nürnberg G; Nürnberg P; Hammerschmidt M; Zhu Y; Tong DR; Katz C; Martin GM; Oshima J; Prives C; Kubisch C
[Ad] Endereço:Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:Dysfunction of the MDM2/p53 axis is linked to premature aging.
[So] Source:J Clin Invest;127(10):3598-3608, 2017 Oct 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The tumor suppressor p53, a master regulator of the cellular response to stress, is tightly regulated by the E3 ubiquitin ligase MDM2 via an autoregulatory feedback loop. In addition to its well-established role in tumorigenesis, p53 has also been associated with aging in mice. Several mouse models with aberrantly increased p53 activity display signs of premature aging. However, the relationship between dysfunction of the MDM2/p53 axis and human aging remains elusive. Here, we have identified an antiterminating homozygous germline mutation in MDM2 in a patient affected by a segmental progeroid syndrome. We show that this mutation abrogates MDM2 activity, thereby resulting in enhanced levels and stability of p53. Analysis of the patient's primary cells, genome-edited cells, and in vitro and in vivo analyses confirmed the MDM2 mutation's aberrant regulation of p53 activity. Functional data from a zebrafish model further demonstrated that mutant Mdm2 was unable to rescue a p53-induced apoptotic phenotype. Altogether, our findings indicate that mutant MDM2 is a likely driver of the observed segmental form of progeria.
[Mh] Termos MeSH primário: Senilidade Prematura
Mutação em Linhagem Germinativa
Proteínas Proto-Oncogênicas c-mdm2
Proteína Supressora de Tumor p53
Proteínas de Peixe-Zebra
Peixe-Zebra
[Mh] Termos MeSH secundário: Senilidade Prematura/genética
Senilidade Prematura/metabolismo
Animais
Apoptose/genética
Linhagem Celular Tumoral
Modelos Animais de Doenças
Seres Humanos
Proteínas Proto-Oncogênicas c-mdm2/genética
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Peixe-Zebra/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 (TP53 protein, human); 0 (Tumor Suppressor Protein p53); 0 (Zebrafish Proteins); EC 2.3.2.27 (MDM2 protein, human); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2); EC 2.3.2.27 (mdm2 protein, zebrafish)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE


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[PMID]:28792007
[Au] Autor:Kubben N; Misteli T
[Ad] Endereço:National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
[Ti] Título:Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases.
[So] Source:Nat Rev Mol Cell Biol;18(10):595-609, 2017 Oct.
[Is] ISSN:1471-0080
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ageing is the predominant risk factor for many common diseases. Human premature ageing diseases are powerful model systems to identify and characterize cellular mechanisms that underpin physiological ageing. Their study also leads to a better understanding of the causes, drivers and potential therapeutic strategies of common diseases associated with ageing, including neurological disorders, diabetes, cardiovascular diseases and cancer. Using the rare premature ageing disorder Hutchinson-Gilford progeria syndrome as a paradigm, we discuss here the shared mechanisms between premature ageing and ageing-associated diseases, including defects in genetic, epigenetic and metabolic pathways; mitochondrial and protein homeostasis; cell cycle; and stem cell-regenerative capacity.
[Mh] Termos MeSH primário: Senilidade Prematura/metabolismo
Senilidade Prematura/patologia
Envelhecimento/metabolismo
Envelhecimento/patologia
[Mh] Termos MeSH secundário: Envelhecimento/genética
Senilidade Prematura/genética
Animais
Reparo do DNA
Epigênese Genética
Instabilidade Genômica
Seres Humanos
Progéria/genética
Progéria/metabolismo
Progéria/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1038/nrm.2017.68


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[PMID]:28701312
[Au] Autor:Kooman JP; Dekker MJ; Usvyat LA; Kotanko P; van der Sande FM; Schalkwijk CG; Shiels PG; Stenvinkel P
[Ad] Endereço:Maastricht University Medical Center, Maastricht, Netherlands; Jeroen.kooman@mumc.nl.
[Ti] Título:Inflammation and premature aging in advanced chronic kidney disease.
[So] Source:Am J Physiol Renal Physiol;313(4):F938-F950, 2017 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic inflammation in end-stage renal disease is an established risk factor for mortality and a catalyst for other complications, which are related to a premature aging phenotype, including muscle wasting, vascular calcification, and other forms of premature vascular disease, depression, osteoporosis, and frailty. Uremic inflammation is also mechanistically related to mechanisms involved in the aging process, such as telomere shortening, mitochondrial dysfunction, and altered nutrient sensing, which can have a direct effect on cellular and tissue function. In addition to uremia-specific causes, such as abnormalities in the phosphate-Klotho axis, there are remarkable similarities between the pathophysiology of uremic inflammation and so-called "inflammaging" in the general population. Potentially relevant, but still somewhat unexplored in this respect, are abnormal or misplaced protein structures, as well as abnormalities in tissue homeostasis, which evoke danger signals through damage-associated molecular patterns, as well as the senescence-associated secretory phenotype. Systemic inflammation, in combination with the loss of kidney function, can impair the resilience of the body to external and internal stressors by reduced functional and structural tissue reserves, and by impairing normal organ crosstalk, thus providing an explanation for the greatly increased risk of homeostatic breakdown in this population. In this review, the relationship between uremic inflammation and a premature aging phenotype, as well as potential causes and consequences, are discussed.
[Mh] Termos MeSH primário: Senilidade Prematura/imunologia
Insuficiência Renal Crônica/complicações
Insuficiência Renal Crônica/imunologia
Uremia/complicações
Uremia/imunologia
[Mh] Termos MeSH secundário: Envelhecimento/imunologia
Animais
Seres Humanos
Insuficiência Renal Crônica/fisiopatologia
Uremia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00256.2017


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[PMID]:28636628
[Au] Autor:Chan YC; Hwang JH
[Ad] Endereço:Department of Food and Nutrition, Providence University, Taichung, Taiwan.
[Ti] Título:Effects of Spirulina on the functions and redox status of auditory system in senescence-accelerated prone-8 mice.
[So] Source:PLoS One;12(6):e0178916, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To our knowledge, the effects of Spirulina platensis water extract (SP) on hearing function have not yet been reported. This study investigated the effects of SP on the function and redox status of the auditory system. Auditory brainstem responses and redox status were compared between two groups of 3-month-old senescence-accelerated prone-8 (SAMP8) mice: the control group was fed a normal diet, and the experimental group was fed a normal diet with oral supplementation of SP for 6 weeks. Compared with the control group, the experimental group had significantly lower hearing thresholds according to auditory brainstem responses measured using click sounds and 8-kHz tone burst sound stimulation at the end of this study. The experimental group had a shorter I-III interval of auditory brainstem responses with 16-kHz tone burst stimulation than the control group that was of borderline significance. Additionally, the experimental group had significantly higher mRNA expression of the superoxide dismutase and catalase genes in the cochlea and brainstem and significantly higher mRNA expression of the glutathione peroxidase gene in the cochlea. Further, the experimental group had significantly lower malondialdehyde levels in the cochlea and brainstem than the control group. However, tumor necrosis factor-α mRNA expression was not significantly different between the control and experimental groups. SP could decrease hearing degeneration in senescence-accelerated prone-8 mice possibly by increasing superoxide dismutase, catalase, and glutathione peroxidase gene expression and decreasing damage from oxidative stress in the cochlea and brainstem.
[Mh] Termos MeSH primário: Senilidade Prematura/prevenção & controle
Doença de Alzheimer/prevenção & controle
Senescência Celular/fisiologia
Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia
Estresse Oxidativo
Spirulina/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Modelos Animais de Doenças
Masculino
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:170622
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0178916


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[PMID]:28335035
[Au] Autor:Rouzier C; Moore D; Delorme C; Lacas-Gervais S; Ait-El-Mkadem S; Fragaki K; Burté F; Serre V; Bannwarth S; Chaussenot A; Catala M; Yu-Wai-Man P; Paquis-Flucklinger V
[Ad] Endereço:Université Côte d'Azur, CHU, Inserm, CNRS, IRCAN, France.
[Ti] Título:A novel CISD2 mutation associated with a classical Wolfram syndrome phenotype alters Ca2+ homeostasis and ER-mitochondria interactions.
[So] Source:Hum Mol Genet;26(9):1599-1611, 2017 May 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Wolfram syndrome (WS) is a progressive neurodegenerative disease characterized by early-onset optic atrophy and diabetes mellitus, which can be associated with more extensive central nervous system and endocrine complications. The majority of patients harbour pathogenic WFS1 mutations, but recessive mutations in a second gene, CISD2, have been described in a small number of families with Wolfram syndrome type 2 (WFS2). The defining diagnostic criteria for WFS2 also consist of optic atrophy and diabetes mellitus, but unlike WFS1, this phenotypic subgroup has been associated with peptic ulcer disease and an increased bleeding tendency. Here, we report on a novel homozygous CISD2 mutation (c.215A > G; p.Asn72Ser) in a Moroccan patient with an overlapping phenotype suggesting that Wolfram syndrome type 1 and type 2 form a continuous clinical spectrum with genetic heterogeneity. The present study provides strong evidence that this particular CISD2 mutation disturbs cellular Ca2+ homeostasis with enhanced Ca2+ flux from the ER to mitochondria and cytosolic Ca2+ abnormalities in patient-derived fibroblasts. This Ca2+ dysregulation was associated with increased ER-mitochondria contact, a swollen ER lumen and a hyperfused mitochondrial network in the absence of overt ER stress. Although there was no marked alteration in mitochondrial bioenergetics under basal conditions, culture of patient-derived fibroblasts in glucose-free galactose medium revealed a respiratory chain defect in complexes I and II, and a trend towards decreased ATP levels. Our results provide important novel insight into the potential disease mechanisms underlying the neurodegenerative consequences of CISD2 mutations and the subsequent development of multisystemic disease.
[Mh] Termos MeSH primário: Senilidade Prematura/genética
Perda Auditiva Neurossensorial/genética
Proteínas de Membrana/genética
Doenças Mitocondriais/genética
Atrofia Óptica/genética
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Retículo Endoplasmático/genética
Retículo Endoplasmático/metabolismo
Homeostase
Seres Humanos
Masculino
Proteínas de Membrana/metabolismo
Meia-Idade
Mitocôndrias/genética
Mitocôndrias/metabolismo
Linhagem
Síndrome de Wolfram/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ERIS protein, human); 0 (Membrane Proteins); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx060


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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


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[PMID]:28011874
[Au] Autor:Chaiprasongsuk A; Lohakul J; Soontrapa K; Sampattavanich S; Akarasereenont P; Panich U
[Ad] Endereço:Department of Pharmacology (A.C., J.L., K.S., S.S., P.A. and U.P.) and Center of Applied Thai Traditional Medicine, Faculty of Medicine (P.A.), Siriraj Hospital, Mahidol University, Bangkok, Thailand.
[Ti] Título:Activation of Nrf2 Reduces UVA-Mediated MMP-1 Upregulation via MAPK/AP-1 Signaling Cascades: The Photoprotective Effects of Sulforaphane and Hispidulin.
[So] Source:J Pharmacol Exp Ther;360(3):388-398, 2017 Mar.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UVA irradiation plays a role in premature aging of the skin through triggering oxidative stress-associated stimulation of matrix metalloproteinase-1 (MMP-1) responsible for collagen degradation, a hallmark of photoaged skin. Compounds that can activate nuclear factor E2-related factor 2 (Nrf2), a transcription factor regulating antioxidant gene expression, should therefore serve as effective antiphotoaging agents. We investigated whether genetic silencing of Nrf2 could relieve UVA-mediated MMP-1 upregulation via activation of mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) signaling using human keratinocyte cell line (HaCaT). Antiphotoaging effects of hispidulin (HPD) and sulforaphane (SFN) were assessed on their abilities to activate Nrf2 in controlling MMP-1 and collagen expressions in association with phosphorylation of MAPKs (extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38), c-Jun, and c-Fos, using the skin of BALB/c mice subjected to repetitive UVA irradiation. Our findings suggested that depletion of Nrf2 promoted both mRNA expression and activity of MMP-1 in the UVA-irradiated HaCaT cells. Treatment of Nrf2 knocked-down HaCaT cells with MAPK inhibitors significantly suppressed UVA-induced MMP-1 and AP-1 activities. Moreover, pretreatment of the mouse skin with HPD and SFN, which could activate Nrf2, provided protective effects against UVA-mediated MMP-1 induction and collagen depletion in correlation with the decreased levels of phosphorylated MAPKs, c-Jun, and c-Fos in the mouse skin. In conclusion, Nrf2 could influence UVA-mediated MMP-1 upregulation through the MAPK/AP-1 signaling cascades. HPD and SFN may therefore represent promising antiphotoaging candidates.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Flavonas/farmacologia
Isotiocianatos/farmacologia
Fator 2 Relacionado a NF-E2/metabolismo
Envelhecimento da Pele
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: Senilidade Prematura/etiologia
Senilidade Prematura/metabolismo
Animais
Antimutagênicos/farmacologia
Linhagem Celular
Ativação Enzimática/efeitos da radiação
Seres Humanos
Queratinócitos
Sistema de Sinalização das MAP Quinases/efeitos da radiação
Metaloproteinase 1 da Matriz/metabolismo
Camundongos
Estresse Oxidativo
Pele/metabolismo
Envelhecimento da Pele/efeitos dos fármacos
Envelhecimento da Pele/efeitos da radiação
Fator de Transcrição AP-1/metabolismo
Regulação para Cima/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimutagenic Agents); 0 (Flavones); 0 (Isothiocyanates); 0 (NF-E2-Related Factor 2); 0 (Transcription Factor AP-1); 9007-34-5 (Collagen); EC 3.4.24.7 (Matrix Metalloproteinase 1); GA49J4310U (sulforafan); N7F61604C2 (hispidulin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161225
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.116.238048


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[PMID]:28005395
[Au] Autor:Clark NC; Pru CA; Yee SP; Lydon JP; Peluso JJ; Pru JK
[Ad] Endereço:Department of Animal Sciences, Center for Reproductive Biology, Washington State University, Pullman, Washington.
[Ti] Título:Conditional Ablation of Progesterone Receptor Membrane Component 2 Causes Female Premature Reproductive Senescence.
[So] Source:Endocrinology;158(3):640-651, 2017 03 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nonclassical progesterone receptors progesterone receptor membrane component (PGRMC) 1 and PGRMC2 have been implicated in regulating cell survival of endometrial and ovarian cells in vitro and are abundantly expressed in these cell types. The objective of this study was to determine if Pgrmc1 and Pgrmc2 are essential for normal female reproduction. To accomplish this objective, Pgrmc1 and/or Pgrmc2 floxed mice (Pgrmc2fl/fl and Pgrmc1/2fl/fl) were crossed with Pgr-cre mice, which resulted in the conditional ablation of Pgrmc1 and/or Pgrmc2 from female reproductive tissues (i.e.,Pgrmc2d/d and Pgrmc1/2d/d mice). A breeding trial revealed that conditional ablation of Pgrmc2 initially led to subfertility, with Pgrmc2d/d female mice producing 47% fewer pups/litter than Pgrmc2fl/fl mice (P = 0.001). Pgrmc2d/d mice subsequently underwent premature reproductive senescence by parities 2 to 5, producing 37.8% fewer litters overall during the trial compared with Pgrmc2fl/fl mice (P = 0.020). Similar results were observed with Pgrmc1/2d/d mice. Based on ovarian morphology and serum P4, the subfertility/infertility was not due to faulty ovulation or luteal insufficiency. Rather an analysis of midgestation implantation sites revealed that postimplantation embryonic death was the major cause of the subfertility/infertility. As with our previous report of Pgrmc1d/d mice, Pgrmc2d/d and Pgrmc1/2d/d mice developed endometrial cysts consistent with accelerated aging of this tissue. Given the timing of postimplantation embryonic demise, uterine decidualization may be disrupted in mice deficient in PGRMC2 or PGRMC1/2. Overall, this study revealed that Pgrmc1 and/or Pgrmc2 are required for the maintenance of uterine histoarchitecture and normal female reproductive lifespan.
[Mh] Termos MeSH primário: Fertilidade
Proteínas de Membrana/fisiologia
Ovário/fisiologia
Receptores de Progesterona/fisiologia
Útero/fisiologia
[Mh] Termos MeSH secundário: Senilidade Prematura/genética
Senilidade Prematura/patologia
Animais
Perda do Embrião
Feminino
Camundongos
Camundongos Transgênicos
Útero/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (PGRMC1 protein, mouse); 0 (PGRMC2 protein, mouse); 0 (Receptors, Progesterone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1701


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Fotocópia
[PMID]:27893337
[Au] Autor:Alfano CM; Peng J; Andridge RR; Lindgren ME; Povoski SP; Lipari AM; Agnese DM; Farrar WB; Yee LD; Carson WE; Kiecolt-Glaser JK
[Ad] Endereço:Catherine M. Alfano, American Cancer Society, Washington, DC; Juan Peng, Monica E. Lindgren, Stephen P. Povoski, Adele M. Lipari, Doreen M. Agnese, William B. Farrar, Lisa D. Yee, William E. Carson III, Janice K. Kiecolt-Glaser, The Ohio State University College of Medicine; Rebecca R. Andridge, The
[Ti] Título:Inflammatory Cytokines and Comorbidity Development in Breast Cancer Survivors Versus Noncancer Controls: Evidence for Accelerated Aging?
[So] Source:J Clin Oncol;35(2):149-156, 2017 Jan 10.
[Is] ISSN:1527-7755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose The sequelae of cancer treatment may increase systemic inflammation and create a phenotype at increased risk of functional decline and comorbidities, leading to premature mortality. Little is known about how this trajectory compares with natural aging among peers of the same age without cancer. This longitudinal study investigated proinflammatory cytokines and comorbidity development over time among breast cancer survivors and a noncancer control group. Methods Women (N = 315; 209 with breast cancer and 106 in the control group) were recruited at the time of their work-up for breast cancer; they completed the baseline questionnaire, interview, and blood draw (lipopolysaccharide-stimulated production of interleukin [IL] -6, tumor necrosis factor-α, and IL-1ß). Measures were repeated 6 and 18 months after primary cancer treatment (cancer survivors) or within a comparable time frame (control group). Results There were no baseline differences in comorbidities or cytokines between survivors and the control group. Over time, breast cancer survivors had significantly higher tumor necrosis factor-α and IL-6 compared with the control group. Survivors treated with surgery, radiation, and chemotherapy accumulated a significantly greater burden of comorbid conditions and suffered greater pain associated with inflammation over time after cancer treatment than did the control group. Conclusion Survivors who had multimodal treatment had higher cytokines and comorbidities, suggestive of accelerated aging. Comorbidities were related to inflammation in this sample, which could increase the likelihood of premature mortality. Given that many comorbidities take years to develop, future research with extended follow-up beyond 18 months is necessary to examine the evidence of accelerated aging in cancer survivors and to determine the responsible mechanisms.
[Mh] Termos MeSH primário: Senilidade Prematura/etiologia
Neoplasias da Mama/terapia
[Mh] Termos MeSH secundário: Neoplasias da Mama/sangue
Neoplasias da Mama/complicações
Neoplasias da Mama/mortalidade
Terapia Combinada
Comorbidade
Citocinese/fisiologia
Feminino
Seres Humanos
Interleucina-1beta/sangue
Interleucina-6/sangue
Estudos Longitudinais
Meia-Idade
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL6 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170910
[Lr] Data última revisão:
170910
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE



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