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1.
J Hazard Mater ; 467: 133717, 2024 Apr 05.
Artigo em Inglês | MEDLINE | ID: mdl-38325100

RESUMO

Nitrogen (N2)-fixing legumes can be used for phytoremediation of toxic heavy metal Mercury (Hg) contaminated soil, but N2-fixation highly relies on phosphorus (P) availability for nodule formation and functioning. Here, we characterized the significance of P deficiency for Hg accumulation and toxicity in woody legume plants. Consequences for foliar and root traits of rhizobia inoculation, Hg exposure (+Hg) and low P (-P) supply, individually and in combination were characterized at both the metabolite and transcriptome levels in seedlings of two Robinia pseudoacacia L. provenances originating from contrasting climate and soil backgrounds, i.e., GS in northwest and the DB in northeast China. Our results reveal that depleted P mitigates the toxicity of Hg at the transcriptional level. In leaves of Robinia depleted P reduced oxidative stress and improved the utilization strategy of C, N and P nutrition; in roots depleted P regulated the expression of genes scavenging oxidative stress and promoting cell membrane synthesis. Rhizobia inoculation significantly improved the performance of both Robinia provenances under individual and combined +Hg and -P by promoting photosynthesis, increasing foliar N and P content and reducing H2O2 and MDA accumulation despite enhanced Hg uptake. DB plants developed more nodules, had higher biomass and accumulated higher Hg amounts than GS plants and thus are suggested as the high potential Robinia provenance for future phytoremediation of Hg contaminated soils with P deficiency.


Assuntos
Fabaceae , Mercúrio , Robinia , Peróxido de Hidrogênio , Mercúrio/toxicidade , Solo , Nitrogênio/química
2.
J Reprod Dev ; 69(2): 125-128, 2023 Apr 03.
Artigo em Inglês | MEDLINE | ID: mdl-36724993

RESUMO

Japanese native horses, which consists of 8 breeds, are threatened with extinction. Embryo transfer (ET) is used to reproduce endangered animals in various mammalian species. We aimed to perform ET using native ponies from Kiso and Hokkaido as donors and recipients, respectively. ET operation included long-distance transport of non-cryopreserved embryos from Nagano Prefecture to Hokkaido. Embryos were transported 1500 km over 9 h in a container maintained at 22°C. After transferring two embryos to two recipients, one mare delivered a healthy live foal. These results demonstrated that reciprocal ET with long-distance transportation of fresh embryos between the isolated breeds may allow for the proliferation of Japanese native horses.


Assuntos
Transferência Embrionária , Mamíferos , Animais , Cavalos , Feminino , Transferência Embrionária/veterinária
3.
PLoS One ; 9(6): e100298, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24941323

RESUMO

BACKGROUND: MicroRNAs (miRNAs) regulate a lot of physiological and pathological processes, including myocardial ischemia/reperfusion. Recent studies reported that knockdown of miR-92a could attenuate ischemia/reperfusion-induced myocardial injury. In the present study, we examined the potential anti-apoptotic effects of miR-92a in a rat myocardiocyte cell line, and the possible role of Smad7 in such actions. METHODOLOGY AND RESULTS: In a preliminary bioinformatic analysis, we identified SMAD family member 7 (Smad7) as a potential target for miR-92a. A luciferase reporter assay indeed demonstrated that miR-92a could inhibit Smad7 expression. Myocardial ischemia/reperfusion was simulated in rat H9c2 cells with 24-h hypoxia followed by 12-h reoxygenation. Prior to hypoxia/reoxygenation, cells were transfected by miR-92a inhibitor. In some experiments, cells were co-transfected with siRNA-Smad7. The miR-92a inhibitor dramatically reduced the release of lactate dehydrogenase and malonaldehyde, and attenuated cardiomyocyte apoptosis. The miR-92a inhibitor increased SMAD7 protein level and decreased nuclear NF-κB p65 protein. Effects of the miR-92a inhibitor were attenuated by co-transfection with siRNA-Smad7. CONCLUSION: Inhibiting miR-92a can attenuate myocardiocyte apoptosis induced by hypoxia/reoxygenation by targeting Smad7.


Assuntos
MicroRNAs/genética , Miócitos Cardíacos/metabolismo , Proteína Smad7/genética , Fator de Transcrição RelA/genética , Animais , Apoptose/efeitos dos fármacos , Hipóxia Celular , Linhagem Celular , Regulação da Expressão Gênica , L-Lactato Desidrogenase/metabolismo , Malondialdeído/metabolismo , MicroRNAs/antagonistas & inibidores , MicroRNAs/metabolismo , Modelos Biológicos , Mimetismo Molecular , Traumatismo por Reperfusão Miocárdica/genética , Traumatismo por Reperfusão Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/patologia , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/patologia , Oligonucleotídeos/farmacologia , Oxigênio/farmacologia , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Ratos , Transdução de Sinais , Proteína Smad7/antagonistas & inibidores , Proteína Smad7/metabolismo , Fator de Transcrição RelA/antagonistas & inibidores , Fator de Transcrição RelA/metabolismo
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