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1.
Genet Mol Res ; 15(4)2016 Dec 19.
Artículo en Inglés | MEDLINE | ID: mdl-28002580

RESUMEN

In this study, we compared the functional properties of endothelial progenitor cells (EPCs) derived from halfpipe-snowboarding athletes who train under hyperoxic conditions with those derived from normal subjects who lived under normoxic conditions. Peripheral blood-derived EPCs were isolated from both halfpipe-snowboarding athletes and normal humans. Cellular growth dynamics, lipoprotein transport, and gene expression of cultured EPCs were compared between the two groups of cells. Results indicate that cytoactivity of EPCs from athletes was higher than that of EPCs from control subjects. This study suggests that function of EPCs from snowboarding athletes may be better than that of EPCs from normal humans, which demonstrates the benefits of training under hyperoxic conditions.


Asunto(s)
Células Progenitoras Endoteliales/citología , Ejercicio Físico , Expresión Génica , Lipoproteínas/metabolismo , Atletas , Hipoxia de la Célula , Proliferación Celular , Células Cultivadas , Células Progenitoras Endoteliales/metabolismo , Humanos , Esquí
2.
Genet Mol Res ; 14(4): 12921-30, 2015 Oct 21.
Artículo en Inglés | MEDLINE | ID: mdl-26505445

RESUMEN

The genes of top athletes are a valuable genetic resource for the human race, and could be exploited to identify novel genes related to sports ability, as well as other functions. We analyzed the expressed sequence tags from top half-pipe snowboarding athletes using the SMART complementary DNA (cDNA) library construction method to elucidate the characteristics of the athlete genome and the differential expression of the genes it contains. Overall, we established a full-length cDNA library from the lymphocytes of half-pipe snowboarding athletes and analyzed the inserted gene fragments. We also classified those genes according to molecular function, biological characteristics, cellular composition, protein types, and signal paths. A total of 201 functional genes were noted, which were distributed in 27 pathways. TXN, MDH1, ARL1, ARPC3, ACTG1, and other genes measured in sequence may be associated with physical ability. This suggests that the SMART cDNA library constructed from the genetic material from top athletes is an effective tool for preserving genetic sports resources and providing genetic markers of physical ability for athlete selection.


Asunto(s)
Atletas , Etiquetas de Secuencia Expresada , Biblioteca de Genes , Genes/genética , Linfocitos , Esquí , Clonación Molecular , Humanos
3.
Genet Mol Res ; 14(4): 17692-8, 2015 Dec 22.
Artículo en Inglés | MEDLINE | ID: mdl-26782414

RESUMEN

Mutations in mitochondrial DNA have been found to be associated with hypertension. Of these, mitochondrial transfer RNA (mt-tRNA) is a hot spot for these pathogenic mutations. It is generally believed that these mutations may result in the failure of mt-tRNA metabolism, thereby worsening mitochondrial dysfunction and resulting in hypertension. mt-tRNA is known for its high frequency of polymorphisms and mutations, and the number of reports regarding mt-tRNA mutations and hypertension is increasing significantly. To better understand the molecular basis of maternally inherited hypertension, we reassessed the link between four mt-tRNA mutations (G15927A in tRNA(Thr), C7492T in tRNA(Ser(UCN)), A4386G in tRNA(Gln), and C14686T in tRNA(Glu)) and hypertension. We first used the phylogenetic approach to investigate the deleterious roles of these mutations, then we used RNA Fold Web Server to predict the minimum free energy of these mt-tRNAs with and without mutations. Using the pathogenicity scoring system, we found that the G15927A and C7492T mutations are classified as pathogenic while all other studied mutations are neutral polymorphisms. Our study provides valuable information for the detection of pathogenic mt-tRNA mutations in hypertension.


Asunto(s)
ADN Mitocondrial/genética , Hipertensión/genética , Filogenia , ARN de Transferencia/genética , Humanos , Hipertensión/patología , Mitocondrias/genética , Mutación , Polimorfismo Genético
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