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1.
Clin Transl Oncol ; 23(3): 572-581, 2021 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-32705492

RESUMEN

PURPOSE: This study aimed to down-regulate LINC00667 and inhibit apoptosis and fibrosis of renal tubular epithelial cells through miR-34c. METHODS: Altogether, 98 patients with chronic kidney disease treated in our hospital were selected as the study group, and 67 normal people were selected as the control group. Epithelial cells of proximal convoluted tubules in human renal cortex were purchased. TGF-ß1 was used to induce fibrosis of HK-2 renal tubular epithelial cells. The expression of LINC00667, miR-34c, type I collagen (Col 1) and type III collagen (Col 3) were detected by qRT-PCR and WB. RESULTS: LINC00667 was highly expressed in cancer tissues and HK-2, while miR-34c was poorly expressed. Inhibition of LINC00667 and over-expression of miR-34c could inhibit the proliferation and invasion of chronic kidney disease cells, but increase the apoptosis rate. Down-regulation of LINC00667 could significantly reduce of Col 1 and Col 3 in renal interstitial fibroblasts induced by TGF-ß1, while up-regulation of miR-34c could also achieve this effect. Double luciferase report confirmed that there was a targeted regulatory relationship between LINC00667 and miR-34c. CONCLUSION: LINC00667 could reduce the proliferation and invasion of chronic kidney disease cells, increase the apoptosis rate by regulating miR-34c, and improve renal fibrosis.


Asunto(s)
Células Epiteliales/fisiología , Túbulos Renales Proximales/metabolismo , MicroARNs/metabolismo , ARN Largo no Codificante/metabolismo , Insuficiencia Renal Crónica/metabolismo , Apoptosis , Estudios de Casos y Controles , Proliferación Celular , Colágeno Tipo I/metabolismo , Colágeno Tipo III/metabolismo , Regulación hacia Abajo , Células Epiteliales/patología , Fibroblastos/metabolismo , Fibrosis , Humanos , Túbulos Renales Proximales/patología , Invasividad Neoplásica , Insuficiencia Renal Crónica/patología , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Crecimiento Transformador beta1
2.
Genet Mol Res ; 10(4): 3338-46, 2011 Oct 31.
Artículo en Inglés | MEDLINE | ID: mdl-22057994

RESUMEN

Graves' disease (GD) is an organ-specific autoimmune thyroid disease; 25-50% of GD patients will develop Graves' ophthalmopathy (GO). The etiology of GD and GO may be multifactorial, but the immune response plays a central role. Many studies have reported that IL-21 has crucial roles in autoimmune diseases. We examined whether IL-21 is associated with the development of GD and GO. The serum concentration of IL-21 was tested in 40 primary GD patients, 42 treated GO patients and 24 healthy controls. Our data show that the serum level of IL-21 is associated with the development of GD. We also made an association study with the IL-21 gene polymorphisms rs4833837, rs907715 and rs13143866 in a comparison of 633 patients and 612 healthy controls from the Chinese population. This case-control association study demonstrated that rs907715 SNP is significantly associated with GD, while the rs13143866 A allele is significantly associated with GO. The haplotypes A-G-G and A-A-A were found at higher and lower frequencies, respectively, in GD patients, suggesting a protective role for A-A-A. However, there were no significant differences in the frequencies of these haplotypes between the GO patients and the control group. We found no association between IL-21 gene polymorphisms and the age of GD onset. We conclude that IL-21 is associated with GD and GO.


Asunto(s)
Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Enfermedad de Graves/genética , Interleucinas/genética , Adolescente , Adulto , Edad de Inicio , Anciano , Anciano de 80 o más Años , Estudios de Casos y Controles , Niño , China/epidemiología , Femenino , Marcadores Genéticos , Enfermedad de Graves/epidemiología , Oftalmopatía de Graves/genética , Haplotipos/genética , Humanos , Interleucinas/sangre , Masculino , Persona de Mediana Edad , Polimorfismo de Nucleótido Simple/genética , Adulto Joven
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