Role of TGF-β1 in Sertoli cells and tight junction / 中华男科学杂志
National Journal of Andrology
;
(12): 510-516, 2017.
Artigo
em Chinês
| WPRIM
| ID: wpr-812733
ABSTRACT
Objective@#To explore the role of TGF-β1 in the proliferation and apoptosis of Sertoli cells and its effect on the expressions of tight junction-related proteins and genes in rats.@*METHODS@#Rat Sertoli cells were isolated in vitro, primarily cultured, and divided into groups A (blank control), B (TGF-β1 receptor blocker), C (TGF-β1), and D (TGF-β1 + receptor blocker). The proliferation and apoptosis of the cells were detected by CCK-8 and flow cytometry, respectively. After establishment of the dual-chamber model for the primary culture of Sertoli cells, the trans-epithelia electrical resistance (TER) value was measured and the relative expressions of Occludin, ZO-1 and Claudin Ⅱ determined by RT-PCR and Western blot.@*RESULTS@#The OD value of the proliferation of the Sertoli cells was markedly higher in group C than in groups A and D (0.79 ± 0.04 vs 0.66 ± 0.05 and 0.68 ± 0.02, P0.05). The TER value was dramatically decreased in group C as compared with groups A and D ([176.37 ± 16.61] vs [281.42 ± 9.83] and [254.37 ± 13.55] /cm2, P0.05) or their protein expressions (F = 0.28 and 1.31, P>0.05). Both the mRNA and protein expressions of Occludin were markedly lower in group C than in A and D (P<0.01 and P<0.05), with statistically significant differences among the four groups (F = 6.86 and 6.87, P<0.01).@*CONCLUSIONS@#TGF-β1 can promote the proliferation of Sertoli cells in rats and act on the tight junction of the cells by regulating the expression of Occludin.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fisiologia
/
Células de Sertoli
/
RNA Mensageiro
/
Células Cultivadas
/
Apoptose
/
Junções Íntimas
/
Biologia Celular
/
Proliferação de Células
/
Fator de Crescimento Transformador beta1
/
Ocludina
Tipo de estudo:
Estudo prognóstico
Limite:
Animais
Idioma:
Chinês
Revista:
National Journal of Andrology
Ano de publicação:
2017
Tipo de documento:
Artigo
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