Protective effect of calretinin on testicular Leydig cells via the inhibition of apoptosis.
Aging (Albany NY)
; 9(4): 1269-1279, 2017 04.
Article
em En
| MEDLINE
| ID: mdl-28437248
ABSTRACT
The core mechanism of Late-onset hypogonadism (LOH) is the deficiency of androgen due to the functional and quantitative decline of testicular Leydig cells. Here we explored the protective effect of calretinin, a Ca2+-binding protein, on Leydig cells. We found in MLTC-1 cells transfected with LV-calb2, the cell viability and optical density (OD) were higher (p<0.05), cells in the S phase of the cell cycle were increased (p<0.01) and p-ERK1/2 and p-AKT levels were significantly higher (p<0.01 and p<0.05), while in R2C cells transfected with LV-siRNA-calb2, all of the results mentioned above were adverse (p<0.05). The cell apoptotic index after calretinin over-expressed was significantly lower (p<0.001), while the expression levels of mitochondria-related apoptotic factors such as cleaved caspase-9 and cytochrome C (cyto C) were lower and ratio of Bcl2/Bax was higher (p<0.05). After calretinin down-regulated, the apoptotic index was higher (p<0.05), while the expression levels of mitochondria-related apoptotic factors were higher and the ratio of Bcl2/Bax was lower (p<0.05). Therefore, calretinin increases Leydig cell viability and proliferation, possibly via ERK1/2 and AKT pathways, and suppresses apoptosis possibly via the mitochondria-related apoptotic pathway, which could be beneficial in understanding the pathophysiology of LOH and could lead to the study of new treatments.
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Texto completo:
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Testículo
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Apoptose
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Calbindina 2
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Células Intersticiais do Testículo
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article