scholarly journals MicroRNA-126 regulates the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT) pathway in SLK cells in vitro and the expression of its pathway members in Kaposiʼs sarcoma tissue

Medicine ◽  
2018 ◽  
Vol 97 (35) ◽  
pp. e11855 ◽  
Author(s):  
Gaihui Lu ◽  
Xiujuan Wu ◽  
Zongfeng Zhao ◽  
Yuan Ding ◽  
Peng Wang ◽  
...  
2008 ◽  
Vol 326 (1) ◽  
pp. 348-353 ◽  
Author(s):  
Linda B. Kidd ◽  
Gernot A. Schabbauer ◽  
James P. Luyendyk ◽  
Todd D. Holscher ◽  
Rachel E. Tilley ◽  
...  

Zygote ◽  
2021 ◽  
pp. 1-7
Author(s):  
T.J.S. Macedo ◽  
V.G. Menezes ◽  
R.S. Barberino ◽  
R.L.S. Silva ◽  
B.B. Gouveia ◽  
...  

Summary This study evaluated the effects of leptin on primordial follicle survival and activation after in vitro culture of ovine ovarian tissue and if leptin acts through the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) pathway. Ovarian fragments were fixed for histology (fresh control) or cultured for 7 days in control medium (α-MEM+) alone or supplemented with leptin (1, 5, 10, 25 or 50 ng/ml). Follicle morphology, activation and apoptosis were analyzed. Next, the fragments were cultured in the medium that showed the best results in the absence or the presence of the PI3K inhibitor (LY294002), and immunohistostaining of p-Akt protein was assessed. After culture, the percentage of normal follicles decreased (P < 0.05) in all treatments compared with the fresh control. Moreover, control medium and 1 ng/ml leptin had similar (P > 0.05) percentages of normal follicles, which were significantly higher than those in other treatments. However, culture with 1 ng/ml leptin maintained apoptosis similarly (P > 0.05) to that of the fresh control and lower (P < 0.05) than that in α-MEM+. Leptin did not influence follicle activation (P > 0.05) compared with the control medium (α-MEM+). Culture in 1 ng/ml leptin with LY294002 decreased the normal follicles and increased apoptosis, inhibited follicle activation (P < 0.05), and reduced p-Akt immunostaining, compared with the medium containing 1 ng/ml leptin without PI3K inhibitor. In conclusion, leptin at 1 ng/ml reduces apoptosis and promotes the activation of primordial follicles compared with the fresh control after in vitro culture of ovine ovarian tissue possibly through the PI3K/Akt pathway.


2018 ◽  
Vol 30 (11) ◽  
pp. 1503 ◽  
Author(s):  
Maria É. S. Bezerra ◽  
Ricássio S. Barberino ◽  
Vanúzia G. Menezes ◽  
Bruna B. Gouveia ◽  
Taís J. S. Macedo ◽  
...  

We investigated the effects of insulin-like growth factor 1 (IGF-1) on the morphology and follicular activation of ovine preantral follicles cultured in situ and whether the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway is involved in IGF-1 action in the sheep ovary. Ovine ovarian fragments were fixed for histological and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) analyses (fresh control) or cultured in supplemented alpha-minimum essential medium (α-MEM+; control) or α-MEM+ with IGF-1 (1, 10, 50, 100 or 200 ng mL−1) for 7 days. Follicles were classified as normal or atretic, primordial or growing and the oocyte and follicle diameters were measured. DNA fragmentation was evaluated by TUNEL assay. Proliferating cell nuclear antigen (PCNA) immunohistochemistry was performed on the fresh control, α-MEM+ and 100 ng mL−1 IGF-1 samples. Inhibition of PI3K activity was performed through pretreatment with the PI3K inhibitor LY294002 and phosphorylated AKT (pAKT) expression was analysed after culture in the absence or presence of LY294002. IGF-1 at 100 ng mL−1 increased (P < 0.05) follicular activation compared with α-MEM+ and decreased TUNEL-positive cells (P < 0.05) compared with other treatments. PCNA-positive cells also increased (P < 0.05) in 100 ng mL−1 IGF-1. LY294002 significantly inhibited follicular activation stimulated by α-MEM+ and 100 ng mL−1 IGF-1 and reduced pAKT expression in follicles. Overall, IGF-1 at 100 ng mL−1 promoted primordial follicle activation, cell proliferation and reduced DNA fragmentation after in situ culture through the PI3K/AKT pathway.


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