The decrease of selenoprotein K induced by selenium deficiency in diet improves apoptosis and cell progression block in chicken liver via the PTEN/PI3K/AKT pathway

• Published in: Free radical biology & medicine 2022-08, Vol.189, p.20-31
• Main Authors: Zhang, Wenyue, Yin, Kai, Shi, Jiahui, Shi, Xu, Qi, Xue, Lin, Hongjin
• Format: Article
• Language: English
• Subjects: Apoptosis; Calcium homeostasis; Cell cycle; Chicken liver; ERS; SELK
• ISSN: 0891-5849; 1873-4596
• DOI: 10.1016/j.freeradbiomed.2022.07.005

Selenoprotein K (SELK) is imperative for normal development of chicken. It does regulate to chicken's physiological function. However, the injury of SELK-deficiency done on chicken liver and its underlying mechanism involved has not yet been covered. Therefore, we built SELK- deficiency model by feeding diet which contained low concentration of selenium (Se) to discuss SELK's regulation mechanism. Through using TUNEL, TEM, western blot and qRT-PCR we found apoptosis occurred in chicken liver in the SELK-deficiency groups. In the meanwhile, our study showed there were differentially expressed of the PTEN/PI3K/AKT pathway, calcium homeostasis, endoplasmic reticulum healthy and cell cycle progression in SELK-deficiency chicken liver tissues. In order to claim the regulation mechanism of SELK, we set SELK-knock down model in the LMH. The results in vitro were coincided with those in vivo. In the SELK-deficiency groups, the PTEN/PI3K/AKT pathway was activated and then induced ERS which eventually resulted in apoptosis in chicken liver. As the same time, the PTEN/PI3K/AKT pathway also regulated the combined effective of MDM2-p53, which leaned liver cells to G1/S blocking. Our findings support the potential of SELK in maintain the health of chicken liver, and indicate that adding proper amount of Se on the daily dietary may alleviate the deficiency of selenium. [Display omitted] •To elucidate the damage in chicken liver caused by Se-deficiency diet.•SELK deficiency caused liver apoptosis.•SELK deficiency influenced cell cycle progression.•SELK regulated the PTEN/PI3K/AKT pathway to influence the combination effective of MDM2-p53.