MiR-144-3p targets STC1 to activate PI3K/AKT pathway to induce cell apoptosis and cell cycle arrest in selenium deficiency broilers.

Selenium (Se) is an indispensable trace element in vertebrate. Se deficiency can damage the immune system. Studies have shown that Se deficiency can cause immune organ damage by regulating the expression of microRNA. Bursa of Fabricius is a special immune organ in poultry. In order to explore the mechanism of bursa of Fabricius injury caused by Se deficiency and the role of miRNA in this process. Firstly, we established the Se deficient model of broilers in vivo and found that Se deficiency could induce apoptosis and cell cycle arrest of bursa of Fabricius cells through Phosphoinositide 3-kinase (PI3K)/Protein Kinase B (AKT) pathway. Secondly, we inferred miRNA (miR-144-3p) and target gene Stanniocalcin 1 (STC1) that may regulate PI3K/AKT pathway through biological analysis system, and further predicted and determined the targeting relationship between them through dual luciferase, it was found that miR-144-3p was highly expressed in the process of cell apoptosis and cell cycle arrest induced by Se deficiency. Finally, in order to further understand whether miR-144-3p/STC1 axis is involved in the process, miR-144-3p knockdown and overexpression experiments were carried out, it was found that miR-144-3p inhibitor can reduce the occurrence of cell apoptosis and cell cycle arrest. In conclusion, Se deficiency can induce apoptosis and cell cycle arrest of bursa of Fabricius in Broilers by up regulating miR-144-3p targeting STC1 and activating PI3K/AKT pathway, leading to injury of bursa of Fabricius in broilers.

Selenium-deficient diet induces inflammatory response in the pig adrenal glands by activating TLR4/NF-κB pathway via miR-30d-R_1.

Selenium (Se) is an important trace element to maintain the body's dynamic balance. Lack of Se can cause inflammation. Studies have shown that inflammation often leads to disorders of the hypothalamic-pituitary-adrenal axis, but the mechanism by which Se deficiency causes inflammation of the porcine adrenal glands is still unclear. In order to study the effect of Se deficiency on the adrenal glands of pigs, we obtained Se-deficient pig adrenal glands through a low-Se diet. The results of mass spectrometry showed that the Se content in the Se-deficient group was only one-tenth of the control group. We detected the expression of the toll-like receptor 4 (TLR4) and downstream factors by qRT-PCR and Western blotting, and found that the lack of Se affected the TLR4/NF-κB pathway. It is known that miR-155-3p, miR-30d-R_1, and miR-146b have all been verified for targeting relationship with TLR4. We confirmed by qRT-PCR that miR-30d-R_1 decreased most significantly in the Se-deficient pig model. Then we tested 25 selenoproteins and some indicators of oxidative stress. It is confirmed that Se deficiency reduces the antioxidant capacity and induces oxidative stress in pig adrenal tissue. In short, a diet lacking Se induces oxidative stress in pig adrenal tissues and leads to inflammation through the miR-30d-R_1/TLR4 pathway. This study provides a reference for the prevention of adrenal inflammation in pigs from a nutritional point of view.