Effect Of Mouse Leydig Cell Apoptosis Induced By Endoplasmic Reticulum Stress

Leydig cells are the main source of male animals to secrete testosterone. The testosteronelevel in the body is closely related to proliferation and apoptosis of leydig cells. It is veryimportant to take a full understanding of the sperm production and male sterility by makingthe molecular mechanisms of proliferation and apoptosis in the leydig cells clear.Endoplasmic reticulum, one of the major organelles of eukaryotic cells,is a important place ofprotein folding and modificating. The homeostasis of endoplasmic reticulum can be brokenand endoplasmic reticulum stress will caused by many physiological and pathological factors.The recent studies have shown that endoplasmic reticulum stress signaling pathways involvedin death process of some kinds of cells. This experiment is determined to make it clear thatwether endoplasmic reticulum stress is involved in apoptosis and signaling pathways in leydigcells or not. The results can lay the foundation to further reveal the regulation mechanism byendoplasmic reticulum stress to apoptosis in the leydig cells.Using collagenase to isolate andculture mouse leydig cells. Adding the inducer agents of specific endoplasmic reticulumstress--thapsigargin(Tg),tunicamycin(Tm) and FCM to detect cell apoptosis rate. The mRNAlevels of GRP78, CHOP and Caspase-12will be detected by Real-Time PCR.Usingcollagenase to isolate and culture in vitro mouse leydig cells, Tm and Tg can significantlyinduce apoptosis in mouse Leydig cells of the testes in a dose and time dependent. The mRNAexpression level of GRP78increased significantly at24h in the culture, while48h showed adownward trend. The level of the expression of mRNA of CHOP and Caspase-12increasesignificantly with the increasing apoptosis rate.We have got mouse leydig cells in a highpurity by the collagenase method. Endoplasmic reticulum stress involved in apoptosis ofmouse leydig cells of the testis through CHOP and Caspase-12signaling pathway.