小鼠β-1,4-N-acetyl-galactosaminyl transferase 2於賽特利細胞之生理功能探討

Abstract

Sda β-1,4-N-acetyl-galactosaminyl transferaseⅡis a kind of carbohydrate transferases, whose main function is to catalyze and transfer GalNAc to Gal of [Neu5Acα2-3]Galβ1-4GlcNAcβ1-3Gal through β-1,4 bond, so that carbohydrate is linked to form the Sda structure. The structure was earliest found in the antigen structure on the blood corpuscle surface; in fact, however, it is widely distributed in the tissues and body fluids of the mammals, including stomach, intestine, kidney, serum, urine, and milk. Recent studies showed that the B4GALNT2 expression was obviously reduced in the gastric cancer and colon cancer cells of human being, causing decrease in the Sda antigen, and the said reduction was closely correlated with the metastasis of the cancer cells; this indicated the importance of B4GALNT2 and its correlation with the bio-system. However, very few studies have been conducted on its physiological functions. In 2003, the research team led by Dell first found the Sda structure in the female reproductive system. Before the physiological functions of the Sda structure was learned about, its invertase B4galnt2 needed to be studied. The research showed that B4galnt2 was correlated with the mouse’s embryo implantation and the maturation of its oocytes. It was presumed that the Sda structure played an important role in the female reproductive system. Therefore, to infer the role of the Sda structure, the regulation and control by the Sda invertase should be learned. The laboratory has found B4galnt2 in the cell strains (TM4) of the Sertoli cells, so it was supposed that B4galnt2 might play a certain role in the male reproductive system, but its functions in the male reproductive system remained unknown yet. In the experiment, a male mouse was taken as the subject. The Quantitative Real-Time PCR and immune fluorescent staining method were used to confirm the existence of B4galnt2 on the cell membranes of the primary Sertoli cells and Sertoli cell strains. The observation indicated that whether the proliferation of the Sertoli cells was declined or enhanced after the cell strains were treated with follicle stimulating hormone, the B4galnt2 gene expression showed no marked difference. In this way, it was presumed that B4galnt2 did not participate in the proliferation of the Sertoli cells. By using hormone to treat the Sertoli cell strains, the Sertoli cells might be induced into the state of maturity. The maturity of the Sertoli cells could be confirmed by the mature marker genes and post-maturation physiological features. In the process of maturation, the B4galnt2 gene expression was increased. The RNAi suppress gene expression experiment showed that when the B4galnt2 expression was reduced, the maturation marker gene expression decreased accordingly. This showed that the Sertoli cells could not enter the state of maturity. To sum up, it was presumed that B4galnt2 participated in the maturation of the Sertoli cells. In addition, the experiment on the primary Sertoli cells showed that the B4galnt2 expression in the mouse coming close to the puberty was higher than that when it was born. When the immature primary Sertoli cells were induced to be mature, the B4galnt2 gene expression in them was raised. Thus, it was presumed that B4galnt2 might participate in the maturation of the Sertoli cells in the mouse.