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Abstract

Rat testicular N-cadherin: Its complementary deoxyribonucleic acid cloning and regulation 
Chung,Sanny S.W.; Mo,Meng-Yun; Silvestrini,Bruno; Lee,William M.; Cheng,Chuen-yan
Endocrinology 139(4): 1853-1862
Publication date: 1998



Using primer sets specific for mouse N-cadherin and rat testicularRNA for RT-PCR, a full-length complementary DNA (cDNA) codingfor rat testicular N-cadherin was isolated. The deduced amino acidsequence of rat N-cadherin yielded a 883-amino acid polypeptide thatdisplayed a 98.6% identity with the mouse homolog. N-Cadherinwas found to be expressed by Sertoli and germ cells in the rattestis by RT-PCR. Using Sertoli-germ cell cocultures, it wasfound that the N-cadherin expression increased with time inculture. To assess whether this is due to a soluble factor(s)released from germ cells that affects Sertoli cell N-cadherinexpression, germ cell-conditioned media (GCCM) were fractionatedby preparative anion-exchange HPLC, and the resulting fractionswere divided into 14 pools. Pool 4 was found to contain a factor(s)that induced a dose-dependent stimulation on Sertoli cell N-cadherin expression with a maximal stimulation at 2 µgprotein/dish/4.5 x 10 Sertoli cells. At higher doses between12 and 32 µg protein/dish, this pool relinquished its effecton Sertoli cell N-cadherin expression suggestive of a biphasic effect.This biphasic effect was confirmed using increasing doses of crudeGCCM on Sertoli cell cultures. Since nonviable germ cells failed tostimulate Sertoli cell N-cadherin expression, it illustratesthe observed stimulatory effect by GCCM is likely to be mediatedvia a soluble factor(s) releasing from viable germ cells. Theseresults reveal the presence of a stimulatory factor(s) in GCCMthat can modulate Sertoli cell N-cadherin expression in vitro. SinceN-cadherin plays a crucial role in facilitating invasive capacity ofmetastatic tumor cells, the observation of germ cell-released factor(s)in affecting Sertoli cell N-cadherin expression may suggest itspossible role in facilitating germ cell migration during spermatogenesis.