Evaluation of cholesteryl ester transfer in the seminiferous tubule cells of immature rats in vivo and in vitro

Abstract

Sertoli cells and germ cells are separated from the interstitial blood capillaries by an extracellular matrix and the peritubular cells, which constitute a barrier to the movement of plasma lipoproteins. The present study was undertaken to evaluate in vivo and in vitro the high density lipoprotein (HDL) cholesteryl ester transfer from plasma to seminiferous tubule cells in the testis of 30-day-old rats. Firstly, the transfer of HDL cholesteryl oleate from plasma to testicular compartments was evaluated and, secondly, the role of apolipoproteins A-I and E in the uptake of cholesteryl ester by Sertoli cells was investigated. At 2 h after the administration of HDL reconstituted with [3H]cholesteryl ester, dimyristoyl phosphatidylcholine and apolipoproteins, the tissue space in the interstitial cells (740 +/- 60 microliters g-1 cell protein) was fourfold higher than that in the seminiferous tubule cells (170 +/- 10 microliters g-1). Sertoli cells were isolated and incubated with [3H]cholesteryl ester HDL reconstituted with apolipoprotein A-I or E to evaluate the mechanisms of cholesteryl ester influx. At the same apolipoprotein concentration (50 micrograms apolipoprotein ml-1 medium), the uptake of [3H]cholesteryl oleate from phospholipid-apolipoprotein E vesicles was twofold higher than that with phospholipid-apolipoprotein A-I vesicles. The presence of heparin reduced the uptake of cholesteryl ester from apolipoprotein E vesicles but not with apolipoprotein A-I vesicles, indicating that uptake of apolipoprotein A-I vesicles via a secretion of apolipoprotein E by the cells themselves was not involved. These results demonstrate that plasma lipoprotein cholesterol is able to cross the testis lamina propria and that Sertoli cells take up cholesteryl ester for seminiferous tubule cell metabolism mainly via an apolipoprotein E pathway.

Cholesterol metabolism and Cx43, Cx46, and Cx50 gap junction protein expression and localization in normal and diabetic and obeseob/obanddb/dbmouse testes

“…Cholesterol substrate requirements exceed the capacity of the Sertoli cell, requiring part of cholesterol to be imported from the blood circulation into tubules through HDL (28) with participation of the multiligand transporter (5,75). The basement membrane allows entry of cholesterol ester-rich HDL (27) into seminiferous tubules, where it is a major source of cholesterol (28), but not cholesterol ester-rich LDL. In addi-tion, cholesterol originates from by-products of the phagocytosis of lipid-containing residual bodies, lipid-rich cell membranes, and apoptotic germ cell remnants (36,71,74).…”

Mevalonate pathway and male reproductive aging

“…During different stages of spermatogenesis, a Sertoli cell interacts with approximately 30–50 germ cells, and signaling between them is necessary to regulate spermatogenesis (Weber et al, 1983; Wong & Russell, 1983). During spermatogenesis, the cholesterol required for the synthesis of new plasma membranes is synthesized in spermatocytes, while Sertoli cells synthesize a small amount of cholesterol through acetate and can also import cholesterol from external high‐density lipoprotein through transporters (Akpovi et al, 2006; Fofana et al, 2000).…”

Dysregulation of Testicular Cholesterol Metabolism Following Spontaneous Mutation of the Niemann-Pick C1 Gene in Mice1

“…Unlike SR-BI, SR-BII carries an endocytic motif in the carboxyl terminus that mediates rapid clathrin-dependent endocytosis and targets the receptor to the endosome compartment [31]. Since Npc1 protein is an endosome/lysosome resident, both proteins may act to mobilize cholesterol from circulating lipoproteins [2]. We localized Npc1 to small dots in Sertoli cell cytoplasm.…”

“…Cultured seminiferous tubules from immature rats are believed to import HDL cholesterol but not LDL cholesterol [35] as the major source of cholesterol for Sertoli cells in vivo [2]. Cholesterol is, in part, imported by Sertoli cells from the blood [35].…”

“…Sertoli cells and germ cells synthesize cholesterol de novo from acetate [1], but whether this synthesis is sufficient to meet cellular requirements is unknown. It is generally accepted that cholesterol must be imported in part from circulating lipoproteins [2] via cholesterol transporters [3]. In addition, cholesterol contained in residual bodies [4] or in apoptotic germ cell membranes engulfed by Sertoli cells is partly recovered in the endosome/lysosome compartment.…”