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.

Male germ cell-specific knockout of cholesterogenic cytochrome P450 lanosterol 14α-demethylase (Cyp51)

“…Because the cholesterol required to support spermatogenesis exceeds the biosynthetic capacity in Sertoli cells, cholesterol could be imported from circulation via specialized cholesterol transporters ( 28 ). Sertoli cells mainly depend on cholesterol acquired from HDLs by the apoE-dependent pathway ( 29,30 ). The other important source of cholesterol might be the recycling of lipid-rich residual bodies and apoptotic germ cells, constantly phagocytized by Sertoli cells ( 31 ).…”

The ATP-binding cassette transporter 1 mediates lipid efflux from Sertoli cells and influences male fertility

“…Although apoA1 is not synthesized within the testis, HDL penetrates the testicular lamina propria and serves as the primary source of cholesterol for Sertoli cells (50). Uptake of cholesterol by cultured Sertoli cells is facilitated by the presence of apoA1 and apoE, and Sertoli cells express both scavenger receptor class B type I (SR-BI) and LDL receptor-related protein receptors (32,(51)(52)(53).…”

Germ cells and fatty acids induce translocation of CD36 scavenger receptor to the plasma membrane of Sertoli cells

“…Lipid metabolism is essential for hormonal regulation as well as structural differentiation leading to the production of spermatozoa. It has been shown in Leydig and Sertoli cells that hypercholesterolemia can have a detrimental effect on the secretary functions and the overall sperm fertilizing capacity (Fofana et al, 2000). In apoE-deficient mice submitted to chow diet, CD36 mRNAs levels are upregulated by at least 100%.…”