Abstract
There is a tight relationship between fertility and changes in cholesterol metabolism during spermatogenesis. In the testis, class B scavenger receptors (SR-B) SR-BI, SR-BII, and LIMP II mediate the selective uptake of cholesterol esters from HDL, which are hydrolyzed to unesterified cholesterol by hormone-sensitive lipase (HSL). HSL is critical because HSL knockout (KO) male mice are sterile. The aim of the present work was to determine the effects of the lack of HSL in testis on the expression of SR-B, lipid raft composition, and related cell signaling pathways. HSL-KO mouse testis presented altered spermatogenesis associated with decreased sperm counts, sperm motility, and infertility. In wild-type (WT) testis, HSL is expressed in elongated spermatids; SR-BI, in Leydig cells and spermatids; SR-BII, in spermatocytes and spermatids but not in Leydig cells; and LIMP II, in Sertoli and Leydig cells. HSL knockout male mice have increased expression of class B scavenger receptors, disrupted caveolin-1 localization in lipid raft plasma membrane microdomains, and activated phospho-ERK, phospho-AKT, and phospho-SRC in the testis, suggesting that class B scavenger receptors are involved in cholesterol ester uptake for steroidogenesis and spermatogenesis in the testis.
Highlights
There is a tight relationship between fertility and changes in cholesterol metabolism during spermatogenesis
We observed that body weight was significantly reduced (27%) in adult HSLϪ/Ϫ mice compared with hormone-sensitive lipase (HSL)+/+ mice (Fig. 1A)
Plasma total cholesterol levels were significantly higher in HSLϪ/Ϫ mice than in controls, whereas the triglyceride concentration did not differ between groups (Fig. 1C)
Summary
There is a tight relationship between fertility and changes in cholesterol metabolism during spermatogenesis. The aim of the present work was to determine the effects of the lack of HSL in testis on the expression of SR-B, lipid raft composition, and related cell signaling pathways. HSL-KO mouse testis presented altered spermatogenesis associated with decreased sperm counts, sperm motility, and infertility. HSL knockout male mice have increased expression of class B scavenger receptors, disrupted caveolin-1 localization in lipid raft plasma membrane microdomains, and activated phosphoERK, phospho-AKT, and phospho-SRC in the testis, suggesting that class B scavenger receptors are involved in cholesterol ester uptake for steroidogenesis and spermatogenesis in the testis.—Casado, M. HSL-knockout mouse testis exhibits class B scavenger receptor upregulation and disrupted lipid raft microdomains. This article is available online at http://www.jlr.org intermediates in the cholesterol biosynthesis pathway, such as follicular fluid meiosis activating sterol (FF-MAS) and testicular meiosis activating sterol (T-MAS), are biologically active as stimulators of meiosis in the gonads [10]
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