ArticleReproduction (Cambridge, England)2017
Hormone-sensitive lipase deficiency alters gene expression and cholesterol content of mouse testis.
Article in Reproduction (Cambridge, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Cloning and Molecular Characterization of HSL and Its Expression Pattern in HPG Axis and Testis during Different Stages in Bactrian Camel.Current issues in molecular biology · 2022Article
- Relationship between semen quality and seminal plasma cholesterol, triacylglycerols and proteins in the domestic cat.Journal of feline medicine and surgery · 2020Article
- Regulation of [CaReproductive biology and endocrinology : RB&E · 2020Article
- Genome Wide Analysis for Growth at Two Growth Stages in A New Fast-Growing Common Carp Strain (Cyprinus carpio L.).Scientific reports · 2020Article
- Lipid droplets in granulosa cells are correlated with reduced pregnancy rates.Journal of ovarian research · 2020Observational
- Mitochondrial CaFrontiers in cell and developmental biology · 2020Article
- Article
- Cholesterol: A Gatekeeper of Male Fertility?Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hormone-sensitive lipase-knockout (HSL-/-) mice exhibit azoospermia for unclear reasons. To explore the basis of sterility, we performed the following three experiments. First, HSL protein distribution in the testis was determined. Next, transcriptome analyses were performed on the testes of three experimental groups. Finally, the fatty acid and cholesterol levels in the testes with three different genotypes studied were determined. We found that the HSL protein was present from spermatocyte cells to mature sperm acrosomes in wild-type (HSL+/+) testes. Spermiogenesis ceased at the elongation phase of HSL-/- testes. Transcriptome analysis indicated that genes involved in lipid metabolism, cell membrane, reproduction and inflammation-related processes were disordered in HSL-/- testes. The cholesterol content was significantly higher in HSL-/- than that in HSL+/+ testis. Therefore, gene expression and cholesterol ester content differed in HSL-/- testes compared to other testes, which may explain the sterility of male HSL-/- mice.
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