Key result
CBS-derived H2S restores testosterone synthesis by inhibiting PDE and activating cAMP/PKA signaling.
Why the study?
Testosterone deficiency increases mortality in men, and the regulatory role of H2S in testosterone synthesis and related signaling pathways was unclear.
Does H2S catalyzed by CBS regulate testosterone synthesis in vitro and in vivo?
Does H2S catalyzed by CBS regulate testosterone synthesis in vitro and in vivo?
H2S catalyzed by CBS recovers testosterone synthesis by inhibiting PDE expression via sulfhydryl modification and activating the cAMP/PKA pathway.
Testosterone deficiency resulted in increased mortality in men. Our previous work found that hydrogen sulphide (H2S) significantly alleviated the spermatogenesis disorder. To investigate whether H2S could regulate testosterone synthesis and the relative signalling pathways. Disorder model of testosterone synthesis was constructed in vitro and in vivo. The cell viability was detected using CCK‐8 method. The concentration of H2S and testosterone were examined using ELISA kits. The relative mRNA and protein expression of CBS, PDE4A, PDE8A and proteins related to testosterone synthesis were detected by RT‐qPCR and western blotting. PAS staining was used to detect the inflammatory status of testis. The sulfhydryl level of PDE4A and PDE8A was determined by Biotin Switch Technique. CBS overexpression inhibited while knockdown promoted LPS + H2O2 induced injury in testosterone synthesis of MLTC‐1 cells, though regulating the level of H2S. The LPS + H2O2 induced inhibition on cAMP and p‐PKA was recovered by CBS overexpression, while addition of the specific inhibitor of PKA had opposite effects. CBS overexpression alleviated the inflammation status in testis and promoted the expression of StAR, P450scc, P450c17 and 3β‐HSD. CBS could also exhibit its protective role through promoting sulfhydrylation of PDE4A and PDE8A. H2S catalysed by CBS could recover testosterone synthesis in vitro and in vivo through inhibiting PDE expression via sulfhydryl modification and activating cAMP/PKA pathway.
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Wang et al. (2021) studied Testosterone deficiency. H2S catalysed by CBS vs. LPS + H2O2 induced injury / CBS knockdown was evaluated on Testosterone synthesis and relative signalling pathways. H2S catalysed by CBS recovered testosterone synthesis in vitro and in vivo by inhibiting PDE expression via sulfhydryl modification and activating the cAMP/PKA pathway.
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