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Real-Time Imaging of Acrosomal Calcium Dynamics and Exocytosis in Live Mouse Sperm
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Published on: October 13, 2023

Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca2+-ATPase

Shing-Hwa Lu1, Yuan-Kuei Yen, Thai-Yen Ling

  • 1Department of Urology, National Yang-Ming University School of Medicine, Taipei City Hospital, Taipei, Taiwan.

Journal of Cellular Biochemistry
|August 19, 2010
PubMed
Summary

Mouse seminal vesicle autoantigen (SVA) prevents premature sperm capacitation by targeting membrane sphingomyelin and regulating calcium levels. This decapacitation mechanism ensures sperm are ready for fertilization.

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Using an Extracellular Flux Analyzer to Measure Changes in Glycolysis and Oxidative Phosphorylation during Mouse Sperm Capacitation
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Published on: January 22, 2020

Area of Science:

  • Reproductive Biology
  • Sperm Physiology
  • Molecular Mechanisms of Fertilization

Background:

  • Sperm capacitation and decapacitation are crucial for successful fertilization.
  • Dysregulated decapacitation leads to premature acrosome reactions and infertility.
  • Seminal plasma inhibits capacitation, but its mechanisms are not fully understood.

Purpose of the Study:

  • To elucidate the decapacitation mechanism of mouse seminal vesicle autoantigen (SVA).
  • To investigate SVA's potential targets, including membrane sphingomyelin (SPM) and plasma membrane Ca(2+)-ATPase (PMCA).

Main Methods:

  • Assessed SVA's effect on sperm capacitation induced by BSA, PAF, and CD.
  • Measured intracellular calcium ([Ca(2+)](i)) and cAMP ([cAMP](i)) levels.
  • Utilized a PMCA inhibitor (carboxyeosin) to evaluate SVA's impact on calcium regulation.
  • Determined binding affinity between SVA and SPM.
  • Examined SVA's effect on PAI-1 expression in epithelial cells.

Main Results:

  • SVA suppressed sperm capacitation induced by various factors.
  • SVA significantly decreased [Ca(2+)](i) and NaHCO(3)-induced [cAMP](i).
  • PMCA inhibition reversed SVA's suppression of [Ca(2+)](i), indicating PMCA regulation.
  • High binding affinity between SVA and SPM suggested membrane lipid raft targeting.
  • SVA enhanced TGF-β-stimulated PAI-1 expression in epithelial cells.

Conclusions:

  • SVA acts as a decapacitation factor by targeting membrane SPM and regulating PMCA activity.
  • This regulation lowers intracellular calcium, subsequently reducing cAMP levels and preventing premature sperm capacitation.
  • SVA's mechanism involves membrane lipid raft interactions and impacts cellular signaling pathways.