Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca2+-ATPase (PMCA)-mediated intracellular calcium

Shing Hwa Lu, Yuan Kuei Yen, Thai Yen Ling, Kur Ta Cheng, Jye An Shu, Heng Kien Au, Yen Hua Huang

研究成果: 雜誌貢獻文章

5 引文 (Scopus)

摘要

Successful fertilization is tightly regulated by capacitation and decapacitation processes. Without appropriate decapacitation regulation, sperm would undergo a spontaneous acrosome reaction which leads to loss of fertilization ability. Seminal plasma is known to negatively regulate sperm capacitation. However, the suppressive mechanisms still remain unclear. In this study, we demonstrate the decapacitation mechanism of mouse seminal vesicle autoantigen (SVA) might target membrane sphingomyelin (SPM) and regulate plasma membrane Ca2+-ATPase (PMCA) activity. The SVA was shown to suppress sperm capacitation induced by a broad panel of capacitation factors (bovine serum albumin (BSA), PAF, and cyclodextrin (CD)). Furthermore, SVA significantly decreased [Ca2+]i and NaHCO3-induced [cAMP]i. Cyclic AMP agonists bypassed the SVA's suppressive ability. Importantly, the SVA may regulate PMCA activity which was evidenced by the fact that the SVA decreased the [Ca2+]i and intracellular pH (pHi) of sperm; meanwhile, a PMCA inhibitor (carboxyeosin) could reverse SVA's suppression of [Ca2+]i. The potential target of the SVA on membrane SPM/lipid rafts was highlighted by the high binding affinity of SPM-SVA (with a Kd of ∼3 μM) which was close to the IC50 of SVA's suppressive activity. Additionally, treatment of mink lung epithelial cells with the SVA enhanced plasminogen activator inhibitor (PAI)-1 expression stimulated by tumor growth factor (TGF)-β and CD. These observations supported the membrane lipid-raft targeting of SVA. In summary, in this paper, we demonstrate that the decapacitation mechanism of the SVA might target membrane sphingolipid SPM and regulate PMCA activity to lower [Ca 2+]i, thereby decreasing the [cAMP]i level and preventing sperm pre-capacitation.

原文英語
頁(從 - 到)1188-1198
頁數11
期刊Journal of Cellular Biochemistry
111
發行號5
DOIs
出版狀態已發佈 - 十二月 1 2010

指紋

Calcium-Transporting ATPases
Cell membranes
Cell Membrane
Calcium
Sphingomyelins
Sperm Capacitation
Cyclodextrins
Membrane Lipids
Membranes
Fertilization
Spermatozoa
seminal vesicle autoantigen
Acrosome Reaction
Mink
Sphingolipids
Plasminogen Activator Inhibitor 1
Bovine Serum Albumin
Semen
Cyclic AMP
Inhibitory Concentration 50

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

引用此文

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title = "Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca2+-ATPase (PMCA)-mediated intracellular calcium",
abstract = "Successful fertilization is tightly regulated by capacitation and decapacitation processes. Without appropriate decapacitation regulation, sperm would undergo a spontaneous acrosome reaction which leads to loss of fertilization ability. Seminal plasma is known to negatively regulate sperm capacitation. However, the suppressive mechanisms still remain unclear. In this study, we demonstrate the decapacitation mechanism of mouse seminal vesicle autoantigen (SVA) might target membrane sphingomyelin (SPM) and regulate plasma membrane Ca2+-ATPase (PMCA) activity. The SVA was shown to suppress sperm capacitation induced by a broad panel of capacitation factors (bovine serum albumin (BSA), PAF, and cyclodextrin (CD)). Furthermore, SVA significantly decreased [Ca2+]i and NaHCO3-induced [cAMP]i. Cyclic AMP agonists bypassed the SVA's suppressive ability. Importantly, the SVA may regulate PMCA activity which was evidenced by the fact that the SVA decreased the [Ca2+]i and intracellular pH (pHi) of sperm; meanwhile, a PMCA inhibitor (carboxyeosin) could reverse SVA's suppression of [Ca2+]i. The potential target of the SVA on membrane SPM/lipid rafts was highlighted by the high binding affinity of SPM-SVA (with a Kd of ∼3 μM) which was close to the IC50 of SVA's suppressive activity. Additionally, treatment of mink lung epithelial cells with the SVA enhanced plasminogen activator inhibitor (PAI)-1 expression stimulated by tumor growth factor (TGF)-β and CD. These observations supported the membrane lipid-raft targeting of SVA. In summary, in this paper, we demonstrate that the decapacitation mechanism of the SVA might target membrane sphingolipid SPM and regulate PMCA activity to lower [Ca 2+]i, thereby decreasing the [cAMP]i level and preventing sperm pre-capacitation.",
keywords = "calcium, cAMP, decapacitation, plasma membrane Ca-ATPase (PMCA), protein tyrosine phosphorylation, seminal vesicle, sperm",
author = "Lu, {Shing Hwa} and Yen, {Yuan Kuei} and Ling, {Thai Yen} and Cheng, {Kur Ta} and Shu, {Jye An} and Au, {Heng Kien} and Huang, {Yen Hua}",
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TY - JOUR

T1 - Capacitation suppression by mouse seminal vesicle autoantigen involves a decrease in plasma membrane Ca2+-ATPase (PMCA)-mediated intracellular calcium

AU - Lu, Shing Hwa

AU - Yen, Yuan Kuei

AU - Ling, Thai Yen

AU - Cheng, Kur Ta

AU - Shu, Jye An

AU - Au, Heng Kien

AU - Huang, Yen Hua

PY - 2010/12/1

Y1 - 2010/12/1

N2 - Successful fertilization is tightly regulated by capacitation and decapacitation processes. Without appropriate decapacitation regulation, sperm would undergo a spontaneous acrosome reaction which leads to loss of fertilization ability. Seminal plasma is known to negatively regulate sperm capacitation. However, the suppressive mechanisms still remain unclear. In this study, we demonstrate the decapacitation mechanism of mouse seminal vesicle autoantigen (SVA) might target membrane sphingomyelin (SPM) and regulate plasma membrane Ca2+-ATPase (PMCA) activity. The SVA was shown to suppress sperm capacitation induced by a broad panel of capacitation factors (bovine serum albumin (BSA), PAF, and cyclodextrin (CD)). Furthermore, SVA significantly decreased [Ca2+]i and NaHCO3-induced [cAMP]i. Cyclic AMP agonists bypassed the SVA's suppressive ability. Importantly, the SVA may regulate PMCA activity which was evidenced by the fact that the SVA decreased the [Ca2+]i and intracellular pH (pHi) of sperm; meanwhile, a PMCA inhibitor (carboxyeosin) could reverse SVA's suppression of [Ca2+]i. The potential target of the SVA on membrane SPM/lipid rafts was highlighted by the high binding affinity of SPM-SVA (with a Kd of ∼3 μM) which was close to the IC50 of SVA's suppressive activity. Additionally, treatment of mink lung epithelial cells with the SVA enhanced plasminogen activator inhibitor (PAI)-1 expression stimulated by tumor growth factor (TGF)-β and CD. These observations supported the membrane lipid-raft targeting of SVA. In summary, in this paper, we demonstrate that the decapacitation mechanism of the SVA might target membrane sphingolipid SPM and regulate PMCA activity to lower [Ca 2+]i, thereby decreasing the [cAMP]i level and preventing sperm pre-capacitation.

AB - Successful fertilization is tightly regulated by capacitation and decapacitation processes. Without appropriate decapacitation regulation, sperm would undergo a spontaneous acrosome reaction which leads to loss of fertilization ability. Seminal plasma is known to negatively regulate sperm capacitation. However, the suppressive mechanisms still remain unclear. In this study, we demonstrate the decapacitation mechanism of mouse seminal vesicle autoantigen (SVA) might target membrane sphingomyelin (SPM) and regulate plasma membrane Ca2+-ATPase (PMCA) activity. The SVA was shown to suppress sperm capacitation induced by a broad panel of capacitation factors (bovine serum albumin (BSA), PAF, and cyclodextrin (CD)). Furthermore, SVA significantly decreased [Ca2+]i and NaHCO3-induced [cAMP]i. Cyclic AMP agonists bypassed the SVA's suppressive ability. Importantly, the SVA may regulate PMCA activity which was evidenced by the fact that the SVA decreased the [Ca2+]i and intracellular pH (pHi) of sperm; meanwhile, a PMCA inhibitor (carboxyeosin) could reverse SVA's suppression of [Ca2+]i. The potential target of the SVA on membrane SPM/lipid rafts was highlighted by the high binding affinity of SPM-SVA (with a Kd of ∼3 μM) which was close to the IC50 of SVA's suppressive activity. Additionally, treatment of mink lung epithelial cells with the SVA enhanced plasminogen activator inhibitor (PAI)-1 expression stimulated by tumor growth factor (TGF)-β and CD. These observations supported the membrane lipid-raft targeting of SVA. In summary, in this paper, we demonstrate that the decapacitation mechanism of the SVA might target membrane sphingolipid SPM and regulate PMCA activity to lower [Ca 2+]i, thereby decreasing the [cAMP]i level and preventing sperm pre-capacitation.

KW - calcium

KW - cAMP

KW - decapacitation

KW - plasma membrane Ca-ATPase (PMCA)

KW - protein tyrosine phosphorylation

KW - seminal vesicle

KW - sperm

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