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小鼠貯精囊自體抗原對精子獲能機制調控之探討

小鼠貯精囊自體抗原對精子獲能機制調控之探討.

meredith-anchoret
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小鼠貯精囊自體抗原對精子獲能機制調控之探討

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  1. 小鼠貯精囊自體抗原對精子獲能機制調控之探討小鼠貯精囊自體抗原對精子獲能機制調控之探討 精子獲能作用是指射精後，精子經雌性生殖道中存在的一些獲能因子活化，經過一連串的生化反應，包括使精子具有超泳動性、具有進行頂體反應的能力。去獲能作用則是指精子為了避免與卵受精前提早活化使能量消耗殆盡，所以在雄性生殖道中也存在一些去獲能因子使精子不被提早活化。自從1951年前後由Chang以及Austin等人提出後獲能及去獲能的觀念後，精子獲能作用機制雖已被廣泛討論，但是在獲能作用與去獲能作用之間的相互協調機制，仍未十分清楚。本實驗室之前研究指出，小白鼠貯精囊液中存在一個19 kDa的醣蛋白，命名為貯精囊自體抗原(seminal vesicle autoantigen, SVA)。SVA已知可以結合於精子細胞膜上富含膽鹼(choline)的磷脂質，如神經磷脂(sphingomyelin)和磷脂膽鹼(phosphatidylchoine)，並可抑制獲能因子如BSA及PAF所引發精子細胞內鈣離子濃度、pH值及cAMP濃度的上升、酪蛋白磷酸化、精子的高度泳動力等獲能作用的現象: 此外也發現SVA可藉由調節PMCA (Ca2+-ATPase通道)來降低精子內的鈣離子濃度，並進而抑制精子的頂體反應。然而SVA作用於精子細胞膜上的分子作用及相關的訊息傳遞機制仍未清楚，因此本篇論文主要為探討SVA蛋白和精子細胞膜上Lipid raft的作用關係，並釐清SVA與sAC(soluble adenylyl cyclases)之抑制現象。

  2. Regulation Mechanism of Seminal Vesicle Autoantigen on Mouse Sperm Capacitation • Capacitation processes are complex biological events for sperm to aquire the ability for fertilization. It was tightly regulated by capacitation factors and decapacitation factors. Many attempts have been shown to demonstrate the capacitation mechanisms; however, the decapacitation regulation remains unclear. In the past ten years, our lab has been demonstrated a seminal vesicle autoantigen (SVA), a novel 19 kDa phospholipids-binding protein in seminal plasma, could play a role as a decapacitation factor to suppress the capacitation factor (like BSA, PAF, and cyclodextran)-induced mouse sperm capacitation. The mechanism of SVA suppression including decrease of the intracellular calcium and cAMP levels, capacitation-associated protein tyrosine phosphorylation, sperm motility, and acrosome reaction. In addition, SVA also enhanced the Ca2+ efflux through activation of the plasma membrane Ca2+-ATPase (PMCA) activity, and, decreased the mitochondria membrane potential of sperm cells. Given SVA interacts with sphingomyelin (SPM) which is a major component in lipid raft, we therefore tried to exam the interaction of SVA and lipid raft on sperm membrane. In our results, we found that SVA is able to suppress the cyclodextran-induced capacitation and its-associated protein tyrosine phosphorylation in sperm. However, by using GM1 and caveolin as markers, we could not observe the inhibition effect of SVA on the BSA-induced distribution pattern of lipid-raft on sperm membrane. This result is further supported by the cell model of cyclodextran-TGF-beta induced PAI-1 gene expression. In addition, SVA significantly suppressed the sAC activity of mouse sperm. In summary, SVA may interact with non-lipid raft region on sperm membrane, by which to suppress the sAC and intracellular signals. As how SVA signal pathway through non-lipid raft region to downstream molecular events still requires further studies.

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