Role of cholesterol in sperm capacitation
Role of cholesterol in sperm capacitation
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DOI：
10.1095/biolreprod59.1.7
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发表时间：
1998-07-01
影响因子：
3.6
通讯作者：
Cross, NL
中科院分区：
文献类型：
--
作者：
Cross, NL
40年前，MC Chang发现，将获能的兔子精子暴露于精浆中，使它们无法在体内受精卵[1]。这个相当非生理学的实验结果对精子获能的研究产生了强烈的影响，这是Chang [2]和Austin [3]在六年前发现的。人们普遍认为，了解精浆如何逆转获能将有助于了解精子如何获得获能，并投入了大量精力来鉴定精浆中的抑制剂。候选物包括蛋白质、肽和脂质[4，5]。从他对精浆抑制活性的研究开始，Brian Davis和他的同事建立了一个强有力的案例，说明脂质在获能中起着重要作用。Davis表明，精子可以被从精浆中制备的囊泡部分“去活化”（综述见[6]）。部分提取的脂质的馏分的活动减少，并可以模仿含有胆固醇的合成磷脂囊泡。戴维斯认为，囊泡改变了精子质膜的脂质组成，其次，这种变化是相反的变化，通常发生在capacitation.In戴维斯的模型中，精子质膜的胆固醇/磷脂（C/PL）的比例决定了精子的获能状态。新鲜射出的精子具有高的C/PL比率;并且在获能期间，胆固醇从精子膜移动到可溶性蛋白质受体，和/或磷脂移动到精子膜中。在建立该模型时，人们普遍认为获能导致精子自发地发生顶体反应（即，不暴露于特定的诱导剂）。在戴维斯的模型中，C/PL比率的下降引发了顶体反应。这种情况如何发生的解释是基于在其他系统中获得的信息;有人认为，较低的C/PL比降低了膜微粘度，放松了膜中磷脂的包装，并可能允许更大的钙内流，所有这些都导致通过未指定的中间步骤融合质膜和顶体外膜。支持胆固醇在控制精子功能中的作用的早期工作已被广泛审查[6-9]。本综述将强调最近的工作，并将总结目前的信息，胆固醇可能会采取行动。符合格式
Forty years ago, MC Chang found that exposing capacitated rabbit sperm to seminal plasma made them incapable of fertilizing eggs in vivo [1]. The results of this rather unphysiological experiment had a strong impact on the study of sperm capacitation, which Chang [2] and Austin [3] had discovered six years earlier. It was widely believed that understanding how seminal plasma reverses capacitation would shed light on how sperm become capacitated, and considerable effort was devoted to identifying the inhibitory agents in seminal plasma. The candidates included proteins, peptides, and lipids [4, 5]. Beginning with his work on the inhibitory activity of seminal plasma, Brian Davis and his coworkers built a strong case for lipids playing an important role in capacitation. Davis showed that sperm could be ‘‘decapacitated’’by a vesicle fraction prepared from seminal plasma (reviewed in [6]). The activity of the fraction was diminished by partially extracting the lipids and could be mimicked by synthetic phospholipid vesicles containing cholesterol. Davis suggested that the vesicles changed the lipid composition of the sperm plasma membrane and, secondly, that the changes were the reverse of alterations that normally occur during capacitation.In Davis’s model the cholesterol/phospholipid (C/PL) ratio of the sperm plasma membrane determines the capacitation state of the sperm. A freshly ejaculated sperm has a high C/PL ratio; and during capacitation, cholesterol moves from the sperm membrane to soluble protein acceptors, and/or phospholipid moves into the sperm membrane. At the time this model was formulated, it was generally believed that capacitation caused sperm to acrosome-react spontaneously (that is, without exposure to a specific inducer). In Davis’s model, the falling C/PL ratio triggered an acrosome reaction. Explanations for how this might happen were based on information obtained in other systems; and it was suggested that a lower C/PL ratio decreased the membrane microviscosity, relaxed the packing of phospholipids in the membrane, and perhaps permitted greater calcium influx, all leading through unspecified intermediate steps to fusion of the plasma and outer acrosomal membranes. The early work that supported a role for cholesterol in the control of sperm function has been extensively reviewed [6–9]. The present review will emphasize more recent work and will summarize current information regarding how cholesterol might act. To conform to the format of