Abstract
In mammals, fertilization occurs via a comprehensive progression of events. Freshly ejaculated sperm have yet to acquire progressive motility or fertilization ability. They must first undergo a series of biochemical and physiological changes, collectively known as capacitation. Capacitation is a significant prerequisite to fertilization. During the process of capacitation, changes in membrane properties, intracellular ion concentration and the activities of enzymes, together with other protein modifications, induce multiple signaling events and pathways in defined media in vitro or in the female reproductive tract in vivo. These, in turn, stimulate the acrosome reaction and prepare spermatozoa for penetration of the egg zona pellucida prior to fertilization. In the present review, we conclude all mainstream factors and pathways regulate capacitation and highlight their crosstalk. We also summarize the relationship between capacitation and assisted reproductive technology or human disease. In the end, we sum up the open questions and future avenues in this field.
Highlights
The phenomenon of mammalian spermatozoa must await a period of time in the female reproductive tract to acquire their fertilizing capacity was first described by Min Chueh Chang and Colin Russell Austin in 1951 in rabbits and rats respectively [1,2], the specific term ‘capacitation’ was proposed by Austin in 1952 [3]
Many reports have confirmed that increased intracellular cyclic adenosine monophosphate levels with the related activation of protein kinase A activity and induction of tyrosine phosphorylation are required for the induction of mammalian sperm capacitation [177,178]
In view of the notion that capacitation in the female reproductive tract is essential for fertilization, there is a need to unravel the molecular processes involved in this
Summary
The phenomenon of mammalian spermatozoa must await a period of time in the female reproductive tract to acquire their fertilizing capacity was first described by Min Chueh Chang and Colin Russell Austin in 1951 in rabbits and rats respectively [1,2], the specific term ‘capacitation’ was proposed by Austin in 1952 [3]. Changes influence each other to regulate sperm functions while some evidence showed there were channels sensitive to membrane potential and pHi because artificial intracellular alkalinization add of HCO3- and increase the beat frequency of sperm [119]. ROS in capacitation is dose-dependent, ROS is required for capacitation as key regulators to promote cholesterol efflux [116], cAMP production [146,147] and PTP [145, 148,149,150] while excessive concentration are toxic due to the destroy of polyunsaturated fatty acid in sperm surface [151,152,153], sperm-zona pellucida interaction [154], induce an intrinsic apoptotic-like pathway [155] and resulting in embryo development fail [156].
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