Abstract: Ejaculated spermatozoon of mammalians should undergo a serious of modification in female to production tract before they acquire the ability to fuse with the oocytes in order to have a successful fertilization. This process is generally termed “capacitation”. The molecular mechanism of capacitation is still far from understanding, despite of the reports about the capacitation-related events, including the rearrangement of plasma membrane lipid, hyperactivated motility, intracellular Ca2+ elevation and protein tyrosine phosphorylation. Insulin-like growth factor-1 (IGF-1) is well known to stimulate the tyrosine kinase of its receptor (IGF-IR) in the regulation of cellular activity. In the seminal vesicle fluid, I could demonstrate IGF-1 by ELISA. Moreover, I could detect IGF-1 mRNA in any sexual glands of adult mice, and examine also IGF-IR on the mouse sperm head by indirect fluorescence technique. These data together prompted me to assess whether IGF-IR is involved in the capacitation-related protein tyrosine phosphorylation. I found the ability of IGF-1 to elicit the capacitation-related protein phosphorylation. The biochemical event could be suppressed by AG538, an inhibitor of IGF-IR. Meanwhile, the sperm capacitation induced by BSA caused the tyrosine phosphorylation of IGF-IR, and the protein tyrosine phosphorylation associated the capacitation could be greatly reduced by AG538. These data suffer ligand-independent IGF-IR on sperm head in the capacitation-related protein phosphorylation.
Publication Year: 2009
Publication Date: 2009-01-01
Language: en
Type: article
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