Abstract
Purpose
The aim of this study was to determine whether altered expression and distribution of calcium- and integrin-binding protein-1 (CIB1) is involved in the pathogenesis of patients with oligoasthenozoospermia.
Methods
Sperm samples were obtained from 25 infertile Chinese men who had failed to achieve conception after a period of 1–2 y and had been referred to the Reproductive Laboratory of the second hospital affiliated to the Shandong University of Traditional Chinese Medicine. Participants were divided into two groups: oligoasthenozoospermia (n = 13) and asthenozoospermia (n = 12); as a third group, fertile men (n = 19) were included as controls. The expression levels of mRNA and protein levels of CIB1 and cyclin-dependent kinase 1 (CDK1) were measured using qRT-PCR and western blotting.
Results
mRNA and protein expression levels of CIB1 were decreased in the oligoasthenozoospermia patients. Interestingly mRNA and protein expression levels of CDK1 were increased in the oligoasthenozoospermia patients.
Conclusion
The results of the present study indicate that that CIB1 may be involved in the pathogenesis of oligoasthenozoospermia by the CDK1 signaling pathway.
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Acknowledgments
This work was supported by the National Natural Science Foundation of China (81102653) and the Shandong Natural Science Foundation (ZR2012HL21 and ZR2011HM013). The authors wish to thank all the couples who participated in this study. We are also indebted to staffs of the reproductive medical center of the Second Hospital affiliated to Shandong University of Traditional Chinese Medicine for sample collection.
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Capsule CIB1 mRNA and protein expression patterns oppose those of CDK1 in sperm of oligoasthenozoospermia patients. CIB1 may be involved in the pathogenesis of oligoasthenozoospermia by the CDK1 signaling pathway.
Wei Sun and Qun Guan contributed equally to this work.
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Sun, W., Guan, Q., Wen, J. et al. Calcium- and integrin-binding protein-1 is down-regulated in the sperm of patients with oligoasthenozoospermia. J Assist Reprod Genet 31, 541–547 (2014). https://doi.org/10.1007/s10815-014-0177-4
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DOI: https://doi.org/10.1007/s10815-014-0177-4