CATSPER2 Membrane Protein Introduction

Introduction of CATSPER2

Diethylstilbestrol, which activates CatSper and disturbs prCatSper gene, is a member of cation channel sperm family and has an essential role in sperm motility and male fertility. Following varicocele, sperm parameters, especially sperm movement, decreases. For this reason, the expression of CatSper gene might be reduced after varicocele induction in an animal model. Ogesterone acts in human spermatozoa. CATSPER-related male infertility results from abnormalities in sperm and can be either CATSPER-related nonsyndromic male infertility (NSMI) or the deafness-infertility syndrome (DIS) when associated with non-progressive prelingual sensorineural hearing loss. Males with NSMI have infertility while females have no symptoms. Males with DIS have both infertility and hearing loss, while females have only hearing loss.

Function of CATSPER2 Membrane Protein

The CatSper channel is confined to the principal piece of sperm flagellum as shown by localization pattern in mice and humans. Influx of Ca²⁺ leads to a rise in sperm intracellular calcium concentration, which facilitates vigorous and faster sperm movements. Moreover, this unique class of Ca²⁺ channel has been shown to be essential for hyperactivated sperm motility, sperm detachment from the epithelium of the female reproductive tract, egg coat penetration and fertility. Hyperactivated motility, which is characterized by asymmetrical high amplitude and lower frequency flagellar beating, is essential for releasing sperm from the isthmic reservoir to reach the site of fertilization that is followed by penetration through the egg's zona pellucida, the extracellular coat that surrounds the egg. The CatSper channel, in association with other ion channels and pumps, facilitates the entry of calcium necessary for rapid changes in sperm motility, allowing the spermatozoa to navigate through the hurdles of the female reproductive tract in order to locate the egg for fertilization. The spermatozoon is likely to receive multiple signals in the female reproductive tract, which provide cues and information to the spermatozoon for gaining hyperactivated motility and fertilizing the egg. CatSper channel mutations in humans have been associated with infertility.

Fig.1 Hypermotility: normal sperm display vigorous and asymmetrical flagellar beating termed as hypermotility, which is essential for propagation through viscous ovi-ductal fluid. CatSper null sperm show only basal motility and are unable to propagate to destination and penetrate protective layers of the egg. (Singh, 2015)

Application of CATSPER2 Membrane Protein in Literature

1. Park E.H., et al. Panax ginseng induces the expression of CatSper genes and sperm hyperactivation. Asian J Androl. 2014, 16(6):845-851. PubMed ID: 24969054
   
   

   This study indicated that P. ginseng plays an important role in improving sperm hyperactivation via CatSper gene expression.

2. Jaiswal D., et al. Chromosome microarray analysis: a case report of infertile brothers with CATSPER gene deletion. Gene. 2014, 542(2):263-265. PubMed ID: 24690399
   
   

   This article reports the first familial case report from India on occurrence of CATSPER gene deletion in human male infertility.

3. Mohammadi S., et al. Effects of Vitamin-E treatment on CatSper genes expression and sperm quality in the testis of the aging mouse. Iran J Reprod Med. 2013, 11(12):989-998. PubMed ID: 24639725
   
   

   In this study, authors find that the vitamin E treatment significantly improves the sperm quality, especially in terms of sperm motility, count and morphology rate. Furthermore, CatSper genes expression could be up-regulated by the vitamin E treatment.

4. Smith J.F., et al. Disruption of the principal, progesterone-activated sperm Ca²⁺ channel in a CatSper2-deficient infertile patient. Proc Natl Acad Sci U S A. 2013, 110(17):6823-6828. PubMed ID: 23530196
   
   

   These results unambiguously establish an important role of CatSper channel in human sperm nongenomic progesterone signaling and demonstrate that the molecular mechanism responsible for activation of CatSper by progesterone arises early in sperm development concurrently with the CatSper channel itself.

5. Zhang Z., et al. Regulation of fertilization in male rats by CatSper2 knockdown. Asian J Androl. 2012, 14(2):301-309. PubMed ID: 22002435
   
   

   This study demonstrates that it is feasible to achieve male contraception by silencing the expression of CatSper2, the key protein involved in sperm hyperactivation.

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Reference

1. Singh A P and Rajender S. (2015). CatSper channel, sperm function and male fertility. Reprod Biomed Online. 30(1), 28-38.

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