NLRP2 Protein Found to Influence Fertility

A PROTEIN, known as NLRP2, has been found to play a key role in early embryogenesis and affect maternal fertility later in life in animal models. As a similar protein exists in humans, it is hoped that this finding will eventually lead to greater comprehension of human reproductive disorders and shed light on novel treatment paths. The study’s lead author, Prof Mohamed Lamkanfi, VIB Center for Inflammation Research, University of Ghent, Ghent, Belgium, elucidated: “At the same time as our research was being conducted, small human studies provided anecdotal evidence that mutations in human NLRP2 might be linked with increased susceptibility to reproductive disorders. Our findings further support a role for the protein in the reproductive system.”

Today, around one in six couples have fertility issues; maternal age is viewed as the major factor driving demand for reproductive technologies. With little currently known about the mechanisms that govern early embryogenesis; this study offered new insights in that regard. The research was carried out in mice and implied that mutations in NLRP2 may lead to early menopause and further conditions linked with the pathological decline of maternal fertility. Furthermore, older adult NLRP2-deficient mice had significantly lower rates of reproduction when compared with younger mice deficient in NLRP2.  This suggests that NLRP2 has an age-linked influence on fertility, becoming more crucial with age.

Prior to conducting this research, it was expected that NLRP2 would be found to play a role in the immune system, with similar proteins having been discovered to have important functions in regulating inflammation and controlling infections. The team were surprised by what they found, with Prof Lamkanfi explaining: “Contrary to expectations, we failed to find any role for NLRP2 in immunity and inflammation. As a result, we refocussed our studies on reproduction after discovering that NLRP2 is specifically produced by egg cells, or oocytes, showing that the protein is critical to the maintenance of oocyte quality later in life.”

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