Immunolocalization of SP22 (Park7) on the Human Sperm Membrane is Indicative of Live Birth
Abstract:
With the decline in sperm quality over recent decades, there is little doubt that the decreased efficiency of spermatogenesis in men reflects
their increasing susceptibility to environmental and pharmaceutical exposures that can compromise male fecundity. More than twenty
years have passed since we discovered a novel sperm membrane protein (SP22) derived from the Park7 gene that is highly correlated with
the fertility of rat sperm exposed to epididymal toxicants., We subsequently discovered that SP22 originates in the testis and is also
compromised during exposure to testicular toxicants. Recently, we were given an opportunity to test the hypothesis that human sperm may
also have reduced fertility when levels of SP22 are significantly decreased. Using a recombinant antibody to the functional
epitope of SP22, we compared sperm from donors who achieved a live birth to donors who were not able to achieve a pregnancy.
Sperm SP22 was significantly reduced in a group of donors not able to achieve a pregnancy. A similar reduction in birth was also observed
among specific Park7 and SP22 exons when a group of donors unable to achieve a pregnancy was compared to the live birth donors. To
our knowledge, this is the first demonstration that SP22 expression can be compromised in men with reduced fertility. This opens the
door to incorporating SP22 analyses in future epidemiology studies, as well as developing over-the-counter testing for men with suspected
male infertility.