Re­searchers close in on de­vel­op­ing men’s birth con­trol pill

The Hamilton Spectator - - HEALTH - KRIS­TEN JOR­DAN SHAMUS

Sci­en­tists at Michi­gan State Univer­sity might have un­cov­ered the key to de­vel­op­ing an ef­fec­tive male birth con­trol pill.

In study­ing the causes of male fer­til­ity and in­fer­til­ity and us­ing a new gene edit­ing tech­nol­ogy, re­searchers dis­cov­ered that they can ef­fec­tively block the gene that con­trols sperm pro­duc­tion in mice, ren­der­ing them in­fer­tile.

Chen Chen, PhD, an as­sis­tant pro­fes­sor of an­i­mal sci­ence at MSU, said his team’s dis­cov­ery is a first step in find­ing drug treat­ments that could sim­i­larly block the ge­netic ex­pres­sion of this gene, called PNLDC1, in hu­mans.

“More than 500,000 men get va­sec­tomies ev­ery year,” Chen said. “There’s a huge mar­ket for this re­search, and now we fur­ther un­der­stand the ge­netic un­der­pin­nings of sperm de­vel­op­ment in mam­mals.

“I think for the gen­eral pub­lic there is great need in an­other male con­tra­cep­tive method.”

The ge­netic edit­ing tech­nol­ogy knocked out or com­pletely blocked the PNLDC1 ex­pres­sion in male mice em­bryos, mak­ing the male mice in­fer­tile. Since mice are mam­mals and use many of the same genes as hu­mans in re­pro­duc­tion, it sug­gests a sim­i­lar ap­proach could be used in de­vel­op­ing a form of hu­man male con­tra­cep­tion.

In the mice Chen and his team stud­ied, the ster­il­iza­tion was per­ma­nent.

“If you delete the gene from birth, it would cause per­ma­nent steril­ity,” he said. “How­ever, be­cause the sys­tem we are study­ing func­tions both neona­tally and post­na­tally, there is a good chance that if you block the same pro­tein func­tion later on, it would have the same ef­fect ... but it’s not af­fect­ing per­ma­nent sperm pro­duc­tion. In or­der to have a per­ma­nent ster­il­iza­tion, you would need to ab­late the stem cell pool be­cause the stem cells are the pro­gen­i­tors (of ) ma­ture sperm.”

The hope is that they would be able to find a drug treat­ment that could block the func­tion of that gene tem­po­rar­ily, al­low­ing pa­tients to block healthy sperm pro­duc­tion for a short time, and then per­mit the re­turn of healthy sperm pro­duc­tion later, if de­sired.

The hor­mone testos­terone, Chen said, is known to be ef­fec­tive for lim­it­ing sperm pro­duc­tion. But, he said, its side-ef­fects make it a poor can­di­date for wide­spread use.

“Testos­terone can act on other tis­sues and or­gans and not ev­ery sin­gle man would re­spond the same way,” he said. “So for the field, it’s bet­ter to de­velop a non­hor­monal tar­get. It does not mess with hor­mones and me­tab­o­lism. In this case, PNLDC1 is in­ter­est­ing be­cause it pri­mar­ily is ex­pressed in germ cells, but not in nor­mal tis­sue like the brains or heart or liver.

“That’s why, if you could tar­get his pro­tein specif­i­cally in the testes, it can block sper­mato­ge­n­e­sis, sperm pro­duc­tion, but with no ad­verse ef­fect on other tis­sues and or­gans.”

Ge­net­i­cally al­tered mice who’ve been part of the PNLDC1 stud­ies have been shown to have smaller testes, but that ap­pears to be the only phys­i­o­log­i­cal dif­fer­ence. It doesn’t ap­pear to have any ef­fect on sex­ual func­tion, Chen said.

“So far we haven’t ob­served any mat­ing be­hav­iour changes,” he said. “Sperm is dra­mat­i­cally de­creased, and ... if you look at the mor­phol­ogy of the cells, we see ab­nor­mally shaped sperm. Very few are ac­tu­ally re­leased into the epi­didymis. You do see some spermlike cells, but they are not func­tional.”

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