Mechanism that regulates stem-cell differentiation in mice may trigger degenerative disease in humans: Research

January 24, 2016

Several key regulators of spermatogonial stem cell self-renewal have been identified, but knowledge of molecules that control spermatogonial stem cell differentiation is lacking, Oatley explained.

"In this study, we found that impairment of STAT3 signaling enhances spermatogonial stem cell self-renewal without affecting general proliferation of the cells. That indicates an alteration in the balance of spermatogonial stem cell fate decisions that inhibited differentiation in favor of self-renewal."

Much stem-cell research is done of necessity with mice, noted Oatley, who pointed out that scientists who use the mouse as a model for human biology make the assumption that what they learn about in a mouse is identical to what happens in a human.

"Ideally, any of us who work with mice would love to translate our work into humans, but the problem is that you can't get the tissue samples from humans, and you can't manipulate the genetics of humans to show what we want to learn," he said.

Oatley said he believes his research is a solid first step in helping scientists learn how to regulate STAT2 levels to treat or control degenerative disease in humans.

Source: Penn State