In the body, repair is constant process. So it’s a good thing the body has a Star Trek-like replicator in the mesenchymal stem cell. These act as the raw material for future muscles, cartilage, or bone cells, to name a few. But scientists at Mayo report that if the ship isn’t healthy, the replicator may suffer too.
Researcher Lilach Lerman, M.D., Ph.D., led the team that examined how mesenchymal stem cells act in an animal model of metabolic syndrome —a set of conditions that increase risk for cardiovascular diseases and diabetes. They report that stem cells in pigs with metabolic syndrome are shifted down a pathway that leads to stasis instead of repair, as compared to lean pigs.
Stasis for a cell is a state called senescence. These senescent cells hover between life and death, spewing out inflammatory molecules to disrupt the function of cells in their vicinity. It’s not a good condition, but it may be a necessary one: If a cell is headed down the road toward cancer, it may receive instructions to die, but if it can’t then it may enter this senescent state.
Dr. Lerman and team had previously observed that pigs with metabolic syndrome had fewer functional mesenchymal stem cells and more senescent stem cells than lean pigs. In their recent publication in the journal Cell Transplantation, they expand on those findings and show one way that metabolic syndrome might affect the stem cells.
It goes like this: biological effects of high blood pressure, abnormal cholesterol or triglycerides, excessive blood sugar, and/or excess body weight around the waist shift the directions cells are given and send them down the road of senescence and the senescence associated disruption that comes with it. The directions, the researchers report, come in the form of short bits of RNA called microRNA. These short fragments interfere with the ability of messenger RNA to take instructions received from the DNA to a ribosome so protein a can be made.
In lean and metabolic syndrome animals, the researchers found differences in 10 microRNAs that, collectively, are linked with 35 senescence-associated genes.
Next, the researchers will explore these genes and the molecules that regulate these pathways in greater detail, in the hope of improving stem cell function for humans managing a chronic disease state.
And to help move us into the era of Star Trek, the team hopes their information improve the use of stem cells gathered from the body as a regenerative medicine tool. Ship or body, replicator or mesenchymal stem cell, understanding how to keep the repair system in good working order means a smoother ride for all.
This article originally appeared in Mayo Clinic's research magazine, Discovery's Edge.
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