I am a scientist, businessman, author, and philanthropist. For nearly two decades, I was a professor at Harvard Medical School and Harvard School of Public Health where I founded two academic research departments, the Division of Biochemical Pharmacology and the Division of Human Retrovirology.
Odds are you’ve never heard of microRNAs. Even if you have, you might not care much. New research, published in, might convince you otherwise: microRNA-141-3p increases with age, and alongside it a number of issues, including weakened bones, chronic inflammation, and shrinking muscle mass. The findings suggest that blocking this microRNA may be able to rescue bone, immune, and muscle health.Although almost all of our cells contain the same DNA, many perform vastly different functions.
Which protein does microRNA-141-3p block from being made? AU-rich RNA-binding factor 1 . Usually, AUF1 is involved in the regulation of messenger RNA stability and in determining which proteins are made. In younger people, AUF1 actively suppresses the production of pro-inflammatory proteins, which, if left unchecked, might otherwise lead to chronic inflammation —. AUF1 also helps curb “cell senescence”, which is when cells become old and lose their ability to function normally.
The scientists treated elderly mice, around 60 in human years, with the antagomir for three months, administering the molecule by injection twice a week. Afterward, they analyzed the spleen, muscles, and bones of the mice and compared them to a control group that did not receive the antagomir treatment.
Specifically, proteins in the blood that upregulate inflammation —tumor necrosis factor alpha , interleukin-1 beta , and interferon gamma — declined with antagomir treatment. In the spleen, treated mice had a higher proportion of M2 macrophages. These are immune cells that helpand repair tissue damage. M1 macrophages, in turn, are known to promote inflammation and were substantially higher in the untreated mice.
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