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Scientists at the University of California-San Francisco have shown that cellular antennae called cilia, found on fat-forming cells and interspersed in muscles, play a key role in the muscle-to-fat transformation.
The findings, revealed in experiments with mice and published on Thursday in Cell, could open up new prospects for regenerative medicine, and one day enable researchers to improve muscle renewal during aging and disease, Xinhua news agency reported.
As we age, our muscle cells are slowly exchanged, one by one, for fat cells.
The process quickens when we injure a muscle, and an extreme form of this process is seen in muscle-wasting diseases such as Duchenne muscular dystrophy (DMD).
High levels of intra-muscular fat have long been associated with a loss of strength and impaired mobility, and more fall in elderly or obese individuals and in patients with DMD.
"The frailty of age is a huge biomedical problem," said Jeremy Reiter, a professor of biochemistry and biophysics at UCSF and senior author of the paper. "This study paves the way to learn how muscles normally age, and provides a new way to possibly improve muscle repair."
Primary cilia are tiny cellular appendages a bit like cellular tentacles that paramecia and other single-celled critters use to move and gather food.
But unlike those motile cilia, primary cilia do not move at all. They stand stiff and solitary on the surface of nearly all of our cells, including neurons, skin cells, bone cells and certain stem cells.
Recent work at Reiter's lab has revealed that primary cilia act much like cellular antennae, receiving molecular cues from neighbouring cells, and processing environmental signals such as light, temperature, salt balance and even gravity.
Previous work has shown that when muscle is injured, fat-forming cells that live alongside muscle cells, called fibro/adipogenic progenitors (FAPs) divide and differentiate into fat cells.
Daniel Kopinke, a postdoctoral fellow in the Reiter lab and first author of the study, found that, unlike muscle cells, the fat-forming FAPs are more likely to carry primary cilia, and muscle injury further increased the abundance of FAPs with cilia.
The group has discovered that genetically engineering cells without cilia result in a low-level activation of the Hedgehog pathway, which is enough to block fatty degeneration of skeletal muscle.
"Now for the first time we have a handle on the cell type that turns muscle into fat, and we have a handle on the signaling pathway that controls the conversion," Kopinke said. "Maybe one day we could use this knowledge to improve muscle function."
(This story has not been edited by Business Standard staff and is auto-generated from a syndicated feed.)