How does the body heal itself?
Last Updated: Saturday, February 27, 2010, 00:00

Washington: Unlocking the secrets of how the body heals itself, especially when organs become diseased, a new study shows that the presence of small particles known as microvesicles helps cellular communication and enables healing.

Microvesicles are much smaller than a normal cell and contain genetic information such as messenger ribonucleic acid (RNA), other species of RNA and protein.

Jason Aliotta, physician researcher at the critical care and haematology-oncology departments at Rhode Island Hospital (RIH), and colleagues focussed on these small particles.

During times of cellular injury or stress, or with certain diseases like cancer, infections and cardiovascular disease, these particles are shed and then taken up by other cells in the body.

The genetic information and protein in the microvesicles help to reprogramme the accepting cell to behave more like the cell from which the particle was derived.

Aliotta, also an assistant professor of medicine at the Brown University, said: "What we attempted to understand is how cells within the bone marrow are able to repair organs that are unrelated to those bone marrow cells, such as the lung.

"Our work suggests that when the lung is injured or diseased and cells within it are stressed or dying, they shed microvesicles. Those microvesicles are then consumed by cells within the bone marrow, including stem cells, which are present in small numbers within the circulatory system. Those bone marrow cells then turn into lung cells."

Other researchers have reported similar findings over the last couple of years. Microvesicles have been known for over 40 years and have often been considered irrelevant, says an RIH release.

Aliotta concludes: "We are now recognising the relevance of microvesicles - they are important mediators of cell-to-cell communication."

Their paper is slated for publication in the March edition of Experimental and is now available online.


First Published: Saturday, February 27, 2010, 00:00

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