It turns out the muscle cells on the outside of blood vessels have been wrongly accused for instigating lung disease. New research shows that while these muscle cells are responsible for constricting or dilating the blood vessels, they are not responsible for sensing the amount of oxygen that gets to the lungs. That message comes from the endothelial cells — special cells that line the blood vessels — along a “signalling pathway.”
Dr. Wolfgang Kuebler, a Li Ka Shing Knowledge Institute scientist at St. Michael’s Hospital, has found that the endothelial cells play a much larger role in the constriction of blood vessels in response to the lack of oxygen and in subsequent pulmonary hypertension, than previously believed. The findings of his study, which was conducted on mice, have been published online in the Journal of Clinical Investigation.
“The vascular endothelial cells have always been regarded as a bystander, but we’ve discovered that lung disease in response to low oxygen originates at this level, that the message is sent by these cells,” said Dr. Kuebler. He said that if there were a way to block, or inhibit, this communication along the signalling pathway between the endothelial cells and the smooth muscle cells, we could potentially prevent right heart failure, a fairly common disease among patients with lung disease.
Story Source:
The above story is reprinted from materials provided by St. Michael’s Hospital. The original article was written by Evelyne Jhung.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Liming Wang, Jun Yin, Hannah T. Nickles, Hannes Ranke, Arata Tabuchi, Julia Hoffmann, Christoph Tabeling, Eduardo Barbosa-Sicard, Marc Chanson, Brenda R. Kwak, Hee-Sup Shin, Songwei Wu, Brant E. Isakson, Martin Witzenrath, Cor de Wit, Ingrid Fleming, Hermann Kuppe, Wolfgang M. Kuebler. Hypoxic pulmonary vasoconstriction requires connexin 40–mediated endothelial signal conduction. Journal of Clinical Investigation, 2012; DOI: 10.1172/JCI59176
