http://www.sciencedaily.com/releases/20 ... 165125.htm
ScienceDaily (Feb. 1, 2010) — Most people know that exercise protects against heart attack and stroke, but researchers have spent 30 years unraveling the biochemistry behind the idea.but researchers have spent 30 years unraveling the biochemistry behind the idea. One answer first offered by researchers at the University of Rochester Medical Center is that athletic hearts push blood through arteries with greater force, which alone triggers reactions that protect against dangerous clogs in blood vessels.
In the latest study out of Rochester, published recently in the journal Blood, researchers demonstrated that they are very close to understanding every step in one flow-sensitive chain reaction that protects arteries. Each step provides an opportunity to mimic with drugs the proven ability of fast, steady blood flow to open up blood vessels and avert the inflammation and blood clots that come with atherosclerosis.
Past research at the Medical Center and elsewhere had determined that two genes, Krüppel-like factor 2 (KLF2) and endothelial nitric oxide synthase (eNOS), are turned on by blood flow force to reverse atherosclerosis, but not how. The current study found for the first time that flow causes a structural change in the enzyme histone deacetylase 5 (HDAC5), which in turn influences whether the two key genes are turned on.
"Obviously we should all be exercising to get our hearts pumping fast, which increases blood flow force through our vessels with all of these molecular benefits," said Zheng-Gen Jin, Ph.D., associate professor of Medicine within the Aab Cardiovascular Research Institute (CVRI) at the University of Rochester Medical Center, and corresponding author for the study. "Beyond that, the designers of future therapies may manipulate HDAC5 to fine-tune the action of protective genes."
The current study revolves around a signaling process called phosphorylation, in which enzymes called kinases attach a set of molecules called a phosphate group to a target to switch life processes on or off. In cells lining blood vessels (endothelial cells), the attachment of a phosphate group to an HDAC5 kicks it out of the cell's nucleus, perhaps by hiding a label that says it belongs there.
To study whether blood flow force represents one the signals that cause HDAC5 nuclear export, the team designed a virus to invade the cells and swap out the key building blocks that make possible its phosphorylation via blood flow force. Weiye Wang, also a member of the CVRI and first author of the paper, designed the virus. He also attached a fluorescent tag to HDAC5 in the mutated cells so the team could track it as it moved.
What the team found for the first time is that blood flow force (also called sheer stress) does indeed cause ...
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