- Kelly Servick
Showing posts with label CCR5. Show all posts
Showing posts with label CCR5. Show all posts
Thursday, September 4, 2025
Thursday, February 21, 2019
Unexpected drug emerges for stroke recovery
Well fuck, Call up stroke leadership and get stroke researchers cracking on human trials immediately. If your doctor and stroke hospital don't do that have the president and board of directors fired. We have lots of dead wood in stroke that needs to be removed so saplings can grow and take over the forest.
Unexpected drug emerges for stroke recovery
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Summary
In
the hours after a stroke, the clot-busting treatment tissue plasminogen
activator can limit damage to the brain. But once that damage is done,
no drugs are known to promote recovery. New research suggests such a
therapy could come from an unlikely target: a cellular protein called
CCR5 that allows HIV to infect cells. Scientists found that in mice,
disabling CCR5 helps surviving neurons make new connections, and that
people who carry a CCR5 mutation may recover better from a stroke. They
hope to launch a clinical trial this year that gives stroke patients an
HIV drug that blocks CCR5.
Friday, February 22, 2013
All About Monocyte Migrations
Finally a better understanding of how plaque forms. I wonder if watermelon juice contains this stuff?
http://www.medicalnewstoday.com/releases/256585.php
LMU researchers led by Christian Weber have, for the first time, elucidated how cells that promote the development of atherosclerosis find their way to the blood vessel wall, where they stimulate the formation of obstructive deposits.
Atherosclerosis is one of the commonest causes of death in modern societies. The condition is characterized by the build-up of fatty deposits called atherosclerotic plaques on the inner surfaces of arteries, which restrict, and may eventually cut off, blood flow. The deposits can also be dislodged from their site of origin and may then block major vessels in the heart or the brain, leading to life-threatening myocardial infarction or stroke.
Monocytes, an important class of white blood cells, are known to contribute significantly to the development of atherosclerosis. They are actively recruited to atherosclerotic lesions, and promote plaque development by sustaining a chronic inflammatory reaction.
Inhibition of monocyte recruitment therefore offers a way of interrupting the build-up of plaques. However, one first needs to know how the monocytes are actually localized to the vessel wall. Professor Christian Weber and Dr. Maik Drechsler of the Institute for Prophylaxis and Epidemiology of Cardiovascular Disease at LMU, in collaboration with Oliver Söhnlein of LMU and a team at the Academic Medical Center in Amsterdam, have now shown that the receptor molecules CCR1 and CCR5 are crucially involved in the process by which monocytes are recruited to the vessel wall. This process is made up of a sequence of distinct steps, including adhesion of the endothelial cells that form the arterial wall, and their subsequent transmigration into the bloodstream by infiltration between neighboring endothelial cells, following activation of the receptors by binding of their respective ligands.
The new findings correct a commonly held view of the precise function of the CCR2 receptor in the recruitment of monocytes. "In contrast to what has been assumed so far, this receptor does not mediate the infiltration of monocytes into the vessel wall; instead, like another chemokine receptor, CXCR2, it controls their mobilization from the bone marrow into the bloodstream," says Oliver Söhnlein.
The receptor molecules CCR1 and CCR5 therefore present promising targets for the development of novel approaches to the treatment of atherosclerosis, using agents that inhibit their interaction with their respective binding partners, either directly or indirectly. (EMBO Molecular Medicine)
http://www.medicalnewstoday.com/releases/256585.php
LMU researchers led by Christian Weber have, for the first time, elucidated how cells that promote the development of atherosclerosis find their way to the blood vessel wall, where they stimulate the formation of obstructive deposits.
Atherosclerosis is one of the commonest causes of death in modern societies. The condition is characterized by the build-up of fatty deposits called atherosclerotic plaques on the inner surfaces of arteries, which restrict, and may eventually cut off, blood flow. The deposits can also be dislodged from their site of origin and may then block major vessels in the heart or the brain, leading to life-threatening myocardial infarction or stroke.
Monocytes, an important class of white blood cells, are known to contribute significantly to the development of atherosclerosis. They are actively recruited to atherosclerotic lesions, and promote plaque development by sustaining a chronic inflammatory reaction.
Inhibition of monocyte recruitment therefore offers a way of interrupting the build-up of plaques. However, one first needs to know how the monocytes are actually localized to the vessel wall. Professor Christian Weber and Dr. Maik Drechsler of the Institute for Prophylaxis and Epidemiology of Cardiovascular Disease at LMU, in collaboration with Oliver Söhnlein of LMU and a team at the Academic Medical Center in Amsterdam, have now shown that the receptor molecules CCR1 and CCR5 are crucially involved in the process by which monocytes are recruited to the vessel wall. This process is made up of a sequence of distinct steps, including adhesion of the endothelial cells that form the arterial wall, and their subsequent transmigration into the bloodstream by infiltration between neighboring endothelial cells, following activation of the receptors by binding of their respective ligands.
The new findings correct a commonly held view of the precise function of the CCR2 receptor in the recruitment of monocytes. "In contrast to what has been assumed so far, this receptor does not mediate the infiltration of monocytes into the vessel wall; instead, like another chemokine receptor, CXCR2, it controls their mobilization from the bone marrow into the bloodstream," says Oliver Söhnlein.
The receptor molecules CCR1 and CCR5 therefore present promising targets for the development of novel approaches to the treatment of atherosclerosis, using agents that inhibit their interaction with their respective binding partners, either directly or indirectly. (EMBO Molecular Medicine)
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