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Nerve cells saved from damage by disappearing and reappearingprotein - Multi Port KVM Switch by grehh hernjer





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Nerve cells saved from damage by disappearing and reappearingprotein - Multi Port KVM Switch by
Article Posted: 05/13/2013
Article Views: 42
Articles Written: 1951
Word Count: 595
Article Votes: 0
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Nerve cells saved from damage by disappearing and reappearingprotein - Multi Port KVM Switch


 
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According to researchers at Johns Hopkins, a protein created by thecentral nervous system's support cells (glia) appears to protectnerve cells from damage in two different ways. The study ispublished in Proceedings of the National Academy of Sciences (PNAS) . Reducing the proteins activity appears to trigger glia cells toincrease their protective powers. However, the team found thatincreasing its activity seems to be vital for using those powers toprotect cells from danger.

Glia cells have long been thought to play a vital role inprotecting cells from death after an acute injury, such as a blowto the head, or chronic damage, such as that cause by Parkinson'sor Alzheimer's disease , according to Seth Blackshaw, Ph.D., an associate professor in theSolomon H. Snyder Department of Neuroscience at the Johns HopkinsUniversity School of Medicine. For several decades, glia cells were thought to help hold thecentral nervous system together. When nearby neurons are exposed toan assault, glia cells respond by increasing in size and switchingoff several genes involved in routine maintenance functions. According to earlier studies, when glia cells and neurons areexposed to an assault, the reaction of the glia appeared to power aresponse that protects cells from further damage.

However, whatglia cells are doing when they change in size and gene expressionand whether this response is vital for protection remains unclear,states Blackshaw. Blackshaw notes that it has been impossible for researchers toinvestigate this so-called glial reactivity without treating wholetissues that include neurons and other types of cells that mayapply their own protective effects. As a result, the researchers set out to identify proteins thatcould play a vital role in triggering glial reactivity withoutassaulting entire tissues. In the study the researchers used Mueller glia as their modelsystem as they are extremely likely to act like other gliathroughout the central nervous system. These glia are the mostabundant type in the retina.

The team identified a protein called Lhx2. In mutant mice thatselectively lacked Lhx2 in the glia of the eye, the team found thatthese cells showed the physical and genetic characteristics ofbeing constantly reactive, even without any damaging stimulus.However, they discovered that shinning an extremely bright lightinto the into the animals eyes caused significantly more damage totheir retinas than in normal mice. In order to determine why these reactive glia didn't produce aprotective response, the team set out to identify otherpro-survival proteins that glia cells produce when under attack.These other proteins were missing in the mutant mice, thusindicating that Lhx2 is vital for glia to produce other protectiveproteins, said Blackshaw. Blackshaw explained: "Lhx2 seems to be a master regulator of glialreactivity, and we've shown here that it has two faces." Although the absence of Lhx2 appears to be vital for stimulatingthe physical and genetic changes glia use to protect and helpneurons survive, the presence of Lhx2 is crucial for production ofthese proteins in the first place.

According to Blackshaw, when glia is exposed to an attack, levelsof Lhx2 activity likely drop and then increase, explaining both theinitial glial reactivity researchers see under a microscope as wellas the resulting neural protection. Once this mechanism is understood better, researchers may be ableto develop drugs that trigger glia to generate more pro-survivalproteins, creating new treatments for neurodegenerative diseases,said Blackshaw. Written By Grace Rattue Copyright: Medical News Today Not to be reproduced without permission of Medical News Today Additional References Citations.

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