Accession Number : ADA581642


Title :   Role of Adenosine Receptor A2A in Traumatic Optic Neuropathies


Descriptive Note : Annual rept. 1 Dec 2011-30 Nov 2012


Corporate Author : AUGUSTA STATE UNIV GA


Personal Author(s) : Liou, Gregory I ; Ahmad, Saif ; Naime, Mohammad ; Fatteh, Nadeem ; Khan, Sohail


Full Text : http://www.dtic.mil/dtic/tr/fulltext/u2/a581642.pdf


Report Date : Dec 2012


Pagination or Media Count : 13


Abstract : Our goal is to develop an early therapeutic intervention before the progression of traumatic optic neuropathy (TON), a vision-threatening complication in head injury, becomes irreversible. Under the stress of TON, extracellular levels of adenosine increase due to its increased formation by ecto-5 -nucleotidase (CD73) or decreased metabolism by the intracellular adenosine kinase (AK). Intracellular adenosine is then released through equilibrative nucleoside transporter (ENT). Extracellular adenosine activates an anti-inflammatory pathway through adenosine receptor A2AAR. TON is likely due to an imbalance in adenosine formation and metabolism. We report here how we determine whether AK or CD73 contributes in causing this imbalance. We have demonstrated that hypoxia-induced microglia activation is inhibited by inhibitors of MAP Kinases (ERK and P38) or AK. We have also shown that hypoxia-induced CD73 up-regulation suppresses microglia activation. We now tested the hypothesis that in an in vivo model of TON at least adenosine metabolism by AK contributed to this imbalance.


Descriptors :   *ADENOSINE , *HEAD(ANATOMY) , *VISION , *WOUNDS AND INJURIES , HYPOXIA , INFLAMMATION , METABOLISM , PHOSPHORUS TRANSFERASES , RECEPTOR SITES(PHYSIOLOGY)


Subject Categories : Anatomy and Physiology
      Medicine and Medical Research
      Organic Chemistry


Distribution Statement : APPROVED FOR PUBLIC RELEASE