Free Radicals, Stroke and AngiogenesisDr. Carli Roulston
Bernard O'Brien Institute
(03) 9288 4023
carlir@unimelb.edu.au
http://bobim.org/index.php?option=com_content&task=blogcategory&id=38&Itemid=57Although it is becoming increasingly evident that inhibiting Reactive Oxygen Species (ROS) in the early stages of stroke and reperfusion may prevent the progression of injury, inhibition in the later phase of recovery may indeed prevent optimal histological and function recovery.
NADPH oxidase is a major source of ROS in the vasculature and recently we have identified in the injured brain two homologues of this enzyme, Nox2 and Nox4, which are up-regulated in the early stages of reperfusion concurrently with increased superoxide generation and progression of injury. However, in addition to their deliterious effects, ROS also act as signaling molecules in many aspects of growth factor-mediated physiological responses. Recent reports suggest that ROS play an important role in angiogenesis, a process imperative for tissue regeneration. In this project we will examine angiogenesis following focal ischaemia and reperfusion in the later phase of recovery in conjuntion with assessing the role of NAPDH oxidase and superoxide generation in the process.
Publications: Miller AA, Dusting GJ, Roulston CL, Sobey CG (2006) NADPH-oxidase activity is elevated in penumbral and non-ischemic cerebral arteries following stroke. Brain Res. 1111 (1): 111-116
Jiang F, Drummond GR, Dusting GJ (2004) Suppression of oxidative stress in the endothelium and vascular wall. Endothelium. 11(2):79-88.
Ushio-Fukai M, Alexander RW (2004) Reactive oxygen species as mediators of angiogenesis signaling: role of NAD(P)H oxidase. Molecular & Cellular Biochemistry. 264(1-2):85-97.
Plate KH (1999) Mechanisms of angiogenesis in the brain. Journal of Neuropathology & Experimental Neurology. 58(4):313-320.
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