CD36 is Involved in Astrocyte Activation and Astroglial Scar Formation

Abstract

Inflammation is an essential component for glial scar formation. However, the upstream mediator(s) that triggers the process has not been identified. Previously, we showed that the expression of CD36, an inflammatory mediator, occurs in a subset of astcotyes in the peri-infarct area where the glial scar forms. This study investigates a role for CD36 in astrocyte activation and glial scar formation in stroke. We observed that the expression of CD36 and glial fibrillary acidic protein (GFAP) coincided in control and injured astrocytes and in the brain. Furthermore, GFAP expression was attenuated in CD36 small interfering RNA transfected astrocytes or in the brain of CD36 knockout (KO) mice, suggesting its involvement in GFAP expression. Using an in-vitro model of wound healing, we found that CD36 deficiency attenuated the proliferation of astrocytes and delayed closure of the wound gap. Furthermore, stroke-induced GFAP expression and scar formation were significantly attenuated in the CD36 KO mice compared with wild type. These findings identify CD36 as a novel mediator for injury-induced astrogliosis and scar formation. Targeting CD36 may serve as a potential strategy to reduce glial scar formation in stroke.

Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia

“…In particular, CD36, a class B scavenger receptor, has been implicated in pathological conditions associated with inflammation including stroke and Alzheimer's disease (El Khoury et al, 2003;Febbraio et al, 2000;Kim et al, 2008). This receptor is expressed in many different cell types such as microglia, astrocytes, microvascular endothelial cells, monocytes/macrophages, and platelets (Bao et al, 2012). It has been reported that the activation of astrocytes may be regulated by the presence and function of these transporters (Glatz et al, 2010).…”

Central Nervous System Resident Cells in Neuroinflammation: A Brave New World.

“…However, it has been recently demonstrated that CD36 plays a pivotal role in astrocytic survival, and proliferation In fact, CD36 deficient and CD36 -siRNA treated animals had reduced astrogliosis and wound healing. Thus, it is now accepted that CD36 signaling intimately correlates with astroglial proliferation (Bao Y 2012).…”

Expression of Peroxiredoxin 1 After Traumatic Spinal Cord Injury in Rats

“…During SCI, astrocytes perform proliferation, hypertrophy, and migration (Wu et al 2012;Yin et al 2012). Astrocytes that over-activated would result in formation of glial scar and secretion of multiple neurotoxic molecules which hold back the neuroregeneration after injury (Bao et al 2012). Our study indicated that injury-evoked PRDX1 was expressed in reactive astrocytes in rat spinal cord, while the previous research suggested that PRDX1 was not expressed in astrocytes of mouse brain (Jin et al 2005).…”