Regulation of glial inflammatory mediators synthesis: Possible role of endothelins

Talia Filipovich, Sigal Fleisher-Berkovich

    Research output: Contribution to journalArticlepeer-review

    17 Scopus citations


    Endothelins are well known as modulators of inflammation in the periphery, but little is known about their possible role in brain inflammation. Stimulation of astrocyte prostaglandin, an inflammatory mediator, synthesis was shown so far only by endothelin 3 (ET-3). By contrast, several studies showed no change or slight decrease of basal nitric oxide synthesis after treatment of astrocytes with endothelin 1 (ET-1) and ET-3. However, a significant increase in astrocytic and microglial nitric oxide synthase (NOS) was observed after exposure to ET-1 and ET-3 in a model of forebrain ischaemia. Here we demonstrate that all three endothelins (ET-1, ET-2, ET-3) significantly enhanced the synthesis of prostaglandin E2 and nitric oxide in glial cells. Each of the selective antagonists for ETA and ETB receptors (BQ123 and BQ788 respectively), significantly inhibited endothelins-induced production of both nitric oxide and prostaglandin E2. These results suggest a regulatory mechanism of endothelins, interacting with both endothelin receptors, on glial inflammation. Therefore, inhibition of endothelin receptors may have a therapeutic potential in pathological conditions of the brain, when an uncontrolled inflammatory response is involved.

    Original languageEnglish
    Pages (from-to)2250-2256
    Number of pages7
    Issue number12
    StatePublished - 1 Dec 2008


    • Brain inflammation
    • Endothelins
    • Glial cells
    • Nitric oxide
    • Prostaglandin E


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