Kinins are produced and act at the site of injury and inflammation in various tissues. They are likely to initiate a particular cascade of inflammatory events, which evokes physiological and pathophysiological responses including an increase in blood flow and plasma leakage. In the central nervous system (CNS), kinins are potent stimulators of the production and release of pro-inflammatory mediators represented by prostanoids and cytotoxins. They are known to induce neural tissue damage. Many of the cytotoxins such as cytokines and free radicals and prostanoids are released from glial cells. Among glial cells, astrocytes and oligodendrocytes are known to possess bradykinin (BK) B2 receptors that phosphoinositide (PI) turnover and raise intracellular Ca2+ concentration. The presence of bradykinin receptors in microglia has been of great significance. We recently showed that rat primary microglia express kinin receptors. In resting microglia, B 2 receptors but not B1 receptors are expressed. When the microglia are activated by bradykinin, B1 receptors are up-regulated, while B2 receptors are down-regulated. As observed in other glial cells, electrophysiological measurements suggest that B2 receptors in phosphoinositide turnover and intracellular Ca2+ concentration in microglia. Release of cytotoxins is likely consequent upon the activation of BK receptors. Our study provides the first evidence that microglia express functional kinin receptors and suggests that microglia play an important role in CNS inflammatory responses.
All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience
- Cell Biology