Fig. 5

Schematic diagram showing astrocytic KLF4 regulating the activation of A1/A2 reactive astrocytes following ischemic stroke. After stroke onset, astrocytes are excessively activated. The classically activated astrocytes (A1 subtype) exert neurotoxic effects by releasing pro-inflammatory mediators, such as iNOS, TNF-α and IL-1β, while alternatively activated astrocytes (A2 subtype) perform neuroprotective effects by secreting anti-inflammatory mediators, such as Arg1, IL-1ra and IL-10. Of interest, astrocytic KLF4 inhibited activation of C3 positive A1 astrocytes but promoted S100A10 positive A2 astrocytes polarization following ischemic stroke by modulating expressions of nuclear factor-kB