KA-induced SE was most robustly associated with an alteration in the abundance of proteins involved in neuroinflammation, including heat shock protein beta-1 (HSP27), glial fibrillary acidic protein, and CD44 antigen.
In the present study, we found that the lacking of P2rx7 led to prolonged astroglial HSPB1 induction due to impaired mitogen-activated protein kinase 1/2 (MAPK1/2)-mediated specificity protein 1 (SP1) phosphorylation, following kainic acid-induced SE.
Interestingly, while Hsp32 and Hsp70 expression was transient, Hsp25 demonstrated a sustained induction pattern, which may reflect an additional role of Hsp25 in subsequent remodeling events in the days following SE.