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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: KLF4 alleviates cerebral vascular injury by ameliorating vascular endothelial inflammation and regulating tight junction protein expression following ischemic stroke

Fig. 5

Cellular localization of KLF4 expression and co-expression of KLF4 with Claudin-5 on cerebral blood vessels after focal cerebral ischemia. Images show the dual-IF staining for KLF4 with CD31, GFAP, Mac-1, or Claudin-5 in the ischemic hemisphere from sham-operated mice or mice at days 2 and 7 post-ischemia. Scale bar = 100 μm (inserts = 40 μm). Note that KLF4 immunoreactivity was observed in CD31-positive vessels in the ischemic hemisphere at days 2 and 7 post-ischemia. At day 2 post-ischemia, KLF4 co-localized extensively with Mac-1-positive microglia/inflammatory macrophages in the ischemic hemisphere, especially in the core (core = C); at day 7, the co-expression of KLF4 with activated microglia/inflammatory macrophages can still be seen in the ischemic hemisphere, including the penumbra (penumbra = P) and the core (core = C). Furthermore, KLF4 expression always strongly co-localized with cells expressing high levels of GFAP in the ischemic penumbra (penumbra = P) at days 2 and 7 post-ischemia, especially at day 7, but this co-localization was significantly reduced in the ischemic core (core = C) (a). Meanwhile, KLF4 expression co-localized with Claudin-5 on the blood vessels in the ischemic hemisphere at days 2 and 7 post-ischemia (b)

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