Fig. 5: MiR-98 can inhibit the microglial phagocytosis of “stress but viable” neurons after ischemic stroke through downregulating PAFR. | Cell Death & Disease

Fig. 5: MiR-98 can inhibit the microglial phagocytosis of “stress but viable” neurons after ischemic stroke through downregulating PAFR.

From: Neuronal extracellular vesicle derived miR-98 prevents salvageable neurons from microglial phagocytosis in acute ischemic stroke

Fig. 5

a–b The procedure and localization of intracerebroventricular injection of miR-98 agomir (negative control) in mice. c The representative of miR-98 expression in the ipsilateral regions 1 day and 3 days after ischemic stroke with miR-98 agomir treatment in FISH. (Scale Bar = 200 μm). d The representative immunostainings and Z-stack images of NeuN, IBA1, and PAFR colocalization in mice brain slices of sham group. e–f The representative immunostainings and Z-stack images of NeuN, IBA1, and PAFR colocalization in mice brain slices of mice with NC/miR-98 agomir treatment 1 day after ischemic stroke. g–j The representative immunostainings and Z-stack images, 3D reconstructions of NeuN, IBA1, and PAFR colocalization in mice brain slices of mice with NC/miR-98 agomir treatment 3 days after ischemic stroke. These Z-stack images and 3D reconstructions of original pictures were required by a Confocal Microscopy or two-photon Microscope. (n = 3 independent experiments). k–m Quantification of the fluorescent %area of PAFR and NeuN and microglial engulfment 3 days after ischemic stroke with NC/miR-98 agomir treatment. Data are shown as means±S.E.M., *P < 0.05 vs corresponding control.

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