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Figure 4 | Journal of Neuroinflammation

Figure 4

From: Traumatic brain injury enhances neuroinflammation and lesion volume in caveolin deficient mice

Figure 4

Caveolin (Cav)-1 knock-out (KO) and Cav-3 KO mice have different microglial and astrocyte populations. Primary mixed glia were cultured from brains from wild-type (WT), Cav-1 KO and Cav-3 KO postnatal day 3 pups. (A) Western blot (WB) analysis of GFAP (glial fibrillary acidic protein) and Iba1 (ionized calcium-binding adapter molecule 1) in primary mixed glia cultures normalized to GAPDH. (B) Immunofluorescence microscopy of GFAP (green) and Iba1 (red) in primary mixed glia cultures. Nuclei were stained with DAPI. (C) Sections of hippocampal CA1 and dentate gyrus (DG) regions from WT, Cav-1 KO and Cav-3 KO mice labeled with Iba1 (left) and GFAP (right). (D) Sections of hippocampal CA1 region with the neuronal dendritic marker MAP2 (microtubule associated protein 2). (E) Quantitation of cell numbers from n = 3 animals. A statistically significant increase in Iba1 cells is found in Cav-3 KO mice compared to WT (P < 0.01, left graph). A significant decrease in GFAP labeling is found in Cav-3 KO mice compared to Cav-1 KO (P < 0.01, middle graph), and a trending decrease when compared to WT (not significant). A statistically significant increase in MAP2 labeling is also detected in Cav-3 KO versus Cav-1 KO (P < 0.01, right graph). Data displayed as mean ± SEM. (F) Bottom panels are quantitative WB analysis of Iba1, GFAP and β3-tubulin from mouse hippocampi. Statistically significant increased expression of Iba1 and β3-tubulin and decreased GFAP expression was detected in Cav-3 KO mice. Conversely, decreased Iba1 expression was observed in Cav-1 KO.

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