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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Inhibition of leucine-rich repeats and calponin homology domain containing 1 accelerates microglia-mediated neuroinflammation in a rat traumatic spinal cord injury model

Fig. 2

LRCH1 knockdown enhances the expression of pro-inflammatory cytokines in primed microglia. a GFP expression in lentivirus-infected microglia. Non, non-infected microglia. L-P−, lentiviral infection without puromycin selection. L-P+, lentiviral infection followed by puromycin selection. Note that only the cells infected with control lentivirus are shown here. The data are representative of two independent experiments. b LRCH1 protein in microglia after lentiviral infection and puromycin selection. LC, cells infected with control lentivirus. LL, cells infected with LRCH1 shRNA-encoding lentivirus. The data are representative of two independent experiments. c Microglia apoptosis and necrosis after lentiviral infection. The data are representative of three independent experiments. d mRNA levels of indicated cytokines in microglia after lentiviral infection. ns, non-significant. n = 3 in 3 independent experiments. e LRCH1 mRNA in microglia before (0) or after (1 or 6 h) priming with LPS + ATP. n = 4 in 3 independent experiments. f–h Concentrations of indicated cytokines in the supernatants of lentivirus-infected microglia culture after 6 h priming. Un, no priming. LPS + ATP, priming. n = 6 in 3 independent experiments. i Concentrations of indicated cytokines in the supernatant-lysate mixtures of lentivirus-infected microglia culture. n = 5 in 3 independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001 in comparison to the “LC” group under the same conditions

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