Figure 7.

Inflammatory gene expression and parameters of lung injury were mitigated by Krüppel-like factor 2 (KLF2) transient overexpression in vivo. (A) mRNA expression for Klf2, Rapgef3, Nos3, Tm, Ccl2, Ccl4, and Cxcl2 in mice transfected with KLF2-overexpressing plasmid or control plasmid with or without LPS administration. Mice were transfected with KLF2-overexpressing plasmid or control plasmid via tail vein injection before intratracheal administration with 0.7 mg/kg LPS for 24 hours and killed to collect lung tissues for RNA isolation followed by quantitative real-time polymerase chain reaction. KLF2 overexpression ameliorates Klf2, Rapgef3, and Nos3 reduction by LPS, and reduces up-regulation of Ccl2, Ccl4, and Cxcl2 by LPS. n = 4–5. All data are represented as fold change. Circles represent control plasmid/without LPS; squares represent KLF2-overexpressing plasmid/without LPS; triangles pointing up represent control plasmid/LPS; and triangles pointing down represent KLF2-overexpressing plasmid/LPS. Error bars represent ± SEM. Measurement of bronchoalveolar lavage (BAL) cell count (B) and BAL protein concentration (C) in mice transfected with KLF2-overexpressing plasmid or control plasmid with or without LPS administration. KLF2 overexpression reduces lung injury induced by LPS as measured by protein leak and cell counts. All data are represented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, Student’s t test. Ccl2 = C-C motif chemokine ligand 2; Ccl4 = C-C motif chemokine ligand 4; Cxcl2 = C-X-C motif chemokine ligand 2; ctrl = control; NOS3 = nitric oxide synthase; PBS = phosphate-buffered saline; RAPGEF3 = Rap guanine nucleotide exchange factor 3; TM = thrombomodulin.