Fig. 1 MT-2 ameliorates asthmatic pulmonary resistance.

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Fig. 1 MT-2 ameliorates asthmatic pulmonary resistance. MT-2 ameliorates asthmatic pulmonary resistance. (A) Western blot analyses of metallothionein-2 (MT-2) protein in control and asthmatic lung tissues from ovalbumin (OVA)–sensitized and OVA-challenged rats. Lower panel: Mean density of MT-2 normalized to β-actin (*P < 0.05 versus control, t test; n = 5 per group). (B) Pulmonary resistance (R) in wild-type (WT) and metallothionein knockout (MT-KO) OVA-sensitized mice challenged with vehicle (control) or OVA. (*P < 0.05 versus control and #P < 0.05 versus WT mice challenged with OVA, n = 8 per group). (C) Gel of purified rat MT-2 recombinant protein and molecular weight markers (M). (D) Pulmonary resistance peak value sum of 2 to 4 min (sR2–4) for OVA-challenged rats without treatment (Con) or treated with terbutaline (TB; 0.055 mg/kg), hydrocortisone (HC; 15 mg/kg), or MT-2 (1, 10, and 100 ng/kg). (*P < 0.05 versus Con, n = 8 per group). (E) Isometric tension of isolated tracheal spirals at baseline (control without challenge or treatment), challenged with acetylcholine without treatment (ACh) or treated with TB (1500 nM) or MT-2 (15, 30, and 60 nM) (*P < 0.05 versus ACh and #P < 0.05 versus TB, n = 5 per group). (F) Collagen gel contraction assays of rat airway smooth muscle cells (ASMCs) at baseline (control without treatment) or treated with TB (10,000 nM) or MT-2 (15, 30, and 60 nM) (*P < 0.05 versus baseline, n = 3 per group). (G) Real-time cell analysis of rat ASMCs at baseline (control without challenge or treatment), challenged with acetylcholine without treatment (ACh) or treated with TB (10,000 nM) or MT-2 (60 nM) (*P < 0.05 versus ACh and #P < 0.05 versus TB, n = 4 per group). All data are expressed as means ± SEM. Statistical analyses were performed by one-way analysis of variance (ANOVA) with the Games-Howell/least significant difference (LSD) post hoc test. Lei-Miao Yin et al., Sci Transl Med 2018;10:eaam8604 Published by AAAS