Fig. 5: Inhibition of mitochondrial H₂O₂ abrogates AT2 MCU depletion.

a, b Group data are for baseline AT2 mitochondrial H₂O₂ production following nonlethal LPS (1 mg/kg) instillations. mCAT^F/F, mice floxed for mitochondrial catalase (mCAT): AT2^CAT+/+, mice expressing mCAT in AT2. In b, determinations were made 24 h after indicated instillations. LPS was instilled at a nonlethal dose (1 mg/kg). Bars: mean ± SEM. n = 4 lungs for each group. Groups were compared using one-way ANOVA with Bonferroni correction. c MCU immunoblots and densitometry of AT2 mitochondria from lungs given intranasal PBS or nonlethal LPS (1 mg/kg). Lungs were excised and AT2 isolated 24 h after instillations. Bars: mean ± SEM. n = 3 lungs for each group. Groups were compared using one-way ANOVA with Bonferroni correction. d–f Group data show in situ determinations of AT2 cytosolic (cCa²⁺) and mitochondrial (mCa²⁺) calcium (d), surfactant secretion (e) and lung inflammation (f). All determinations were made 24 h after intranasal instillations. LPS was instilled at a nonlethal dose (1 mg/kg). Bars: mean ± SEM. n = 4 lungs each bar. Groups were compared using one-way ANOVA with Bonferroni correction. n.s., not significant. g Kaplan-Meier plots are for mouse survival after instillations of ALI-inducing lethal LPS (50 mg/kg). n = 10 mice in each group, *p = 0.027 versus mCAT^F/F. p-value is calculated by Log-Rank test.