Fig. 6: LPS causes mitochondrial fragmentation.

a, b In mice expressing mitochondria-targeted dendra-2, we detected AT2 in terms of the lamellar body (LB) localizing dye, LTR. In the PBS-treated lung (alveoli marked by dotted lines), an AT2 is selected in the low magnification image (rectangle). Images i-iii show the AT2 at high magnification, displaying polarized mitochondrial aggregation. LBs co-mingle with mitochondria at the indicated site (arrow). Images v and vii display the channel for mitochondrial fluorescence in AT2 in a lung given intranasal instillation of nonlethal LPS (1 mg/kg, 24 h), and a lung that was given Mdivi-1 prior to the LPS treatment. Images iv, vi, and viii show distribution of mitochondrial fluorescence along the depth axes (y-z). Mitochondrial density was quantified in the depth axis at sites of highest mitochondrial aggregation along the selected lines (dashed lines). Scale bar, 5 µm. Bars: mean ± SEM. n = 20 cells from 4 lungs each bar. Groups were compared using one-way ANOVA with Bonferroni correction. c, d, Phosphorylated Ser616-Drp1 (c) and Drp1 (d) immunoblots and densitometry are for freshly isolated AT2 mitochondria following indicated treatments. LPS was instilled at a nonlethal dose (1 mg/kg). Drp1, dynamin-related protein 1; pSer616, phosphorylated serine 616. Bars: mean ± SEM. n = 4 and 3 lungs each bar respectively, in c and d. In c, p-values are for two-tailed Student’s t-test. In d, groups were compared using one-way ANOVA with Bonferroni correction.