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. 2021 Aug 18;218(10):e20202151. doi: 10.1084/jem.20202151

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© 2021 Huen et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure S3. — Effects of FGF21 deficiency on cardiac markers of inflammation, fatty acid oxidation, acute stress response, and cell apoptosis during endotoxemia. Fgf21^fl/fl and Alb-Cre;Fgf21^fl/fl (Fgf21^ΔLiv) mice given vehicle or 5 mg/kg i.p. LPS treatment, whole heart tissue harvested 20 h after vehicle or LPS treatment. (A) RA of mRNA expression, shown relative to Rpl13a. Vehicle (Veh), n = 7/group; LPS, n = 14–15/group. mRNA data are pooled from four independent experiments. (B) Whole heart tissue protein lysates immunoblotted for caspase-3. Positive control (+ctrl) generated from Hepa1-6 cells treated with 5 μM staurosporine for 24 h. Representative blot from one of two independent experiments. (C) Quantification of TUNEL-positive cells per 400×-power field. n = 5/vehicle group, n = 6/LPS group; data are pooled from two independent experiments. Data are expressed as mean percentage of TUNEL-positive cells per total cells per high-power field (hpf). (D) Representative images of heart sections from the left ventricle using TACS Blue Labeling to stain TUNEL-positive cells and Nuclear Fast Red heart to stain nuclei. Terminal deoxynucleotidyl transferase enzyme was omitted for the unlabeled negative control. TACS-nuclease treatment was used for the positive control. Scale bars represent 100 µm. Two-way ANOVA with Sidak’s multiple comparisons tests were not statistically significant (A and C). Data are expressed as mean ± SEM.