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. 2018 Feb 26;9:816. doi: 10.1038/s41467-018-03105-2

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Reconstitution of cardiomyocyte-specific Hif2a-deficient mice with recombinant amphiregulin. a–c Hif2a^loxP/loxPMyosin-Cre+ of similar age, gender, and weight as control mice were exposed to 60 min of myocardial ischemia, followed by 120 min of reperfusion; infarct sizes were measured by double staining with Evan’s blue and triphenyltetrazolium chloride and serum samples were collected. All Infarct sizes are presented as the percentage of infarcted tissue in relation to the area-at-risk. Serum troponin levels were determined by ELISA. Note that data in (a–c) in the “no treatment group” are used in part in Fig. 1c–e to display and analyze IR injury from similar experimental conditions. a Infarct sizes of Hif2a^loxP/loxPMyosin-Cre+ mice after 60 min of ischemia and 120 min reperfusion that were pre-treated with 10 µg recombinant murine AREG administered over a 15 min period via an indwelling arterial catheter or received no pharmacologic intervention. Data presented as the percentage of infarcted area in relation to area-at-risk. Statistical significance assessed by two-sided, unpaired Student’s t-test (no treatment n = 6; 10 μg AREG n = 9, data presented as mean ± SD). b Representative infarct staining of Hif2a^loxP/loxPMyosin-Cre+ that were pre-treated with 10 µg recombinant murine Areg administered over a 15 min period via an indwelling arterial catheter or received no pharmacologic intervention. c Serum troponin levels of Hif2a^loxP/loxPMyosin-Cre+ mice, after 60 min ischemia, 120 min reperfusion that were pre-treated with 10 µg recombinant murine AREG administered over a 15 min period via an indwelling arterial catheter, or received no pharmacologic intervention. Statistical significance assessed by two-sided, unpaired Student’s t-test (no treatment n = 4; 10 μg AREG n = 7, data presented as mean ± SD). d Hif2a^loxP/loxPMyosin-Cre+ or Myosin-Cre+ mice underwent 60 min myocardial ischemia, followed by 120 min of reperfusion. Then the area-at-risk was excised, protein isolated and immunoblotted for total AKT (tAKT) or phosphorylated Akt (pAKT). Two samples for each condition and genotype are presented. One representative blot out of three experiments is shown. e Quantification by densitometry of pAKT immunoblot results relative to total AKT (tAKT). Data are expressed as mean fold change ± SD normalized to Myosin-Cre+. Statistical significance assessed by two-sided, unpaired Student’s t-test (three individual blots analyzed with n = 7 mice per group)