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. 2017 Mar 24;18:53. doi: 10.1186/s12931-017-0536-7

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 4 — Expression of the autophagic marker, LC3, is upregulated in the RV of the MCT rat model. a, b RT-qPCR of LC3 mRNA expression relative to GAPDH in RV (left) and LV (right) tissue of control and MCT-treated rats. GAPDH was used as a loading control. c, d Representative RV tissue sections immunostained for LC3 protein (dark brown) in control and MCT-treated rats. Note: Dark brown granules in myocardial cell cytoplasm. Black scale represents 50 μm (×200 original magnification). e, f Quantification of LC3 positive protein signal (integrated optical density) in RV (left) and LV (right) tissue sections per field area. g Correlation of pulmonary artery systolic pressure with LC3 positive protein signal in 2, 4, and 6 week MCT-treated rats. ^* P < 0.05, ^** P < 0.01. Values are presented as mean ± standard deviation