Campus Units

Animal Science

Document Type

Article

Publication Version

Published Version

Publication Date

6-2017

Journal or Book Title

Physiological Reports

Volume

5

Issue

12

First Page

e13317

DOI

10.14814/phy2.13317

Abstract

We have previously established that 24 h of environmental hyperthermia causes oxidative stress and have implicated mitochondria as likely contributors to this process. Given this, we hypothesized that heat stress would lead to increased autophagy/mitophagy and a reduction in mitochondrial content. To address this hypothesis pigs were housed in thermoneutral (TN; 20°C) or heat stress (35°C) conditions for 1‐ (HS1) or 3‐ (HS3) days and the red and white portions of the semitendinosus collected. We did not detect differences in glycolytic muscle. Counter to our hypothesis, upstream activation of autophagy was largely similar between groups as were markers of autophagosome nucleation and elongation. LC3A/B‐I increased 1.6‐fold in HS1 and HS3 compared to TN (P < 0.05), LC3A/B‐II was increased 4.1‐fold in HS1 and 4.8‐fold in HS3 relative to TN, (P < 0.05) and the LC3A/B‐II/I ratio was increased 3‐fold in HS1 and HS3 compared to TN suggesting an accumulation of autophagosomes. p62 was dramatically increased in HS1 and HS3 compared to TN. Heat stress decreased mitophagy markers PINK1 7.0‐fold in HS1 (P < 0.05) and numerically by 2.4‐fold in HS3 compared to TN and BNIP3L/NIX by 2.5‐fold (P < 0.05) in HS1 and HS3. Markers of mitochondrial content were largely increased without activation of PGC‐1α signaling. In total, these data suggest heat‐stress‐mediated suppression of activation of autophagy and autophagosomal degradation, which may enable the persistence of damaged mitochondria in muscle cells and promote a dysfunctional intracellular environment.

Comments

This article is published as Brownstein, Alexandra J., Shanthi Ganesan, Corey M. Summers, Sarah Pearce, Benjamin J. Hale, Jason W. Ross, Nicholas Gabler et al. "Heat stress causes dysfunctional autophagy in oxidative skeletal muscle." Physiological reports 5, no. 12 (2017): e13317. doi: 10.14814/phy2.13317.

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

Copyright Owner

The Authors

Language

en

File Format

application/pdf

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