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Int. J. Mol. Sci. 2016, 17(3), 284; doi:10.3390/ijms17030284

Pressure Combined with Ischemia/Reperfusion Injury Induces Deep Tissue Injury via Endoplasmic Reticulum Stress in a Rat Pressure Ulcer Model

1
Department of Nursing, the Affiliated Dongyang People’s Hospital of Wenzhou Medical University, Jinhua 322100, China
2
Department of Nursing School, Wenzhou Medical University, Wenzhou 325035, China
3
School of Pharmacy, Key Laboratory of Biotechnology and Pharmaceutical Engineering, Wenzhou Medical University, Wenzhou 325035, China
4
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
5
Department of Computer Science and Information Engineering, Asia University, Taichung 41354, Taiwan
6
Department of Nursing, The Affiliated Xinhua Hospital of Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Chris Jackson
Received: 4 January 2016 / Revised: 16 February 2016 / Accepted: 17 February 2016 / Published: 25 February 2016
(This article belongs to the Special Issue Inflammatory Skin Conditions)
View Full-Text   |   Download PDF [3440 KB, uploaded 25 February 2016]   |  

Abstract

Pressure ulcer is a complex and significant health problem in long-term bedridden patients, and there is currently no effective treatment or efficient prevention method. Furthermore, the molecular mechanisms and pathogenesis contributing to the deep injury of pressure ulcers are unclear. The aim of the study was to explore the role of endoplasmic reticulum (ER) stress and Akt/GSK3β signaling in pressure ulcers. A model of pressure-induced deep tissue injury in adult Sprague-Dawley rats was established. Rats were treated with 2-h compression and subsequent 0.5-h release for various cycles. After recovery, the tissue in the compressed regions was collected for further analysis. The compressed muscle tissues showed clear cellular degenerative features. First, the expression levels of ER stress proteins GRP78, CHOP, and caspase-12 were generally increased compared to those in the control. Phosphorylated Akt and phosphorylated GSK3β were upregulated in the beginning of muscle compression, and immediately significantly decreased at the initiation of ischemia-reperfusion injury in compressed muscles tissue. These data show that ER stress may be involved in the underlying mechanisms of cell degeneration after pressure ulcers and that the Akt/GSK3β signal pathway may play an important role in deep tissue injury induced by pressure and ischemia/reperfusion. View Full-Text
Keywords: pressure ulcer; deep tissue injury; endoplasmic reticulum stress; Akt/GSK3β pathway; rat model pressure ulcer; deep tissue injury; endoplasmic reticulum stress; Akt/GSK3β pathway; rat model
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MDPI and ACS Style

Cui, F.-F.; Pan, Y.-Y.; Xie, H.-H.; Wang, X.-H.; Shi, H.-X.; Xiao, J.; Zhang, H.-Y.; Chang, H.-T.; Jiang, L.-P. Pressure Combined with Ischemia/Reperfusion Injury Induces Deep Tissue Injury via Endoplasmic Reticulum Stress in a Rat Pressure Ulcer Model. Int. J. Mol. Sci. 2016, 17, 284.

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