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

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.

[Expressions of tumor necrosis factor-alpha and NF-kappa B in skeletal muscles and its effect on apoptosis in deep tissue injury of rats].

Objective: To evaluate the changes of tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) expression in muscle of pressure ulcer rats and explore the relationship with apoptosis.

Methods: Fifty-four male SD rats were randomly divided into nine groups (n = 6), the experiment groups were pressed 9 circles (3 circles/day, 3 days), then observed on the 1st, 3rd, hematoxylin and eosin staining under the microscope; the expression of TNF-alpha was detected by Western blot; the expressions of NF-kappaB and caspase-3 were determined by immunohistochemistry, and evaluated the relationship of TNF-alpha with NF-kappaB and caspase-3; the number of apoptotic cells in compressed muscle tissue was detected by Hoechst 33258 staining under the fluorescence microscope.

Results: Compared with the control group, histology examination showed that the tissue structure in experiment groups was in disorder, inter-space was wider, cell edema and the number of inflammatory cells were increased, the tissue was arranged in order and inflammatory cell recruitment was gradually attenuated.

[Effects of endoplasmic reticulum stress related proteins and their mediated apoptosis in the formation of deep tissue injury of pressure ulcer in rats].

Objective: To explore the effects of endoplasmic reticulum stress (ERS) related proteins and their mediated apoptosis in the formation of deep tissue injury of pressure ulcer in rats.

Methods: Forty male Sprague-Dawley rats were divided into normal control group and groups A, B, C, D according to the random number table, with 8 rats in each group. Rats in group A were loaded with 22.

[Expressions of vascular endothelial growth factor and basic fibroblast growth factor in the late stage of pressure ulcer].

Objective: To study the distribution and expressions of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in the III-IV stage of pressure ulcer wound, and to explore their correlation with ulceration.

Methods: Forty-one patients hospitalized in the two Affiliated Hospital of Wenzhou Medical College from June 2010 to March 2012 were recruited, including twenty-one patients with 23 pressure ulcer of stage III-IV, 14 acute injury patients, and 6 donors of normal skin. Samples harvested from the 41 patients through surgery were divided into four groups, including pressure ulcer centre group (n = 23), pressure ulcer margin group (n = 23), acute wound group (n = 14), and normal skin group (n = 6).

Deubiquitination of CXCR4 by USP14 is critical for both CXCL12-induced CXCR4 degradation and chemotaxis but not ERK ativation.

The chemokine receptor CXCR4 plays important roles in the immune and nervous systems. Abnormal expression of CXCR4 contributes to cancer and inflammatory and neurodegenerative disorders. Although ligand-dependent CXCR4 ubiquitination is known to accelerate CXCR4 degradation, little is known about counter mechanisms for receptor deubiquitination.