Abstract
Pressure ulcers are characterized by chronicity, which results in delayed wound healing due to pressure. Early intervention for preventing delayed healing due to pressure requires a prediction method. However, no study has reported the prediction of delayed healing due to pressure. Therefore, this study focused on biological response-based molecular markers for the establishment of an assessment technology to predict delayed healing due to pressure. We tested the hypothesis that sustained compressive loading applied to three dimensional cultured fibroblasts leads to upregulation of heat shock proteins (HSPs), CD44, hyaluronan synthase 2 (HAS2), and cyclooxygenase 2 (COX2) along with apoptosis via disruption of adhesion. First, sustained compressive loading was applied to fibroblast-seeded collagen sponges. Following this, collagen sponge samples and culture supernatants were collected for apoptosis and proliferation assays, gene expression analysis, immunocytochemistry, and quantification of secreted substances induced by upregulation of mRNA and protein level. Compared to the control, the compressed samples demonstrated that apoptosis was induced in a time- and load- dependent manner; vinculin and stress fiber were scarce; HSP90α, CD44, HAS2, and COX2 expression was upregulated; and the concentrations of HSP90α, hyaluronan (HA), and prostaglandin E2 (PGE2) were increased. In addition, the gene expression of antiapoptotic Bcl2 was significantly increased in the compressed samples compared to the control. These results suggest that compressive loading induces not only apoptosis but also survival activity. These observations support that HSP90α, HA, and, PGE2 could be potential molecular markers for prediction of delayed wound healing due to pressure.
Highlights
A recent study indicates that the prevalence of pressure ulcer (PU) is 13.7% in all care settings, including acute, long-term, rehabilitation, and home care settings [1]
We investigated candidates of molecular markers in order to predict delayed wound healing due to pressure focusing on cellular responses along with apoptosis triggered by the disruption of adhesion for the first time
Our results revealed that sustained compressive loading reduced the cell number and notably induced apoptosis in a time- and load-dependent manner
Summary
A recent study indicates that the prevalence of pressure ulcer (PU) is 13.7% in all care settings, including acute, long-term, rehabilitation, and home care settings [1]. This unacceptably high prevalence may be related to its chronicity, representing delayed wound healing due to pressure, which mainly inhibits tissue granulation in the wound healing process. A PU is continuously exposed to pressure as noted in its definition that PU is a localized damage to the skin and the underlying tissue, mainly caused by continuous exposure to pressure [2]. Some studies about delayed wound healing related with malnutrition or infection has reported [5], no study has reported the prediction of delayed wound healing due to pressure
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