Key result
Acute ischemia/reperfusion pressure ulcers in mice increase ADAMTS-5 expression ~3-fold and upregulate proinflammatory cytokines.
Why the study?
To characterize the early inflammatory cytokine profile and explore the potential role of ADAMTS-5 in extracellular matrix remodeling in an acute ischemia/reperfusion-induced pressure ulcer model.
Does acute ischemia/reperfusion injury increase the mRNA expression of pro-inflammatory cytokines and ADAMTS-5 in a mouse pressure ulcer model?
Does acute ischemia/reperfusion injury increase the mRNA expression of pro-inflammatory cytokines and ADAMTS-5 in a mouse pressure ulcer model?
Proinflammatory cytokines and ADAMTS-5 are activated early during pressure ulcer formation following ischemia/reperfusion injury, suggesting a role for early extracellular matrix degradation.
Suggests early inflammatory targets for pressure ulcer prevention; hypothesis-generating in this animal model and requires human validation.
Objectives: This study aimed to determine the messenger ribonucleic acid (mRNA) expression levels of interleukin (IL)-1α, IL-1β, IL-6, IL-17, and A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) -5 in an acute ischemia/reperfusion (I/R)-induced pressure ulcer (PU) model, in order to characterize the early inflammatory cytokine profile and explore the potential role of ADAMTS-5 in extracellular matrix (ECM) remodeling. Patients and Methods: Ten BALB/c mice were randomly allocated to control and PU groups. Acute PUs were generated on the dorsal skin using a repeated I/R protocol achieved with ceramic magnetic plaques. Skin biopsies obtained from ulcerated and control areas were examined histologically using hematoxylin-eosin staining. mRNA expression levels of IL-1α, IL-1β, IL-6, IL-17, and ADAMTS-5 were analyzed by quantitative real-time PCR and compared statistically between groups. Results: Compared with controls, mRNA expression levels of IL-1α, IL-6, IL-17, and ADAMTS-5 were significantly increased in the PU group (p<0.05). In contrast, IL-1β expression showed an increase that did not reach statistical significance. Conclusion: These findings indicate that proinflammatory cytokines and ADAMTS-5 are activated early during PU formation following I/R injury. The observed upregulation of ADAMTS-5, a molecule that has been rarely examined in PU models, suggests a possible role for early ECM degradation in ulcer development. Further experimental and clinical studies are warranted to clarify the relevance of these pathways for PU progression and targeted local therapies.
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Sağlam et al. (2026) studied Pressure ulcer (n=10). Acute ischemia/reperfusion-induced pressure ulcer model vs. Control (normal skin) was evaluated on ADAMTS-5 mRNA expression (p=0.014). Acute ischemia/reperfusion-induced pressure ulcers in mice significantly upregulated the mRNA expression of proinflammatory cytokines (IL-1α, IL-6, IL-17) and ADAMTS-5 compared to controls.
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