Dataset Information

Longitudinal evaluation of biomarkers in wound fluids of venous leg ulcers treated with a protease-modulating wound dressing

ABSTRACT: Venous leg ulcers (VLU) represent a clinical challenge and impair the patient’s quality of life. Venous insufficiency is underlying the protracted healing. We report the protein expression pattern for biomarkers in VLU wound fluids and compare these with acute split-thickness wound fluids. Fifty-seven patients with VLU were recruited and treated for 12 weeks with a protease-modulating polyacrylate wound dressing and a two-layer bandage compression system. Ten patients with acute wounds were followed for 21 days. Wound size decreased from 18.7 ± 12.3 cm2 to 11.75 ± 11.39 cm2 in the VLU cohort, 10 wounds healed completely. Relative wound area reduction reached 48.9% ± 51.9% at week 12. 61.4% of the patients achieved a relative wound area reduction of ≥40% and 50.9% a relative wound area reduction of ≥60%. IL-1beta, TNF-alpha, and MMP9 concentration ranges were similar in VLU and acute wound fluids. Concentrations of S100A8, S100A9, neutrophil elastase, MMP2, and fibronectin were elevated in VLU wound fluids and decreased significantly in abundance after two weeks of treatment. The values remained low, yet, higher than those of acute wounds. Collagen (I) alpha1 abundance was higher in VLU wound fluids and not significantly regulated. Our data show a robust healing response in venous leg ulcers treated with a protease-modulating polyacrylate wound dressing. The biomarker pattern in VLU wound fluids changed within the first two weeks and we speculate that this might reflect a decrease of STAT3 influence in the wound bed.

ORGANISM(S): Homo Sapiens

SUBMITTER: Ulrich auf dem Keller

PROVIDER: PXD025748 | panorama | Tue Aug 22 00:00:00 BST 2023

REPOSITORIES: PanoramaPublic

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Publications

Longitudinal Evaluation of Biomarkers in Wound Fluids from Venous Leg Ulcers and Split-thickness Skin Graft Donor Site Wounds Treated with a Protease-modulating Wound Dressing.

Mikosiński Jacek J Kalogeropoulos Konstantinos K Bundgaard Louise L Larsen Cathrine Agnete CA Savickas Simonas S Moldt Haack Aleksander A Pańczak Konrad K Rybołowicz Katarzyna K Grzela Tomasz T Olszewski Michał M Ciszewski Piotr P Sitek-Ziółkowska Karina K Twardowska-Saucha Krystyna K Karczewski Marek M Rabczenko Daniel D Segiet Agnieszka A Buczak-Kula Patrycja P Schoof Erwin M EM Eming Sabine A SA Smola Hans H Auf dem Keller Ulrich U

Acta dermato-venereologica 20221213

Venous leg ulcers represent a clinical challenge and impair the quality of life of patients. This study examines impaired wound healing in venous leg ulcers at the molecular level. Protein expression patterns for biomarkers were analysed in venous leg ulcer wound fluids from 57 patients treated with a protease-modulating polyacrylate wound dressing for 12 weeks, and compared with exudates from 10 acute split-thickness wounds. Wound healing improved in the venous leg ulcer wounds: 61.4% of the 57 ...[more]

PMID: 36250733

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Project description:Acute lung injury (ALI), a major cause of acute respiratory failure with high morbidity and mortality, isare characterized by significant pulmonary inflammation and both alveolar and vascular barriers dysfunction. In Pprior studies have highlighted the role of nonmuscle myosin light chain kinase (nmMLCK) as an essential element of inflammatory response with MYLK polymorphisms associated withwhich alters ALI susceptibility. In the present study we sought to further define nmMLCK in acute inflammatory syndromes and examined We examined nmMLCK as a molecular target involved in increase of lung epithelial and endothelial barrier permeability. We utilized in two muirine models of inflammatory lung injury: intratracheal administration of endotoxin/lipopolysaccharide (LPS, 2.5 mg/kg) and VILI (ventilator-induced lung injury, tidal volume 40ml/kg). Two complementary strategies were used to reduce nmMLCK activity or expression. We found that membrane permeant oligopeptide, PIK, inhibited MLC kinase activity in vitro in aand displayed dose-dependent mannerinhibition of MLC kinase activity.. Intravenous delivery of PIK significantly attenuated LPS-induced lung inflammation reflected by decreasing accumulation of bronchoalveolar lavage (BAL) albumin (~ 50% reduction) as well as reduction in BAL cells, tissue MPO activity and tissue albumin in lung homogenates. A second regulatory approach explored targeting murine nmMLCK by administration of siRNA (5mg/kg) 3 days prior to LPS challenge. siRNA decreased of nmMLCK expression in lungs (~ 70% reduction) and resulted in significant attenuation LPS-induced lung inflammation (~ 40% reduction) as reflected by decreased BAL protein level and BAL cells. For targeting pulmonary vessels nmMLCK we used ACE antibody-conjugated liposomes with nmMLCK siRNA in murine ventilator-induced lung injury (VILI) model. Protein silencing of nmMLCK was evident by immunohistochemical analysis with a decrease in relative intensity of fluorescence in lung vessels compared with control animals. Furthermore, the inhibition of nmMLCK expression by siRNA in vessels significantly attenuated VILI lung injury as reflected by decreased BAL protein level (40% reduction). Finally, MLCK knockout mice were significantly protected (reduced BAL protein and albumin) when exposed to a model of severe VILI (4h, 40ml/kg tidal volume). Conclusion: the MLCK gene KO and chemical biology results indicate that the targeting of nmMLCK in vivo attenuate the severity of LPS-induced or VILI acute lung injury. We used microarrays to detail the global programme of gene expression induced by VILI in Wild type and nmMLCK-/- mouse. Experiment Overall Design: four group (n=3) of animals were treated by SB (Spontaneouse breathing) or VILI (4 hours, 30 ml/kg tidal volume) in Wild type or nmMLCK-/- animals;

Dataset Information

Longitudinal evaluation of biomarkers in wound fluids of venous leg ulcers treated with a protease-modulating wound dressing

Publications

Longitudinal Evaluation of Biomarkers in Wound Fluids from Venous Leg Ulcers and Split-thickness Skin Graft Donor Site Wounds Treated with a Protease-modulating Wound Dressing.

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