Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney
| Autor: | Hepokoski, Mark, Englert, Joshua A, Baron, Rebecca M, Crotty-Alexander, Laura E, Fuster, Mark M, Beitler, Jeremy R, Malhotra, Atul, Singh, Prabhleen |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
Vascular Endothelial Growth Factor A
Proteomics Male Kidney Disease Physiology Ventilator-Induced Lung Injury Medical Physiology Clinical Sciences Renal and urogenital Vascular Cell Adhesion Molecule-1 Bioengineering Kidney Inbred C57BL Angiopoietin-2 Mice Rare Diseases Sepsis 2.1 Biological and endogenous factors Animals Aetiology Acute Respiratory Distress Syndrome Lung Assistive Technology Animal Respiration Endothelial Cells lung-kidney crosstalk Hematology Urology & Nephrology respiratory system Up-Regulation respiratory tract diseases Infectious Diseases Disease Models Artificial Respiratory Patient Safety Inflammation Mediators Biomarkers Signal Transduction |
| Zdroj: | Hepokoski, M; Englert, JA; Baron, RM; Crotty-Alexander, LE; Fuster, MM; Beitler, JR; et al.(2017). Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 312(4), F654-F660. doi: 10.1152/ajprenal.00523.2016. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/2nj180wd American journal of physiology. Renal physiology, vol 312, iss 4 |
| DOI: | 10.1152/ajprenal.00523.2016. |
| Popis: | In critical illness, such as sepsis or the acute respiratory distress syndrome, acute kidney injury (AKI) is common and associated with increased morbidity and mortality. Mechanical ventilation in critical illnesses is also a risk factor for AKI, but it is potentially modifiable. Injurious ventilation strategies may lead to the systemic release of inflammatory mediators from the lung due to ventilator induced lung injury (VILI). The systemic consequences of VILI are difficult to differentiate clinically from other systemic inflammatory syndromes, such as sepsis. The purpose of this study was to identify unique changes in the expression of inflammatory mediators in kidney tissue in response to VILI compared with systemic sepsis to gain insight into direct effects of VILI on the kidney. Four groups of mice were compared-mice with sepsis from cecal ligation and puncture (CLP), mice subjected to injurious mechanical ventilation with high tidal volumes (VILI), mice exposed to CLP followed by VILI (CLP+VILI), and sham controls. Protein expression of common inflammatory mediators in kidneys was analyzed using a proteome array and confirmed by Western blot analysis or ELISA. VEGF and VCAM-1 were found to be significantly elevated in kidneys from VILI mice compared with sham and CLP. Angiopoietin-2 was significantly increased in CLP+VILI compared with CLP alone and was also correlated with higher levels of AKI biomarker, neutrophil gelatinase-associated lipocalin. These results suggest that VILI alters the renal expression of VEGF, VCAM-1, and angiopoietin-2, and these proteins warrant further investigation as potential biomarkers and therapeutic targets. |
| Databáze: | OpenAIRE |
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