Pre-B-cell-colony-enhancing factor is critically involved in thrombin-induced lung endothelial cell barrier dysregulation

Ye, Shui Q.; Zhang, Li Q.; Adyshev, Djanybek; Usatyuk, Peter V.; Garcia, Alexander N.; Lavoie, Tera; Verin, Alexander D.; Natarajan, Viswanathan; Garcia, Joe G.N.

doi:10.1016/j.mvr.2005.08.003

Cited by 97 publications

(91 citation statements)

References 46 publications

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“…PBEF/NAMPT is also an inflammatory mediator secreted in the development of VILI (9) and influences ARDS severity (10). Supporting the human and animal ARDS data, PBEF/NAMPT alters vascular barrier integrity via Ca 21 -dependent cytoskeletal rearrangement and enhances the inflammatory response in experimental and clinical sepsis through regulation of neutrophil apoptosis and inflammatory cytokine secretion (11,12). A number of stimuli associated with inflammation and infection (LPS, TNF-a, oxidized low-density lipoprotein, IL-1b, IL-6, and cyclic stretch) up-regulate PBEF/ NAMPT expression (4,(13)(14)(15).…”

Section: Clinical Relevancementioning

confidence: 76%

Mechanical Stress Induces Pre–B-cell Colony-Enhancing Factor/NAMPT Expression via Epigenetic Regulation by miR-374a and miR-568 in Human Lung Endothelium

Adyshev

Elangovan

Moldobaeva

et al. 2014

Am J Respir Cell Mol Biol

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Increased lung vascular permeability and alveolar edema are cardinal features of inflammatory conditions such as acute respiratory distress syndrome (ARDS) and ventilator-induced lung injury (VILI). We previously demonstrated that pre-B-cell colony-enhancing factor (PBEF)/NAMPT, the proinflammatory cytokine encoded by NAMPT, participates in ARDS and VILI inflammatory syndromes. The present study evaluated posttranscriptional regulation of PBEF/NAMPT gene expression in human lung endothelium via 39-untranslated region (UTR) microRNA (miRNA) binding. In silico analysis identified hsa-miR-374a and hsa-miR-568 as potential miRNA candidates. Increased PBEF/NAMPT transcription (by RT-PCR) and expression (by Western blotting) induced by 18% cyclic stretch (CS) (2 h: 3.4 6 0.06 mRNA fold increase (FI); 10 h: 1.5 6 0.06 protein FI) and by LPS (4 h: 3.8 6 0.2 mRNA FI; 48 h: 2.6 6 0.2 protein FI) were significantly attenuated by transfection with mimics of hsa-miR-374a or hsa-miR-568 (40-60% reductions each). LPS and 18% CS increased the activity of a PBEF/NAMPT 39-UTR luciferase reporter (2.4-3.25 FI) with induction reduced by mimics of each miRNA (44-60% reduction). Specific miRNA inhibitors (antagomirs) for each PBEF/ NAMPT miRNA significantly increased the endogenous PBEF/ NAMPT mRNA (1.4-3.4 6 0.1 FI) and protein levels (1.2-1.4 6 0.1 FI) and 39-UTR luciferase activity (1.4-1.7 6 0.1 FI) compared with negative antagomir controls. Collectively, these data demonstrate that increased PBEF/NAMPT expression induced by bioactive agonists (i.e., excessive mechanical stress, LPS) involves epigenetic regulation with hsa-miR-374a and hsa-miR-568, representing novel therapeutic strategies to reduce inflammatory lung injury.

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Section: Clinical Relevancementioning

confidence: 76%

Mechanical Stress Induces Pre–B-cell Colony-Enhancing Factor/NAMPT Expression via Epigenetic Regulation by miR-374a and miR-568 in Human Lung Endothelium

Adyshev

Elangovan

Moldobaeva

et al. 2014

Am J Respir Cell Mol Biol

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“…Furthermore, antiapoptotic effects of PBEF are documented in neutrophils (10). Regarding cytokine activities, PBEF induces IL-6 and IL-8 in amniotic cells (11), whereas down-regulation of PBEF results in inhibition of the thrombin-stimulated increase of IL-8 secretion in pulmonary artery endothelial cells (12).…”

mentioning

confidence: 99%

Pre–B cell colony‐enhancing factor/visfatin, a new marker of inflammation in rheumatoid arthritis with proinflammatory and matrix‐degrading activities

Brentano

Schorr

Ospelt

et al. 2007

Arthritis & Rheumatism

238

224

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Objective. To study possible mechanisms that mediate induction of the recently described adipocytokine pre-B cell colony-enhancing factor (PBEF) in joints of patients with rheumatoid arthritis (RA), and to analyze whether levels of PBEF correlate with disease severity and whether PBEF itself has the potential to act as a proinflammatory and destructive mediator in RA.Methods. RA synovial fibroblasts (RASFs) and monocytes were stimulated with Toll-like receptor (TLR) ligands, cytokines, and recombinant human PBEF or were transfected with PBEF expression constructs or with PBEF-specific small interfering RNA. Production of interleukin-6 (IL-6), IL-8, and tumor necrosis factor ␣ (TNF␣) was measured by enzymelinked immunosorbent assay, and expression of matrix metalloproteinases (MMPs) was assessed by real-time polymerase chain reaction. PBEF expression in synovial tissue, synovial fluid, serum, and SFs was assessed by immunohistochemistry, in situ hybridization, Western blotting, and enzyme immunoassays. Results. In RASFs, PBEF was up-regulated by

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“…[9,10] It has been reported that the level of visfatin was significantly increased in the serum and bronchoalveolar lavage fluids of mouse model with acute lung injury, [11] while the peptide products of some visfatin genes increased the risk of acute respiratory distress syndrome and mortality of critical patients in ICU. Another study [12] demonstrated that the plasma level of visfatin in patients with acute pneumonia and septicemia was significantly increased.…”

Section: Discussionmentioning

confidence: 99%

“…If the apoptosis of PMN is delayed, "respiratory burst" will occur, which leads to a vicious cycle and aggravate the SIRS. Visfatin can obviously Vol 2, No 2, 2011 inhibit the neutrophil apoptosis, [10] and the mechanism is related to the decreased activities of cysteine protease causpases-8 and causpases-3. In addition, it was found that visfatin could extend the survival time of neutrophils, activate neutrophils, increase the expression of intercellular adhesion molecule (ICAM-1) and other costimulatory molecules released by neutrophils, and enhance the adhesion of PMN with vascular endothelium.…”

Section: Discussionmentioning

confidence: 99%

Visfatin levels in patients with severe pneumonia

Xie

Shi

et al. 2011

World J Emerg Med

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Pre-B-cell-colony-enhancing factor is critically involved in thrombin-induced lung endothelial cell barrier dysregulation

Cited by 97 publications

References 46 publications

Mechanical Stress Induces Pre–B-cell Colony-Enhancing Factor/NAMPT Expression via Epigenetic Regulation by miR-374a and miR-568 in Human Lung Endothelium

Mechanical Stress Induces Pre–B-cell Colony-Enhancing Factor/NAMPT Expression via Epigenetic Regulation by miR-374a and miR-568 in Human Lung Endothelium

Pre–B cell colony‐enhancing factor/visfatin, a new marker of inflammation in rheumatoid arthritis with proinflammatory and matrix‐degrading activities

Visfatin levels in patients with severe pneumonia

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