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  • TRPV4 channels augment macrophage activation and ventilator-induced lung injury
  • Hamanaka K; Jian MY; Townsley MI; King JA; Liedtke W; Weber DS; Eyal FG; Clapp MM; Parker JC
  • Am J Physiol Lung Cell Mol Physiol 2010[Sep]; 299 (3): L353-62
  • We have previously implicated transient receptor potential vanilloid 4 (TRPV4) channels and alveolar macrophages in initiating the permeability increase in response to high peak inflation pressure (PIP) ventilation. Alveolar macrophages were harvested from TRPV4(-/-) and TRPV4(+/+) mice and instilled in the lungs of mice of the opposite genotype. Filtration coefficients (K(f)) measured in isolated perfused lungs after ventilation with successive 30-min periods of 9, 25, and 35 cmH(2)O PIP did not significantly increase in lungs from TRPV4(-/-) mice but increased >2.2-fold in TRPV4(+/+) lungs, TRPV4(+/+) lungs instilled with TRPV4(-/-) macrophages, and TRPV4(-/-) lungs instilled with TRPV4(+/+) macrophages after ventilation with 35 cmH(2)O PIP. Activation of TRPV4 with 4-alpha-phorbol didecanoate (4alphaPDD) significantly increased intracellular calcium, superoxide, and nitric oxide production in TRPV4(+/+) macrophages but not TRPV4(-/-) macrophages. Cross-sectional areas increased nearly 3-fold in TRPV4(+/+) macrophages compared with TRPV4(-/-) macrophages after 4alphaPDD. Immunohistochemistry staining of lung tissue for nitrotyrosine revealed increased amounts in high PIP ventilated TRPV4(+/+) lungs compared with low PIP ventilated TRPV4(+/+) or high PIP ventilated TRPV4(-/-) lungs. Thus TRPV4(+/+) macrophages restored susceptibility of TRPV4(-/-) lungs to mechanical injury. A TRPV4 agonist increased intracellular calcium and reactive oxygen and nitrogen species in harvested TRPV4(+/+) macrophages but not TRPV4(-/-) macrophages. K(f) increases correlated with tissue nitrotyrosine, a marker of peroxynitrite production.
  • |*Macrophage Activation[MESH]
  • |Animals[MESH]
  • |Disease Susceptibility[MESH]
  • |Genotype[MESH]
  • |Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism[MESH]
  • |Immunohistochemistry/methods[MESH]
  • |In Vitro Techniques[MESH]
  • |Lung/metabolism[MESH]
  • |Macrophages, Alveolar/metabolism/pathology/transplantation[MESH]
  • |Mice[MESH]
  • |Mice, Knockout[MESH]
  • |Permeability[MESH]
  • |Phorbol Esters/pharmacology[MESH]
  • |Pulmonary Edema/physiopathology[MESH]
  • |Pulmonary Ventilation[MESH]
  • |Reactive Nitrogen Species/metabolism[MESH]
  • |Reactive Oxygen Species/metabolism[MESH]
  • |Staining and Labeling[MESH]
  • |TRPC Cation Channels/agonists/deficiency/*metabolism[MESH]
  • |Tyrosine/analogs & derivatives/metabolism[MESH]
  • |Ventilator-Induced Lung Injury/pathology/*physiopathology[MESH]





  • *{{pmid20562229}}
    *<b>[http://www.kidney.de/mlpefetch.php?search=20562229 TRPV4 channels augment macrophage activation and ventilator-induced lung injury ]</b> Am J Physiol Lung Cell Mol Physiol 2010; 299(3) ; L353-62 Hamanaka K; Jian MY; Townsley MI; King JA; Liedtke W; Weber DS; Eyal FG; Clapp MM; Parker JC

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    Am J Physiol Lung Cell Mol Physiol

    L353 3.299 2010