C78 FIBROSIS: MEDIATORS AND MODULATORS: Uncovering The Mysteries Of S100a4 In Fibrosis: Activation And Localization Of Non-Muscle Myosin li Drives Myofibroblast Differentiation

Immunofluorescence or immunoblotting was used to quantify/localize filamentous (F)-actin, alpha-smooth muscle actin (aSMA), NMIIA, and activated myosin (pMLC) in lung fibroblasts. pMLC was quantified by IB (± TGFß) and traction force microscopy on 25 kPa PA gels was performed in primary human lung f...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2017-01, Vol.195
Main Authors: Southern, B D, Grove, L M, Scheraga, R G, Abraham, S, Niese, K A, Mansoor, S, Rosenfeld, S S, Olman, M A
Format: Article
Language:English
Subjects:
Fibroblasts
Localization
Rodents
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Summary:Immunofluorescence or immunoblotting was used to quantify/localize filamentous (F)-actin, alpha-smooth muscle actin (aSMA), NMIIA, and activated myosin (pMLC) in lung fibroblasts. pMLC was quantified by IB (± TGFß) and traction force microscopy on 25 kPa PA gels was performed in primary human lung fibroblasts from normal and IPF patients. Results: As expected, WT fibroblasts developed central F-actin stress fibers with increased incorporation of activated NMIIA and aSMA in response to PA gels of pathophysiologic stiffness (replicating the range of normal to fibrotic lung, 1-25 kPa), and these effects were augmented by TGFß.
ISSN:1073-449X
1535-4970