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Furthermore, a greatly reduced vascular density was observed, along with higher levels of α-smooth muscle actin expression in stromal cells.
The effect of transferrin on stellate cell activation was assessed using western blot analysis for α-smooth muscle actin expression, [3H]Thymidine incorporation, and real-time RT-PCR for procollagen α1(I) mRNA expression.
While cyclic strain reduced both vimentin and alpha-smooth muscle actin compared to unstrained controls, vimentin and alpha-smooth muscle actin expression increased with strain anisotropy and correlated with direction (P < 0.05).
The encapsulated VIC in pure HA hydrogels with lower mechanical stiffness showed a more spreading morphology compared to their stiffer counterparts and dramatically up-regulated alpha smooth muscle actin expression, indicating more activated myofibroblast properties.
Study Design: Immunohistochemical methods were used to evaluate cell proliferation, vascular density, and α-smooth muscle actin expression by stromal cells in a group of 9 age-matched intrauterine growth restricted and control placentas at 25 to 41 weeks of gestation.
CD123+(high endothelial venules) endothelial cells significantly decreased (p = 0.01) after HDIT/HCT in scleroderma patients, although smooth muscle actin expression was not (p = 0.08).
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Activation of alpha-smooth muscle actin (SMA) expression, a cytoskeleton protein normally expressed only in myoepithelial cells, is considered a landmark for the activation of stromal fibroblasts with little however being known regarding the mechanism governing the expression of SMA in the stroma.
Exogenous soluble heparin prevented serum-dependent activation of the classic mitogen-activated protein kinase (MAPK) and induced myofibroblast alpha smooth muscle actin (αSMA) expression and collagen production.
In vitro studies of individual cytokines on fibroblasts has revealed a variety of roles for these cytokines in the regulation of the fibrotic process, such as mitogenic activity, stimulation of extracellular matrix and alpha-smooth muscle actin gene expression, alteration of the contractile phenotype, production of proteases, protease inhibitors, chemokines, cytokines and growth factors [7].
α-Smooth muscle actin (SMA) expression was evaluated on 96 well plates (cell surface ELISA) as previously reported [ 16- 18].
Reduced α-smooth muscle actin (αSMA) expression and matrix metalloproteinase 2 (MMP2) activity in the DDR2-/ wound extracts indicated defective recruitment of skin fibroblasts.
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