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Mouse lung fibroblasts were isolated according to described protocols (Seluanov et al., 2010).
Similar to thrombin, factor Xa increased fibroblast proliferation in human and mouse lung fibroblasts [ 311, 321, 325], and stimulated procollagen-alpha 1 (I) promoter activity and procollagen production in human and mouse lung fibroblasts [ 325].
These effects on collagen were mediated via PAR-1, since factor Xa had no effect on procollagen production in PAR-1 deficient mouse lung fibroblasts [ 325].
Purified mouse lung fibroblasts in DMEM containing 10% calf serum were seeded into 96-well plates and grown in a humidified atmosphere containing 5% CO2.
In mouse lung fibroblasts and macrophages, Akt exhibited control over necroptosis-associated TNF α production but did not have a role in cell death.
CD47/IAP is also shown to be necessary for the electrophysiological response of mouse lung fibroblasts and OV10 carcinoma cells to mechanical stimulation.
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Nanotoxicity evaluation of this multifunctional nHAp carried out on primary human endothelial cells (HUVEC), normal mouse lung fibroblast cell line (L929), human nasopharyngeal carcinoma (KB) and human lung cancer cell line (A549) revealed no apparent toxicity even upto relatively higher doses of 500 μg/mL and 48 h of incubation.
In serum-free medium, only the addition of growth factors could initiate mouse lung fibroblast proliferation [ 16].
In the present work, transfection studies were undertaken with a human ovarian carcinoma cell line and a mouse lung fibroblast cell line, rather than human chondrocytes, in an attempt to provide additional understanding of CD47/IAP involvement in cellular mechanotransduction.
For instance, the response of specific mouse strain-derived lung fibroblasts to asbestos rather than bleomycin as the injurious agent showed that lung fibroblasts from the 129 mouse strain proliferated less than those from the C57BL/6 and SJL strain and showed a reduced response in terms of cell proliferation to PDGF [ 54].
Kitamura, H. et al. Mouse and human lung fibroblasts regulate dendritic cell trafficking, airway inflammation, and fibrosis through integrin αvβ8-mediated activation of TGF-β.
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