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We investigated the effects of visfatin/Nampt on murine osteoblasts for the first time.
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Given the shared genetic and phenotypic features present in MOA and the Mmp2−/− mice, we hypothesized that genetic analysis of MMP-2-deficient murine osteoblasts would provide an excellent model system for investigating the molecular pathways that might be altered in both the mouse model and human disease.
Primary murine osteoblasts (OB) were treated with L51P, BMP2, and Noggin.
The bio-functionality of the coatings has been tested using the correlated characteristics of the coatings with MC3T3-E1 murine osteoblasts response in vitro.
Our results demonstrate that TGF-β1 can decrease TNF-α-induced apoptosis in murine osteoblasts at least in part by attenuating TNF-α-induced caspase gene expression.
To determine the effect of chondroitin sulfate (CS) on inflammatory mediators and proteolytic enzymes induced by interleukin-1β (IL-1β) and related to cartilage catabolism in murine osteoblasts.
Murine osteoblasts express high levels of MIF [ 13].
Interestingly, CREB was not detectible in CnOb, highlighting possible interspecies differences when compared to murine osteoblasts.
Studies in osteoblast cells lines and in murine osteoblasts suggest that hypoxia can mediate osteoblast activity (22, 23), but to our knowledge, the effect of hypoxia on primary osteoblasts isolated from patients with OA has not been reported.
Also, murine osteoblasts do not have TRIF signaling and these studies suggest that TLR signaling in osteoblasts only use MyD88-dependent pathway.
Runx2 can also be negatively regulated by some members of the miR-23a/27a/24-2 cluster in murine osteoblasts [ 62].
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