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Aortic Valve Endothelium Mechanobiology
Published in Juhyun Lee, Sharon Gerecht, Hanjoong Jo, Tzung Hsiai, Modern Mechanobiology, 2021
Rachel L. E. Adams, Craig A. Simmons
KLF2 is a transcription factor predominantly expressed by endothelial cells exposed to shear stress. Well known as atheroprotective, KFL2 regulates pathways that mediate vascular tone [136] and vascular adhesion [137, 138]. In human endothelial cells, KLF2 expression has been shown to be induced by atheroprotective shear stress and not by atheroprone inflammatory cytokines, such as TNF-α4 and IL-1β5 [139]. In vascular endothelial cells exposed to atheroprotective or atherosusceptible waveforms of the vasculature, KLF2 was one of the most responsive genes upregulated by atheroprotective waveforms [140]. KLF2 functions through many pathways, including those involved in angiogenesis, inflammation, oxidative stress, and immune regulation [136]. To date, knowledge of the protective role of KLF2 signaling pathways in aortic valve homeostasis is incomplete.
Nanomaterial-induced toxicity in pathophysiological models representative of individuals with pre-existing medical conditions
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Sreejesh Sreedharan, Georgios Zouganelis, Samantha J Drake, Gyanendra Tripathi, Ali Kermanizadeh
In an in vitro study, the toxic properties of a PEGylated Au nanorod (length approximately 50 nm, diameter approximately 25 nm) were investigated in human umbilical vein endothelial cells with or without LPS stimulus at concentrations of 10 µg/ml of NMs for 24 hr (Li et al. 2019). No significant influence of LPS in terms of NM-induced cytotoxicity or in material uptake was detected. However, Li et al. (2019) noted that KLF2 (Kruppel-like factor a transcription factor important for maintenance of function of vascular walls) was significantly down-regulated by treatment with LPS. Further, mRNA levels of MCP-1 were almost 8-fold higher in LPS and NM-treated cells as compared to NMs alone (Li et al. 2019).