Preconditioning With Electrical Stimulation Promotes Flap Survival by Improving Blood Supply Via ROS/Nrf2/HO1 Pathway
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PROVIDER: PRJNA1176028 | ENA |
REPOSITORIES: ENA
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Project description:We have previously demonstrated that preconditioning flap donor with electrical stimulation (ES) could increase the survival area of pedicled perforator flaps in a rat model. However, the detailed molecular mechanisms remain unclear. In this study, we first verified the effects of ES through in vivo and in vitro experiments. Then we explored the underlying mechanisms in vitro. The results indicated that preconditioning with ES could not only increase the flap survival area but mitigate human umbilical vein endothelial cells (HUVECs) dysfunction. Furthermore, low level reactive oxygen spices (ROS) were produced in HUVECs after ES, serving assignaling molecule to activate the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HOl) pathway. Then ROS scavenger was used to attenuate thegeneration of ROS, resulting that activation of the Nrf2/HOl pathway was inhibited. These results suggest that ROS/Nrf2/HO1 pathway may play pivotal roles in the ES pretreatment induced flap survival.
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Project description:Deletion of the flap loop in the Rp2 subunit of human RNAPII did not alter the ability of human RNAPII to initiate transcription or elongate the initiated transcripts in vivo and in vitro, and was also dispensable for elongation factor-mediated enhancement and inhibition of transcript elongation in vitro. ChIP:chip of wild-type and flap deletion human RNAPII revealed that the mutant RNAPII was not defective for promoter binding, initiation and elongation in vivo. Eight ChIP datasets were generated as log2(IP/input) fluorescence intensities using anti-FLAG IP of wild-type RPB2-FLAG cells in biological triplicate, anti-FLAG IP of delta-FL RPB2 FLAG cells in biological triplicate, and anti-RPB1 CTD, 8WG16 of both wild-type and delta-FL cells in biological duplicate. The two 8WG16- IP datasets were combined to measure the distribution of RPB1 signal.
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