Thus, HIF-1α in CFs provides a critical braking mechanism against excessive post-ischemic CF activation and proliferation through regulation of mitochondrial ROS.
The mitochondrial-targeted antioxidant MitoTEMPO rescued Hif-1a mutant phenotypes. A combination of Matlab, ImageMagick, and Avi-Synth scripts were used to process the data and generate videos and.
#Andor solis video contrast generator#
CF proliferation was associated with higher reactive oxygen species (ROS) as occurred also in wild-type mice treated with the mitochondrial ROS generator MitoParaquat (MitoPQ). Videos were recorded using Andor SOLIS software (for the EMCCD) and VideoHome Technology GrabBee (for the color camera, in conjunction with a StarTech SVID2USB2NS analog video capture cable). Andor Solis T is the option for time resolved work and has additional features to enable control of the iStar camera range.
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After myocardial infarction (MI), however, there was ∼50% increased CF proliferation and excessive scarring and contractile dysfunction, a scenario replicated in 3D engineered cardiac microtissues. Images were acquired on Nikon Eclipse Ti2E microscope fitted with an Andor Zyla 4.2+ camera using Nikon NIS-Elements AR software (4.00.00 build 764 LO, 64 bit) and 20 × objective (Nikon, CFI S Plan Fluor LWD 20XC, Air immersion, 0.7 NA). Andor Solis I provides the user with full control over Andor’s wide range of imaging cameras. CF-specific deletion of Hif-1a resulted in decreased HIF-1 target gene expression and increased mesenchymal progenitors in uninjured hearts and increased CF activation without proliferation following sham injury, as demonstrated using single-cell RNA sequencing (scRNA-seq).
We report that cardiac fibroblasts (CFs) and mesenchymal progenitors are more hypoxic than other cardiac interstitial populations, express more hypoxia-inducible factor 1α (HIF-1α), and exhibit increased glycolytic metabolism.
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