Nigel
Bradley
Subcellular localization of B-Catenin and SNAIL in Endothelial Cells under Normoxia Pulmonary hypertension (PH) is a progressive disease marked by pulmonary vascular remodeling, endothelial dysfunction, and increased pulmonary arterial pressure. One of the contribution mechanisms is endothelial to mesenchymal transition (EndMT). The process includes the attribution of mesenchymal
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Nigel Bradley
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characteristics by endothelial cells (ECs). -catenin and Snail are key drivers in this transition, yet their subcellular localization under PH remain unclear. This study aims to investigate the expression and localization of -catenin and Snail in pulmonary endothelial cells under normoxic conditions. Human pulmonary arterial endothelial cells (HPAECs) will be cultured and followed up by immunofluorescence (IF) staining. The cells will then be imaged and analyzed using ImageJ in order to quantify -catenin and Snail levels in both the cytoplasm and nucleus. We hypothesize that under normoxic conditions -catenin and Snail will exhibit limited nuclear localization and remain local to the cytoplasm. This stabilization of location is consistent with a neutral endothelial state, where EndMT associate transcription factors are inactive. Establishing this control localization is paramount to being able to comprehend the effects of varying pathological conditions, such as hypoxia, inflammation, the dysregulation of bone morphogenic protein receptors (BMPR) and oxidative stress. These findings will serve as a baseline and reference point for assessing how domestic and environmental stressors disrupt EC homeostasis drive vascular remodeling and how the principle contributes to pulmonary hypertension. Nihil Suthy:
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Claflin university / Leadership Alliance-Summer Research Early Identification Program (SR-EIP), FYRE First year research experience
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Nigel Bradley