David
An
86 Program for Research in Science and Engineering KLF2 Regulates Endothelial Cell Size and Morphology
Abstract profile. Full document pending author claim.
Authors:
David An, Guillermo Garc a-Carde a
Date Created:
2025-01-01
Course Title:
Professor:
Not specified
About Paper:
Atherosclerosis develops in regions of disturbed flow, such as Ad-mKLF2 cells showed a 22% increase in surface area (95% bifurcations or curves, where endothelial cells (ECs) exhibit CI: 15%-26%) and adopted a more elongated morphology, a altered gene expression and cuboidal morphology. Suppression shape linked to improved alignment to shear stress and enhanced of kruppel-like factor 2 (KLF2), critical for EC physiology, is a barrier function. While control cells proliferated by 29% over 48 hallmark of these areas. Endothelial cell size, influencing vessel hours(95%CI:9%-48%), mKLF2cellsprioritizedgrowthwithout diameter, perfusion, and vascular responses, is also affected by division, with unchanged nuclear size ruling out senescence or flow. Although KLF2’s role in regulating EC size has been DNA damage. A positive correlation between GFP intensity and shown in zebrafish, its effects on human EC size, morphology, and cell area supports a direct role for KLF2 in modulating cell size downstream targets remain poorly understood. andshape. NosignificantsizedifferencebetweenAd-mKLF2cells with or without L-NAME indicates eNOS is not a key determinant. Human umbilical vein endothelial cells (HUVECs) were We are now examining hundreds of downstream genes to further transduced with murine KLF2 (mKLF2) or GFP-only control elucidate this regulatory network and identify additional pathways vectors under static conditions. Epifluorescent imaging was used: Cellpose enabled segmentation and quantification of cell area, involved. while PolarityJam analyzed morphological features including These findings establish KLF2 as a key regulator of EC size and eccentricity, axis ratio, and orientation. NOS3 expression was morphology, independent of eNOS, and lay the groundwork for quantified in four groups: Ad-GFP control, Ad-mKLF2, Ad- future studies on additional KLF2-regulated pathways to restore mKLF2 with L-NAME (an eNOS inhibitor), and Ad-GFP with vascular homeostasis and combat atherosclerosis. L-NAME.
Abstract:
Atherosclerosis develops in regions of disturbed flow, such as Ad-mKLF2 cells showed a 22% increase in surface area (95% bifurcations or curves, where endothelial cells (ECs) exhibit CI: 15%-26%) and adopted a more elongated morphology, a altered gene expression and cuboidal morphology. Suppression shape linked to improved alignment to shear stress and enhanced of kruppel-like factor 2 (KLF2), critical for EC physiology, is a barrier function. While control cells proliferated by 29% over 48 hallmark of these areas. Endothelial cell size, influencing vessel hours(95%CI:9%-48%), mKLF2cellsprioritizedgrowthwithout diameter, perfusion, and vascular responses, is also affected by division, with unchanged nuclear size ruling out senescence or flow. Although KLF2’s role in regulating EC size has been DNA damage. A positive correlation between GFP intensity and shown in zebrafish, its effects on human EC size, morphology, and cell area supports a direct role for KLF2 in modulating cell size downstream targets remain poorly understood. andshape. NosignificantsizedifferencebetweenAd-mKLF2cells with or without L-NAME indicates eNOS is not a key determinant. Human umbilical vein endothelial cells (HUVECs) were We are now examining hundreds of downstream genes to further transduced with murine KLF2 (mKLF2) or GFP-only control elucidate this regulatory network and identify additional pathways vectors under static conditions. Epifluorescent imaging was used: Cellpose enabled segmentation and quantification of cell area, involved. while PolarityJam analyzed morphological features including These findings establish KLF2 as a key regulator of EC size and eccentricity, axis ratio, and orientation. NOS3 expression was morphology, independent of eNOS, and lay the groundwork for quantified in four groups: Ad-GFP control, Ad-mKLF2, Ad- future studies on additional KLF2-regulated pathways to restore mKLF2 with L-NAME (an eNOS inhibitor), and Ad-GFP with vascular homeostasis and combat atherosclerosis. L-NAME.
Source:
Harvard / Isabelle Agarwal, Kaylee Wells, Lee Rubin / 2025
Topics:
cell, klf2, size, morphology, endothelial, area, control, human, enos, atherosclerosi, flow, gene
