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MEK5 is Activated by Shear Stress, Activates ERK5 And Induces KLF4 To Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells

ABSTRACT: MEK5 is activated by shear stress in large vessel endothelial cells (ECs) and contributes to the suppression of pro-inflammatory changes in the arterial wall. We used microarray analyses of total RNA from MEK5/CA-transduced HDMECs compared to LacZ control-transduced HDMECs to identify distinct classes of several regulated genes, including KLF4, eNOS, and ICAM. We conclude that MEK5 activation by shear stress may modulate inflammatory responses in the microvasculature, and these actions are partly mediated by KLF4. Total RNA was isolated from 8 separate paired (derived from same primary isolate) MEK5/CA and LacZ transduced HDMEC lines

ORGANISM(S): Homo sapiens

SUBMITTER: Adedayo Hanidu

PROVIDER: E-GEOD-25145 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MEK5 is Activated by Shear Stress, Activates ERK5 And Induces KLF4 To Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells

Project description:MEK5 is activated by shear stress in large vessel endothelial cells (ECs) and contributes to the suppression of pro-inflammatory changes in the arterial wall. We used microarray analyses of total RNA from MEK5/CA-transduced HDMECs compared to LacZ control-transduced HDMECs to identify distinct classes of several regulated genes, including KLF4, eNOS, and ICAM. We conclude that MEK5 activation by shear stress may modulate inflammatory responses in the microvasculature, and these actions are partly mediated by KLF4.

2010-12-31 | GSE25145 | GEO

Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

2013-11-03 | GSE47746 | GEO

Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

Project description:To determine if fibroblasts could be reprogrammed to a keratinocyte phenotype p63+KLF4 or LacZ expressing retroviruses were transduced into primary human neonatal fibroblasts. Global gene expression profiling using U133 plus 2.0 arrays were used to deteremine the extent of reprogramming to a keratinocyte phenoypte upon transduction with p63+KLF4. Fibroblasts transduced with p63+KLF4 were also treated +/- high calcium to determine if treatment with calcium could induce differentiation of these cells. Microarray analysis was also performed on cells treated +/- calcium. For gene expression profiling, cultured human fibroblasts were infected with LacZ or p63+KLF4 expressing retroviruses. p63+KLF4 cells were also treated +/- calcium. Microarray analysis using Affymetrix HG-U133 2.0 plus arrays was performed on duplicate samples.

2013-11-03 | E-GEOD-47746 | biostudies-arrayexpress

Homo sapiens

Project description:Gene expression data of fibroblasts transduced with LacZ or p63+KLF4.

| PRJNA207551 | ENA

KLF4 Recruits SWI/SNF to Increase Chromatin Accessibility and Reprogram the Endothelial Enhancer Landscape under Laminar Shear Stress

Project description:Physiologic laminar shear stress (LSS) induces an endothelial gene expression profile that is vasculo-protective. In this report, we delineate how LSS mediates changes in the epigenetic landscape to promote this beneficial response. We show that under LSS, KLF4 interacts with the SWI/SNF nucleosome remodeling complex to increase accessibility at enhancer sites that promote expression of homeostatic endothelial genes. By combining molecular and computational approaches we discovered enhancers that loop to promoters of known and novel KLF4- and LSS-responsive genes that stabilize endothelial cells and suppress inflammation, such as BMPR2 and DUSP5. By linking enhancers to genes that they regulate under physiologic LSS, our work establishes a foundation for interpreting how non-coding DNA variants in these regions might disrupt protective gene expression to influence vascular disease. AP-MS studies: For KLF gain-of-function, pulmonary artery endothelial cells (PAEC) were transduced with adenoviral vectors encoding a constitutively active mutant of MEK5 (caMEK5), or GFP as control. 90h post-transduction cells were lysed and AP was performed using antibodies targeting either KLF (sc166238, Santa Cruz Biotechnology) or FLAG (F7425, Millipore Sigma). Datafiles correspond to: GK: GFP-tranduced controls using anti-KLF antibodies for AP. GF: GFP-tranduced controls using anti-FLAG antibodies for AP. KK: caMEK5-transduced cells with anti-KLF antibodies for AP. KF: caMEK5-tranduced cells with anti-FLAG antibodies for AP.

2020-07-24 | MSV000085825 | MassIVE

Shear stress-induced long non-coding RNA, NIMBUSS, is required for the KLF2-mediated gene expression profile associated with vascular homeostasis II

Project description:To investigate the regulation of the long non-coding RNA (lncRNA) transcriptome of endothelial cells in response to shear stress, gene expression profiling was performed using a microarray for both protein-coding genes and lncRNAs. The expression of known flow-induced protein coding genes, eNOS, KLF2, and KLF4, were quantified using real-time PCR. Identifying lncRNAs that are up-regulated or down-regulated in the presence or absence of laminar flow will provide insight into gene regulatory mechanisms that contribute to vascular homeostasis or disease.

2024-12-01 | GSE142373 | GEO

TRAF7 is an essential regulator of vascular integrity

Project description:Targeted deletion of TRAF7 revealed that it is a crucial part of shear stress-responsive MEKK3-MEK5-ERK5 signaling pathway induced in endothelial cells by blood flow. Similarly, to Mekk3-, Mek5- or Erk5-deficient mice, Traf7-deficient embryos died in utero around midgestation due to impaired endothelial cell integrity. They displayed significantly lower expression of transcription factor Klf2, an essential regulator of vascular hemodynamic forces downstream of the MEKK3-MEK-ERK5 signaling pathway. Deletion of Traf7 in endothelial cells of postnatal mice was also associated with severe cerebral hemorrhage. Here, we show that besides MEKK3 and MEK5, TRAF7 associates with a planar cell polarity protein SCRIB. SCRIB binds with an N-terminal region of TRAF7, while MEKK3 associates with the C-terminal WD40 domain. Downregulation of TRAF7 as well as SCRIB inhibited fluid shear stress-induced phosphorylation of ERK5 in cultured endothelial cells. These findings suggest that TRAF7 and SCRIB may comprise an upstream part of the MEKK3-MEK5-ERK5 signaling pathway. Objective: to present first in vivo experimental evidence of TRAF7 function by using global and endothelium-specific TRAF7 knockout mice and comparing transcriptomes of developing embryos.

2023-06-01 | GSE229698 | GEO

Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ATAC-seq)

Project description:This data set reveals the changes of histone modifications and chromatin accessibility in human umbilical vein endothelial cells (HUVECs) under atheroprotective pulsatile shear (PS), atheroprone oscillatory shear (OS), or with KLF4 overexpression. Using ChIP-Seq, we defined the H3K27ac and H3K4me1 enrichment under PS and OS conditions. Using ATAC-seq, we identified the chromatin accessibility under KLF4 overexpression.

2020-03-11 | GSE128390 | GEO

Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ChIP-seq)

2020-03-11 | GSE128389 | GEO

Identification of NOS3 interacting proteins

Project description:The endothelial nitric oxide (NO) synthase (eNOS, or NOS3) can be activated in response to fluid shear stress and numerous agonists via cellular events such as increased intracellular Ca2+, interaction with substrate, co-factors as well as adaptor and regulatory proteins, protein phosphorylation and S-glutathionylation in addition to shuttling between distinct sub-cellular domains. While some protein interactors modulate enzymatic activity, others can be S-nitrosation targets, which are brought in close proximity to the NO source under specific conditions. The identification of proteins interacting with eNOS in human endothelial cells stimulated with serum and growth factors may provide new insight into the regulation of eNOS activity as well as NO signaling via S-nitrosation.

2021-09-08 | PXD013755 | Pride

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