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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Role of zyxin in the tension-induced expression change in endothelial cells

ABSTRACT: One of the hallmarks in hypertension is a pressure-induced change in endothelial cell phenotype. A cytoskeletal protein zyxin, which was seen to translocate from focal adhesion contacts to the nucleus in response to the increased wall tensionis, mediates the tension-induced endothelial signaling. Microarrays were used to detail the role of zyxin in the tension-induced expression changes in endothelial cells. Primary endothelial cells (Huvec) from four treatment groups were used for RNA extraction and hybridization on Affymetrix microarrays: wild type under normal condition, wild type under tension, Zyxin-SiRNA-treated under normal condition and Zyxin-SiRNA-treated under tension.

ORGANISM(S): Homo sapiens

SUBMITTER: Li Li

PROVIDER: E-GEOD-17814 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Zyxin mediation of stretch-induced gene expression in human endothelial cells.

Wójtowicz Agnieszka A Babu Sahana Suresh SS Li Li L Gretz Norbert N Hecker Markus M Cattaruzza Marco M

Circulation research 20100812 7

<h4>Rationale</h4>Prolonged exposure to enhanced stretch, such as in hypertension, triggers endothelial dysfunction, a hallmark of pathological vascular remodeling processes. Despite its clinical relevance, little is known about stretch-induced gene expression in endothelial cells.<h4>Objective</h4>Here, we have characterized a new stretch-inducible signaling pathway and the subsequent changes in endothelial gene expression in response to stretch.<h4>Methods and results</h4>Using human primary e ...[more]

PMID: 20705921

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Role of zyxin in the tension-induced expression change in endothelial cells

Project description:One of the hallmarks in hypertension is a pressure-induced change in endothelial cell phenotype. A cytoskeletal protein zyxin, which was seen to translocate from focal adhesion contacts to the nucleus in response to the increased wall tensionis, mediates the tension-induced endothelial signaling. Microarrays were used to detail the role of zyxin in the tension-induced expression changes in endothelial cells.

2010-08-16 | GSE17814 | GEO

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [miRNA]

Project description:Hypertrophic scars arise from dysregulated wound healing under prolonged mechanical tension, causing disfiguring fibrosis. However, limited preclinical models replicate key features of human tension-induced scarring. We developed an innovative murine model utilizing suture anchoring to impose persistent transverse-axial stretch across healing incisions, mimicking excessive wound tension that leads to hypertrophy clinically. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage while leaving wound edges on the lower back relaxed. This localized anchoring restrained wound contraction, maintaining high tension throughout remodeling analogous to scars widening under stress. Stretched upper wounds developed profound fibrotic changes compared to relaxed controls. Scars induced by suture-anchored tension displayed macroscopic hypertrophy, hardness, erythema, and pruritis up to 3 months. Histologically, scars induced by suture-anchored tension were hypercellular, hypervascular, hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. MiRNA sequencing revealed the different signature in suture-anchored tension induced hypertrophic scars compared to control normal scars.

2023-09-28 | GSE243948 | GEO

Suture-anchored cutaneous tension induces persistent hypertrophic scarring in a novel murine model [RNA-Seq]

Project description:Hypertrophic scars arise from dysregulated wound healing under prolonged mechanical tension, causing disfiguring fibrosis. However, limited preclinical models replicate key features of human tension-induced scarring. We developed an innovative murine model utilizing suture anchoring to impose persistent transverse-axial stretch across healing incisions, mimicking excessive wound tension that leads to hypertrophy clinically. Dorsal paired incisions were generated in mice, with wound edges on the upper back sutured to the rib cage while leaving wound edges on the lower back relaxed. This localized anchoring restrained wound contraction, maintaining high tension throughout remodeling analogous to scars widening under stress. Stretched upper wounds developed profound fibrotic changes compared to relaxed controls. Scars induced by suture-anchored tension displayed macroscopic hypertrophy, hardness, erythema, and pruritis up to 3 months. Histologically, scars induced by suture-anchored tension were hypercellular, hypervascular, hyperproliferative with disorganized extracellular matrix deposition, and displayed molecular hallmarks of hypertrophic fibrosis. MRNA sequencing revealed the fibrogenic signature in suture-anchored tension induced hypertrophic scars, which exhibited transcriptional overlap with mechanically-stretched scars, human hypertrophic and keloid scars.

2023-09-28 | GSE243949 | GEO

Tension-Induced Osteogenesis in periodontal ligament stem cells

Project description:Orthodontic tooth movement (OTM) relies on alveolar bone remodeling governed by periodontal ligament stem cells (PDLSCs). The mechanotransduction pathways linking mechanical tension to osteogenesis remain unknown. PIEZO1 is a mechanosensitive cation channel that plays a pivotal role in cell function regulation and fate determination. In this study, PIEZO1 knockdown and RNA sequencing were performed to reveal the mechanism of tension-induced osteogenesis.

2026-09-03 | GSE312900 | GEO

Tension sensing by FAK governs nuclear mechanotransduction, trancriptome and fate endothelial transcriptome and fate

Project description:Endothelial cell (EC) attachment to the matrix and adjacent cells generates a mechanical environment that maintains a restrictive barrier against the uncontrolled influx of circulating protein and immune cells. Mechanisms that mediate the transition from restrictive to leaky endothelium, a hallmark of tissue injury exemplified by acute lung injury (ALI), remain elusive. Here, we show that FAK sensing and transmission of mechanical tension to the EC nucleus governs cell fate. In FAK-deleted EC, increased EC tension activated DNMT3a, which induced methylation of the KLF2 promoter leading to impaired synthesis of KLF2 and restrictive EC transcriptome, including S1PR1. FAK suppressed DNMT3a activity by restricting the tyrosine phosphorylation of nuclear envelope protein, emerin at Y74/Y95, and its localization in a nuclear cap. Inhibiting emerin phosphorylation or DNMT3a activity in damaged lungs enabled KLF2 transcription of S1PR1, rescuing the restrictive EC phenotype. Our works reveal a paradigm whereby FAK sensing of tension transmission to the nucleus maintains restrictive EC transcriptome and lung homeostasis.

2022-08-28 | GSE212037 | GEO

Tissue tension fosters macrophage-driven lipid peroxidation-induced DNA damage [WES]

Project description:Tissue tension fosters macrophage-driven lipid peroxidation-induced DNA damage.

2026-03-24 | GSE318365 | GEO

Transcriptome response to oxygen tension and light irradiation in Roseobacter denitrificans OCh114

Project description:Transcriptome profiles of an aerobic photosynthetic bacterium Roseobacter denitrificans OCh114 grown under different oxygen tension and light irradiation conditions were determined by NimbleGen Prokaryotic Expression array (12x135K).

2021-06-30 | GSE152336 | GEO

Cortical actin tension regulates secretory protein trafficking and the endoplasmic reticulum stress response

Project description:We used proximity-based biotinylation assay cells to isolate candidate plasma membrane-associated proteins whose localization are sensitive to cortical tension level. Using membrane-targeting ascorbate peroxidase (APEX2-CAAX) as a bait, we mapped the proteomic landscape at the cell cortex under high and low cortical tension conditions.

2022-06-10 | PXD018975 | Pride

Importin-7 Promotes Tension-Induced Osteogenesis by Regulating RUNX2 Nuclear Translocation during Orthodontic Tooth Movement

Project description:Orthodontic tooth movement (OTM) is primarily driven by alveolar bone remodeling, wherein tension-induced osteogenesis plays a central role. Importin7 (IPO7) has been identified as a highly mechanoresponsive nuclear transport receptor (NTR). However, its role in regulating tension-induced osteogenesis during OTM and its underlying mechanism remains elusive. In the present study, cyclic tensile strain and a rat OTM model were used to investigate the role of IPO7. The results revealed that IPO7 was significantly expressed both in vitro and in vivo following exposure to mechanical stretch. Moreover, IPO7 knockdown inhibited tension-induced osteogenesis in BMSCs. Upon mechanical force stimulation, IPO7 translocated from the cytoplasm to the nucleus. Furthermore, immunoprecipitation (IP) coupled with mass spectrometry (MS) was performed and demonstrated that RUNX2 was one of the IPO7-interacting proteins related to osteogenesis. Although RUNX2 has been established to translocate to the nucleus to facilitate osteogenesis, whether it is IPO7 that regulate RUNX2 nuclear input during tension-induced osteogenesis remains to be determined. Then, the interaction between IPO7 and RUNX2 was further validated via co-immunoprecipitation (co-IP) and colocalization assays in BMSCs using immunofluorescence. Taken together, this study demonstrates that IPO7 promotes tension-induced osteogenesis by regulating the nucleoplasmic localization of RUNX2. Thus, targeting IPO7 may represent a prospective therapeutic strategy for enhancing alveolar bone remodeling and the efficacy of orthodontic treatment.

2025-10-06 | PXD061760 | Pride

Tension-Induced Osteogenesis in periodontal ligament stem cells

Project description:Tension-Induced Osteogenesis in periodontal ligament stem cells

| PRJNA1377575 | ENA