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Analysis of transcriptome in normoxia/hypoxia(21d)-exposed lungs upon KO of Nfat5 in ECs

ABSTRACT: Analysis of transcriptome in normoxia/hypoxia(21d)-exposed lungs upon KO of Nfat5 in ECs

PROVIDER: PRJNA957294 | ENA |

REPOSITORIES: ENA

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Analysis of transcriptome in normoxia/hypoxia(21d)-exposed lungs upon KO of Nfat5 in ECs

Project description:Chronic hypoxic stress stimulates lung endothelial cells to promote vascular remodeling processes, which - in the long run - increase the resistance of pulmonary arteries. While several molecular determinants promoting these maladaptive changes have been delineated, their transcriptional regulation is not well studied. In this context, we revealed that hypoxia activates nuclear factor of activated T-cells 5 (NFAT5/TonEBP) in murine lung endothelial cells (MLECs) - a transcription factor that regulates the adjustment of the cellular transcriptome to cope with osmotic, biomechanical or metabolic environmental stressors. Here, we studied the functional relevance of NFAT5 for the control of endothelial hypoxic stress responses in the lung. Genetic ablation of Nfat5 in endothelial cells did not evoke any obvious phenotypic alterations under normoxia. However, microarray-based transcriptome analyses of lung tissue revealed significant alterations 7 but not 21 days after exposure to normobaric hypoxia (10% O2).

2024-08-08 | GSE230053 | GEO

Impact of Nfat5 on normoxia- and hypoxia-exposed mouse lung endothelial cells

Project description:Chronic hypoxia causes detrimental structural alterations in the lung, which are partially dependent on stress responses of the endothelium. In this context, we revealed that hypoxia-exposed murine lung endothelial cells (MLEC) activate nuclear factor of activated T-cells 5 (NFAT5/TonEBP) - a transcription factor that adjusts the cellular transcriptome to cope with multiple environmental stressors. Here, we studied the impact of NFAT5 on hypoxia-induced gene expression in MLEC by comparing the transcriptome of control and Nfat5-deficient MLEC, which were isolated from mouse lungs after exposure to normoxia and hypoxia for 7 days and processed for scRNA seq.

2024-08-08 | GSE255681 | GEO

Analysis of transcriptome in hypoxia(7d)-exposed lungs upon KO of Nfat5 in ECs

2024-08-08 | GSE230052 | GEO

Analysis of transcriptome in hypoxia-exposed lungs upon KO of Nfat5 in ECs

Project description:Analysis of transcriptome in hypoxia-exposed lungs upon KO of Nfat5 in ECs

| PRJNA957273 | ENA

Analysis of transcriptome in hypoxia(7d)-exposed lungs upon KO of Nfat5 in ECs

Project description:Analysis of transcriptome in hypoxia(7d)-exposed lungs upon KO of Nfat5 in ECs

| PRJNA957286 | ENA

Impact of Nfat5 on normoxia- and hypoxia-exposed mouse lung endothelial cells

Project description:Impact of Nfat5 on normoxia- and hypoxia-exposed mouse lung endothelial cells

| PRJNA1076150 | ENA

NFAT5/TonEBP controls metabolic adaption and tone of pulmonary vascular smooth muscle cells in the hypoxic lung [normoxia vs hypoxia]

Project description:Hypoxia provokes adaptive responses of cells, which ensure their energy supply including the adjustment of the transcriptome to match their metabolism. In this context, we explored the transcriptional impact of nuclear factor of activated T-cells 5 (NFAT5) on the function of vascular smooth muscle cells (VSMC) in the hypoxic lung. Exposure to hypoxia induced a rapid nuclear translocation of NFAT5 in cultured murine VSMCs. SMC-specific ablation of Nfat5 (Nfat5(SMC-/-)) increases the systolic pressure in the right ventricle (RVSP) of the mouse heart and impairs its function upon exposure to hypoxia for 7 and 21 days. Analyses of the transcriptome of the lung revealed a robust increase in the expression genes attributed to mitochondrial respiration. Further analyses of hypoxia-exposed pulmonary artery VSMCs revealed that loss of Nfat5 stimulates the expression of multiple mitochondria-related genes encoding cytochrome oxidases while decreasing the expression of lactate dehydrogenase A (Ldha) and phosphofructokinase 3 (Pfkfb3). Both, inhibition of LDHA or PFKFB3 activity and loss of Nfat5 stimulated the mitochondrial production of reactive oxygen species (ROS) in hypoxic pulmonary artery VSMCs while scavenging of ROS normalized the RVSP values in hypoxia-exposed Nfat5(SMC-/-) mice. In summary, our findings suggest a crucial role for NFAT5 in adjusting the transcriptome of hypoxia-exposed pulmonary artery VSMCs to support an adequate glycolysis-centered metabolism. Loss of Nfat5 impairs this response thereby fueling the mitochondrial respiration and ROS production that amplifies the hypoxia-mediated constriction of pulmonary arteries.

2021-11-26 | GSE178462 | GEO

Knockout of NFAT5 in endothelial cells

Project description:Endothelial cell-specific genetic ablation of Nfat5 was induced in adult mice. These anmials and control mice were exposed to hypoxia (10% oxygen) for 7 days. The lungs were processed for RNA exptraction and further analyses of the transcriptome

2021-11-26 | GSE178461 | GEO

Analysis of transcriptome in hypoxia-exposed lungs upon KO of Nfat5 in ECs

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-08 | GSE230055 | GEO

NFAT5 is a critical regulator of rheumatoid inflammation

Project description:NFAT5 is an osmoprotective transcription factor whose DNA binding domain shares structural homology with NFkappaB and other member of NFAT family, but its role in chronic inflammatory diseases remains unclear. The mRNA profiling of synoviocytes and endothelial cells transfected with NFAT5-targeted siRNA reveals three major changes in cellular processes associated with the pathogenesis of rheumatoid arthritis: cell cycle and survival, angiogenesis, and cell migration. The cells were transfected with NFAT5-targeted siRNA or non-specific scrambled (control) siRNA.

2010-12-31 | E-GEOD-22956 | biostudies-arrayexpress

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