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Transcript profiling of Arabidopsis plasma membrane proton pump mutants

ABSTRACT: Plasma membrane proton pump maintains proton electrochemical gradient and provides energy to secondary transporters. Arabidopsis mutant plants with reduced proton pump activity grow normal under ideal growth conditions; however their growth are reduced compared with wildtype plants when placed under the conditions that stress on protonmotive force (high external pH or high external potassium).

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE34202 | GEO | 2015/04/01

SECONDARY ACCESSION(S): PRJNA149843

REPOSITORIES: GEO

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Transcript profiling of Arabidopsis plasma membrane proton pump mutants

Project description:Plasma membrane proton pump maintains proton electrochemical gradient and provides energy to secondary transporters. Arabidopsis mutant plants with reduced proton pump activity grow normal under ideal growth conditions; however their growth are reduced compared with wildtype plants when placed under the conditions that stress on protonmotive force (high external pH or high external potassium). Seedlings of wildtype, aha1, and aha2 mutant plants were grown under ideal growth condition. Total RNA from those seedlings were subjected to transcriptome analyses using Affymetrix Gene Chip.

2015-04-01 | E-GEOD-34202 | biostudies-arrayexpress

Inter- and Intra-Molecular Interactions of The Arabidopsis Plasma Membrane Proton Pump Revealed Using a Mass Spectrometric-Cleavable Crosslinker

Project description:In plants and fungi, the plasma membrane proton pump (H+-ATPase) establishes an electrochemical gradient across the plasma membrane which serves as the driving force for the secondary transport of ions and nutrients across the cell membrane. This is an essential enzyme that functions in many important processes including stomatal movement, cell elongation, and cellular responses to stimuli from hormones, light, and other environmental conditions. Therefore, understanding how the activity of the H+-ATPase is regulated is important to understand how plants adapt to different growth conditions. The autoinhibitory effect of the C- terminal regulatory domain of H+-ATPase is well established and is thought to be mediated by interactions with the catalytic domains. Here, using the lysine reactive mass spectrometry cleavable crosslinker DSSO, we found that the C-terminal domain of the Arabidopsis H+- ATPase 2 (AHA2) crosslinked extensively with the actuator, nucleotide-binding, and phosphorylation domains, suggesting that the C-terminal domain regulates the catalytic cycle by modulating the relative positions of these domains. Interestingly, several C-terminal crosslinks occurred near a predicted proton binding site (Asp-684 in TM6), suggesting that the C-terminal domain may regulate proton efflux. Additionally, crosslinks between the C-terminal domain and other domains of AHA2 were detected in a monomeric protein resolved on SDS-PAGE, suggesting that intramolecular interactions may also be involved in the regulation of enzyme activity. Finally, we observed mixed-isotope crosslinking between unlabeled (14N-AHA2) and labeled (15N-AHA2) between the C-terminal domain and other domains of AHA2, supporting our model that oligomeric H+-ATPase may autoinhibit the neighboring monomer in a “head to tail” configuration.

2023-06-01 | PXD018219 | Pride

Targeting ATP12A, a non-gastric proton pump alpha subunit, for idiopathic pulmonary fibrosis treatment

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a pathological condition of unknown etiology which results from injury to the lung and an ensuing fibrotic response that leads to thickening of the alveolar walls and obliteration of the alveolar space. The pathogenesis is not clear and there are currently no effective therapies for IPF. Small airway disease and mucus accumulation are prominent features in IPF lungs, similar to Cystic Fibrosis (CF) lung disease. The ATP12A gene encodes the alpha-subunit of the non-gastric H+, K+-ATPase, which functions to acidify the airway surface fluid and impairs mucociliary transport function in cystic fibrosis patients. We hypothesize that the ATP12A protein may play a role in the pathogenesis of IPF. Our studies demonstrate that ATP12A protein is overexpressed in distal small airways from IPF patient lungs compared to normal human lungs. In addition, overexpression of the ATP12A protein in mouse lungs worsened the bleomycin (BLEO)-induced experimental pulmonary fibrosis. This was prevented by a potassium-competitive proton pump blocker, vonoprazan (VON). This data supports the concept that the ATP12A protein plays an important role in the pathogenesis of lung fibrosis. Inhibition of the ATP12A protein has the potential as a novel therapeutic strategy in IPF.

2023-04-01 | GSE205849 | GEO

Proton pump inhibitor treatment aggravates bacterial translocation in patients with advanced liver cirrhosis and portal hypertension

Project description:Blood microbiome and proton pump inhibitor treatment

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Long-term Proton Pump Inhibitor Administration Caused Physiological and Microbiota Changes in Rats

Project description:Long-term Proton Pump Inhibitor Administration Caused Physiological and Microbiota Changes in Rats

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Expression data from young and senescent HCAECs treated with proton pump inhibitors (omeprazole and lansoprazole)

2017-04-18 | GSE77239 | GEO

Targeting ATP12A, a non-gastric proton pump alpha subunit, for idiopathic pulmonary fibrosis treatment

Project description:Targeting ATP12A, a non-gastric proton pump alpha subunit, for idiopathic pulmonary fibrosis treatment

| PRJNA847950 | ENA

Expression data from young and senescent HCAECs treated with proton pump inhibitors (omeprazole and lansoprazole)

Project description:Proton pump inhibitors (PPIs) are among the most frequently prescribed drugs, especially in older people. Although these drugs are usually considered safe, recent evidence suggests that high dose and/or long term use of PPIs may have several detrimental effects, including increased risk of adverse cardiovascular events. The impact of PPI in the aging host environment still need to be characterized. Aged tissues, including vascular tissues, accumulate senescent cells that can communicate with their environment by secreting a myriad of cytokines and growth factors. Human coronary artery endothelial cells (HCAECs) provide an excellent model system to study â??in vitroâ?? most aspects of cardiovascular function and disease related to cellular senescence. The purpose of this study is thus to investigate the in vitro effects of two well-known PPIs (Omeprazole and Lansoprazole) on endothelial gene expression in senescent e non-senescent HCAECs. We used a cDNA microarray method to compare gene expression profiles of young and senescent HCAECs treated with omeprazole and lansoprazole. Young cells were cultured in medium supplemented with vehicle (CTRL) or 100Î¼M PPIs (Omeprazole or Lansoprazole) and grown for subsequent passages until they evidenced senescence-associated phenotypes. Total mRNA was extracted and gene expression profiles were analyzed in senescent endothelial cells (P12) compared to the non-senescent cells (P6) in both untreated (CTRL) and PPI-treated groups by cDNA microarray. All experiments were performed in triplicate for each treatment group.

2017-04-18 | E-GEOD-77239 | biostudies-arrayexpress

Expression data from primary rat aortic smooth muscle cells

Project description:Electrochemical gradients of monovalent cations across the plasma membrane (high intracellular potassium, [K+]i vs low intracellular sodium, [Na+]i) are created by the Na+,K+-pump and determine a large variety of physiologically important processes. We hypothesized that transcriptomics changes triggered by hypoxia are at least partially caused by Na+i/K+i-mediated excitation-transcription coupling . We used microarrays for identification and functional characterization of [Na+]i/]K+]i-sensitive transcriptome in RASMC

2014-09-05 | GSE61131 | GEO

Proton pump inhibitors modulate the barrier dysfunction caused by IL-13 in the epithelium in eosinophilic esophagitis

Project description:Eosinophilic esophagitis (EoE) is a chronic immune-mediated disorder triggered by specific food antigens, characterized by eosinophil-rich multicellular inflammation and structural changes in the epithelium. Treatment options for EoE include dietary therapy, pharmacological therapy, or a combination of both, chosen based on the patient's preference and clinical progression. Pharmacological options include proton pump inhibitors (PPIs), corticosteroids, and biologic therapy. Although PPI therapy is used for EoE management, its underlying mechanism of action remains unclear. To investigate the effects of omeprazole, an orally bioavailable PPI commonly used for EoE therapy, on the dynamics of esophageal epithelial barrier function and inflammation, we employed air-liquid interface (ALI) culture. We examined how omeprazole affects gene expression changes caused by IL-13 treatment. ALI cultures were treated with 100 ng/ml of IL-13 and/or 50 µM of acid-activated omeprazole for 96 hours, and bulk RNA sequencing was performed to analyze the epithelial-specific transcriptomes of IL-13 and/or omeprazole-treated ALI. Our findings suggest potential gene interactions where omeprazole may mitigate transcriptional changes induced by IL-13, indicating that omeprazole may attenuate IL-13 mediated epithelial dysfunction relevant to EoE pathophysiology by modulating pathways associated with inflammation, tissue repair, and cell-cell communication.

2024-09-13 | GSE273039 | GEO

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