ArticleAmerican journal of physiology. Cell physiology2010
Angiotensin II-induced upregulation of AT(1) receptor expression: sequential activation of NF-kappaB and Elk-1 in neurons.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 39 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Ang II-induced contraction is impaired in the aortas of renovascular hypertensive animal model.Vascular biology (Bristol, England) · 2024Article
- Multiple Aspects of Inappropriate Action of Renin-Angiotensin, Vasopressin, and Oxytocin Systems in Neuropsychiatric and Neurodegenerative Diseases.Journal of clinical medicine · 2022Review
- Impact of Peripheral α7-Nicotinic Acetylcholine Receptors on Cardioprotective Effects of Donepezil in Chronic Heart Failure Rats.Cardiovascular drugs and therapy · 2021Article
- Article
- Effects of Statins on Renin-Angiotensin System.Journal of cardiovascular development and disease · 2021Review
- Are losartan and imatinib effective against SARS-CoV2 pathogenesis? A pathophysiologic-based in silico study.In silico pharmacology · 2021Article
- SARS-CoV-2 spike protein promotes IL-6 trans-signaling by activation of angiotensin II receptor signaling in epithelial cells.PLoS pathogens · 2020Article
- The deleterious role of the prostaglandin EAmerican journal of physiology. Heart and circulatory physiology · 2020Article
- AMPK: a balancer of the renin-angiotensin system.Bioscience reports · 2019Review
- Soluble RAGE attenuates AngII-induced endothelial hyperpermeability by disrupting HMGB1-mediated crosstalk between AT1R and RAGE.Experimental & molecular medicine · 2019Article
- High mobility group box-1 in hypothalamic paraventricular nuclei attenuates sympathetic tone in rats at post-myocardial infarction.Cardiology journal · 2019Article
- Angiotensin II Causes Neuronal Damage in Stretch-Injured Neurons: Protective Effects of Losartan, an Angiotensin TMolecular neurobiology · 2018Article
- Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders.Current hypertension reports · 2018Review
- Overexpression of ß-Arrestin1 in the Rostral Ventrolateral Medulla Downregulates Angiotensin Receptor and Lowers Blood Pressure in Hypertension.Frontiers in physiology · 2018Article
- ERK1/2 MAPK signaling in hypothalamic paraventricular nucleus contributes to sympathetic excitation in rats with heart failure after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2016Article
- Molecular variability elicits a tunable switch with discrete neuromodulatory response phenotypes.Journal of computational neuroscience · 2016Article
- BDNF contributes to angiotensin II-mediated reductions in peak voltage-gated K+ current in cultured CATH.a cells.Physiological reports · 2015Article
- Hepatic expression of serum amyloid A1 is induced by traumatic brain injury and modulated by telmisartan.The American journal of pathology · 2015Article
- Endoplasmic reticulum and oxidant stress mediate nuclear factor-κB activation in the subfornical organ during angiotensin II hypertension.American journal of physiology. Cell physiology · 2015Article
- Modulation of angiotensin II signaling following exercise training in heart failure.American journal of physiology. Heart and circulatory physiology · 2015Review
Corrections and comments
- Retraction · 2024-08-02Duplication of/in Image · Investigation by Company/Institution · Investigation by Third Party · · see also: https://pubpeer.com/publications/4A3F0C99CDE7850A23AE06D0D573DA
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
It has been clearly established that increased circulating angiotensin II (ANG II) with concurrent upregulation of brain and peripheral ANG II type 1 receptors (AT(1)R) are important mediators in the pathophysiology of several diseases characterized by sympatho-excitation. In an effort to further understand the regulation of AT(1)R expression in neurons, we determined the role of sequential activation of the transcription factors nuclear factor-kappaB (NF-kappaB) and Ets-like protein 1 (Elk-1) in AT(1)R upregulation. We used CATH.a neurons as our neuronal cell model. Cells were treated with ANG II (100 nM) over a preset time course. Following ANG II activation, there was a temporal increase in the p65 subunit of NF-kappaB that was observed at 30 min, peaked at 1 h, and was sustained up to 24 h. There was a concomitant decrease of IkappaB and increased IkappaK expression. We also observed an increase in AT(1)R expression which followed the temporal increase of NF-kappaB. The activation of NF-kappaB was blocked by using the inhibitors parthenolide or p65 small interfering RNA (siRNA) which both led to a decrease in AT(1)R expression. The expression of Elk-1 was upregulated over a time period following ANG II activation and was decreased following NF-kappaB inhibition. p65-DNA binding was assessed using electrophoretic mobility shift assay, and it was shown that there was a time-dependent increased binding that was inhibited by means of parthenolide pretreatment or siRNA-mediated p65 gene silencing. Therefore, our results suggest a combined role for the transcription factors NF-kappaB and Elk-1 in the upregulation of AT(1)R in the CATH.a cell neuronal model. These data imply a positive feedback mechanism that may impact neuronal discharge sensitivity in response to ANG II.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.