ArticleAmerican journal of physiology. Cell physiology2010
Tumor necrosis factor-{alpha} suppresses angiotensinogen expression through formation of a p50/p50 homodimer in human renal proximal tubular cells.
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. Cited by 27 papers.
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27 citing papers in PubMed, 37 citations in OpenAlex.
- Responses to Ang II (Angiotensin II), Salt Intake, and Lipopolysaccharide Reveal the Diverse Actions of TNF-α (Tumor Necrosis Factor-α) on Blood Pressure and Renal Function.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Identification and verification of vascular cell adhesion protein 1 as an immune-related hub gene associated with the tubulointerstitial injury in diabetic kidney disease.Bioengineered · 2021Article
- Angiotensin II biphasically regulates cell differentiation in human iPSC-derived kidney organoids.American journal of physiology. Renal physiology · 2021Article
- Angiotensin II-induced renal angiotensinogen formation is enhanced in mice lacking tumor necrosis factor-alpha type 1 receptor.Physiological reports · 2021Article
- MicroRNA-133a-Dependent Inhibition of Proximal Tubule Angiotensinogen by Renal TNF (Tumor Necrosis Factor).Hypertension (Dallas, Tex. : 1979) · 2020Article
- Inflammation as a Regulator of the Renin-Angiotensin System and Blood Pressure.Current hypertension reports · 2018Review
- Microbial Degradation of Cellular Kinases Impairs Innate Immune Signaling and Paracrine TNFα Responses.Scientific reports · 2016Article
- Macrophage-derived IL-6 contributes to ANG II-mediated angiotensinogen stimulation in renal proximal tubular cells.American journal of physiology. Renal physiology · 2016Article
- Effects of pyrrolidine dithiocarbamate on proliferation and nuclear factor-κB activity in autosomal dominant polycystic kidney disease cells.BMC nephrology · 2015Article
- Cardiac-specific suppression of NF-κB signaling prevents diabetic cardiomyopathy via inhibition of the renin-angiotensin system.American journal of physiology. Heart and circulatory physiology · 2014Article
- ROCK/NF-κB axis-dependent augmentation of angiotensinogen by angiotensin II in primary-cultured preglomerular vascular smooth muscle cells.American journal of physiology. Renal physiology · 2014Article
- Renal angiotensin-converting enzyme and blood pressure control.Current opinion in nephrology and hypertension · 2014Review
- Therapeutic potential of curcumin in digestive diseases.World journal of gastroenterology · 2013Review
- Tumor necrosis factor-α: regulation of renal function and blood pressure.American journal of physiology. Renal physiology · 2013Review
- Nuclear factor κB mediates suppression of canonical transient receptor potential 6 expression by reactive oxygen species and protein kinase C in kidney cells.The Journal of biological chemistry · 2013Article
- Do multiple nuclear factor kappa B activation mechanisms explain its varied effects in the heart?Ochsner journal · 2013Article
- Angiotensin II blockade and renal protection.Current pharmaceutical design · 2013Review
- Proximal tubule angiotensinogen modulation of arterial pressure.Current opinion in nephrology and hypertension · 2013Review
- Augmented intrarenal and urinary angiotensinogen in hypertension and chronic kidney disease.Pflugers Archiv : European journal of physiology · 2013Review
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Abstract
Angiotensinogen (AGT) expression in renal proximal tubular cells (RPTCs) and intrarenal tumor necrosis factor-α (TNF-α) levels are increased in hypertension and renal diseases However, the contribution of TNF-α to AGT expression in RPTCs has not been established. Therefore, the objective of the present study was to determine influence of TNF-α on AGT expression in RPTCs. Human kidney-2 (HK-2) cells, immortalized human RPTCs, were treated with several concentrations of TNF-α up to 24 h. AGT mRNA and protein expression were evaluated by RT-PCR and ELISA, respectively. Activation of nuclear factor-κB (NF-κB) by TNF-α was evaluated by Western blot analysis, immunocytochemistry, and electrophoretic mobility shift assay (EMSA). TNF-α suppressed AGT mRNA expression in a dose- and time-dependent manner. Maximum AGT mRNA reduction was caused by 40 ng/ml of TNF-α (0.52 ± 0.09, ratio to control, at 24 h) and at 24 h (0.66 ± 0.05, ratio to control, by 10 ng/ml TNF-α). TNF-α reduced AGT protein accumulation in the medium between 8 and 24 h (0.62 ± 0.13 by 40 ng/ml TNF-α, ratio to control). TNF-α activated and induced translocalization of p50 and p65, which are NF-κB subunits. Elevated formation of p50/p65 and p50/p50 dimers by TNF-α were observed by EMSA and supershift assay. Gene silencing of p50, but not p65, attenuated the effect of TNF-α on reduction of AGT expression in RPTCs. These results indicate that TNF-α suppresses AGT expression through p50/p50 homodimer formation in human RPTCs, suggesting a possible counteracting mechanism that limits excessive intrarenal AGT production.
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