ArticleHypertension (Dallas, Tex. : 1979)2011
Contribution of a nuclear factor-kappaB binding site to human angiotensinogen promoter activity in renal proximal tubular cells.
Article in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- N-type calcium channel and renal injury.International urology and nephrology · 2022Review
- Epigenetic modification: a regulatory mechanism in essential hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Review
- Advanced Glycation End Products Stimulate Angiotensinogen Production in Renal Proximal Tubular Cells.The American journal of the medical sciences · 2019Article
- High glucose augments angiotensinogen in human renal proximal tubular cells through hepatocyte nuclear factor-5.PloS one · 2017Article
- HDAC9 is an epigenetic repressor of kidney angiotensinogen establishing a sex difference.Biology of sex differences · 2017Article
- 20-Hydroxyeicosatetraenoic Acid (HETE)-dependent Hypertension in Human Cytochrome P450 (CYP) 4A11 Transgenic Mice: NORMALIZATION OF BLOOD PRESSURE BY SODIUM RESTRICTION, HYDROCHLOROTHIAZIDE, OR BLOCKADE OF THE TYPE 1 ANGIOTENSIN II RECEPTOR.The Journal of biological chemistry · 2016Article
- Augmentation of angiotensinogen expression in the proximal tubule by intracellular angiotensin II via AT1a/MAPK/NF-кB signaling pathways.American journal of physiology. Renal physiology · 2016Article
- 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
- Renal generation of angiotensin II and the pathogenesis of hypertension.Current hypertension reports · 2014Review
- 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
- Evidence for a functional intracellular angiotensin system in the proximal tubule of the kidney.American journal of physiology. Regulatory, integrative and comparative physiology · 2012Review
- Angiotensinogen gene transcription in pulmonary fibrosis.International journal of peptides · 2012Article
- Rho-kinase/nuclear factor-κβ/angiotensinogen axis in angiotensin II-induced renal injury.Hypertension research : official journal of the Japanese Society of Hypertension · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Intrarenal angiotensinogen (AGT) is expressed highly in renal proximal tubular cells (RPTCs) and contributes to the regulation of intrarenal angiotensin II levels. Inhibition of nuclear factor (NF)-κB suppressed human (h)AGT expression in human RPTCs. However, the presence and localization of an NF-κB binding site in the hAGT promoter region have not been determined. Therefore, this study was performed to demonstrate that an NF-κB binding site in the hAGT promoter region contributes to hAGT promoter activity in human RPTCs. The hAGT promoter region was cloned from -4358 to +122 and deletion analysis was performed. A possible NF-κB binding site was removed from the hAGT promoter region (M1) and mutated (M2). Human RPTCs were transfected, and hAGT promoter activity was determined by luciferase assay. The identity of DNA binding proteins from binding assays were determined by Western blot. Progressive 5'-end deletions demonstrated removal of a distal promoter element in hAGT_-2414/+122 reduced promoter activity (0.61 ± 0.12, ratio to hAGT_-4358/+122). Inhibition of NF-κB suppressed promoter activity in hAGT_-4358/+122 (0.51 ± 0.14, ratio to control) and hAGT_-3681/+122 (0.48 ± 0.06, ratio to control) but not in the construct without the NF-κB binding site. Promoter activity was reduced in the domain mutants M1 (0.57 ± 0.08, ratio to hAGT_-4358/+122) and M2 (0.61 ± 0.16, ratio to hAGT_-4358/+122). DNA binding levels of NF-κB protein were reduced in M1. These data demonstrate the functional importance of an NF-κB binding site in the hAGT promoter region, which contributes to hAGT promoter activity in human RPTCs.
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