ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2010
Interleukin-6 stimulates epithelial sodium channels in mouse cortical collecting duct cells.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 79 citations in OpenAlex.
- Sodium-glucose cotransporter 2 inhibitors for hypertension in cardiovascular-kidney-metabolic syndrome.Experimental physiology · 2025Review
- From fat to filter: the effect of adipose tissue-derived signals on kidney function.Nature reviews. Nephrology · 2025Review
- Pharmacological inhibition of the NLRP3 inflammasome attenuates kidney apoptosis, fibrosis, and injury in Dahl salt-sensitive rats.Clinical and experimental nephrology · 2025Article
- The immune-microbiome axis in salt-sensitive hypertension: a focus on renal and neural mechanisms.Frontiers in physiology · 2025Review
- Inflammation and vasopressin hypersecretion in aging.Frontiers in endocrinology · 2025Review
- Sex-specific relationships of inflammatory biomarkers with blood pressure in older adults.GeroScience · 2024Article
- Dissociation of Hypertension and Renal Damage After Cessation of High-Salt Diet in Dahl Rats.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024Review
- Immunomodulation and immunopharmacology in heart failure.Nature reviews. Cardiology · 2024Review
- The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Activation of renal epithelial NaFrontiers in pediatrics · 2024Article
- Aldosterone Antagonism Is More Effective at Reducing Blood Pressure and Excessive Renal ENaC Activity in AngII-Infused Female Rats Than in Males.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Urine Cell Transcriptomes Implicate Specific Renal Inflammatory Pathways Associated With Difficult-to-Control Hypertension.Journal of the American Heart Association · 2023Article
- Role of epithelial sodium channel-related inflammation in human diseases.Frontiers in immunology · 2023Review
- Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron.American journal of physiology. Cell physiology · 2022Article
- Article
- The Immune System in Hypertension: a Lost Shaker of Salt 2021 Lewis K. Dahl Memorial Lecture.Hypertension (Dallas, Tex. : 1979) · 2022Review
- Tubular IL-1β Induces Salt Sensitivity in Diabetes by Activating Renal Macrophages.Circulation research · 2022Article
- Type 1 Angiotensin Receptors on CD11c-Expressing Cells Protect Against Hypertension by Regulating Dendritic Cell-Mediated T Cell Activation.Hypertension (Dallas, Tex. : 1979) · 2022Article
- The antihypertensive effect of remote ischemic conditioning in spontaneously hypertensive rats.Frontiers in immunology · 2022Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The aim of this study is to elucidate the effects of interleukin-6 (IL-6) on the expression and activity of the epithelial sodium channel (ENaC), which is one of the key mechanisms underlying tubular sodium reabsorption. M-1 cortical collecting duct cells were treated with IL-6 (100 ng/ml) for 12 h. Real-time polymerase chain reaction and immunoblotting were employed to examine the mRNA and protein abundance. Transepithelial voltage (V(te)) and resistance (R(te)) were measured with an ohm/voltmeter (EVOM, WPI). The equivalent current was calculated as the ratio of V(te) to R(te.) Treatment with IL-6 (n = 5) increased the mRNA abundance of alpha-ENaC by 11 +/- 7% (P = not significant), beta-ENaC by 78 +/- 14% (P = 0.01), gamma-ENaC by 185 +/- 38% (P = 0.02), and prostasin by 29 +/- 5% (P = 0.01), all normalized by beta-actin. Treatment with IL-6 increased the protein expression of alpha-ENaC by 19 +/- 3% (P = 0.001), beta-ENaC by 89 +/- 21% (P = 0.01), gamma-ENaC by 36 +/- 12% (P = 0.02), and prostasin by 33 +/- 6% (P = 0.02). The amiloride-sensitive sodium current increased by 37 +/- 5%, from 6.0 +/- 0.4 to 8.2 +/- 0.3 muA/cm(2) (P < 0.01), in the cells treated with IL-6 compared with controls (P = 0.01). Aprotinin (28 microg/ml), a prostasin inhibitor, reduced the amiloride-sensitive sodium current by 61 +/- 5%, from 6.1 +/- 0.3 to 3.7 +/- 0.2 muA/cm(2) (P = 0.01). The magnitude of the IL-6-induced amiloride-sensitive sodium current in the presence of aprotinin dropped by 57 +/- 2%, from 8.6 +/- 0.2 to 4.9 +/- 0.2 muA/cm(2) (P < 0.01). This study has identified a novel function of IL-6, namely, IL-6 may activate ENaC. Therefore, renal inflammation mediated by IL-6 likely contributes to impaired pressure natriuresis.
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