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Article

Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension

1
Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut 1107, Lebanon
2
Department of Nutrition and Food Sciences, Faculty of Agricultural and Food Sciences, American University of Beirut, Beirut 1107, Lebanon
3
Epidemiology and Population Health Department, Faculty of Health Sciences, American University of Beirut, Beirut 1107, Lebanon
4
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2024, 25(8), 4402; https://doi.org/10.3390/ijms25084402
Submission received: 9 March 2024 / Revised: 5 April 2024 / Accepted: 9 April 2024 / Published: 16 April 2024
(This article belongs to the Special Issue Recent Advances in Hypertension and Cardiovascular Disease)

Abstract

Sodium chloride (NaCl) activates Th17 and dendritic cells in hypertension by stimulating serum/glucocorticoid kinase 1 (SGK1), a sodium sensor. Memory T cells also play a role in hypertension by infiltrating target organs and releasing proinflammatory cytokines. We tested the hypothesis that the role of T cell SGK1 extends to memory T cells. We employed mice with a T cell deletion of SGK1, SGK1fl/fl × tgCD4cre mice, and used SGK1fl/fl mice as controls. We treated the mice with L-NAME (0.5 mg/mL) for 2 weeks and allowed a 2-week washout interval, followed by a 3-week high-salt (HS) diet (4% NaCl). L-NAME/HS significantly increased blood pressure and memory T cell accumulation in the kidneys and bone marrow of SGK1fl/fl mice compared to knockout mice on L-NAME/HS or groups on a normal diet (ND). SGK1fl/fl mice exhibited increased albuminuria, renal fibrosis, and interferon-γ levels after L-NAME/HS treatment. Myography demonstrated endothelial dysfunction in the mesenteric arterioles of SGK1fl/fl mice. Bone marrow memory T cells were adoptively transferred from either mouse strain after L-NAME/HS administration to recipient CD45.1 mice fed the HS diet for 3 weeks. Only the mice that received cells from SGK1fl/fl donors exhibited increased blood pressure and renal memory T cell infiltration. Our data suggest a new therapeutic target for decreasing hypertension-specific memory T cells and protecting against hypertension.
Keywords: inflammation; hypertension; SGK1; memory T cells; immunologic memory; T-lymphocytes inflammation; hypertension; SGK1; memory T cells; immunologic memory; T-lymphocytes

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MDPI and ACS Style

Maaliki, D.; Itani, M.; Jarrah, H.; El-Mallah, C.; Ismail, D.; El Atie, Y.E.; Obeid, O.; Jaffa, M.A.; Itani, H.A. Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension. Int. J. Mol. Sci. 2024, 25, 4402. https://doi.org/10.3390/ijms25084402

AMA Style

Maaliki D, Itani M, Jarrah H, El-Mallah C, Ismail D, El Atie YE, Obeid O, Jaffa MA, Itani HA. Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension. International Journal of Molecular Sciences. 2024; 25(8):4402. https://doi.org/10.3390/ijms25084402

Chicago/Turabian Style

Maaliki, Dina, Maha Itani, Hala Jarrah, Carla El-Mallah, Diana Ismail, Yara E. El Atie, Omar Obeid, Miran A. Jaffa, and Hana A. Itani. 2024. "Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension" International Journal of Molecular Sciences 25, no. 8: 4402. https://doi.org/10.3390/ijms25084402

APA Style

Maaliki, D., Itani, M., Jarrah, H., El-Mallah, C., Ismail, D., El Atie, Y. E., Obeid, O., Jaffa, M. A., & Itani, H. A. (2024). Dietary High Salt Intake Exacerbates SGK1-Mediated T Cell Pathogenicity in L-NAME/High Salt-Induced Hypertension. International Journal of Molecular Sciences, 25(8), 4402. https://doi.org/10.3390/ijms25084402

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