ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: SA-PO772

Loss of Serum and Glucocorticoid Kinase 1 (SGK) in T Cells Abrogates Memory T Cell Formation, Hypertension, and End-Organ Damage

Session Information

  • Hypertension and CVD: Mechanisms
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Hypertension and CVD

  • 1503 Hypertension and CVD: Mechanisms


  • Maaliki, Dina, American University of Beirut, Beirut, Lebanon
  • Itani, Maha M., American University of Beirut, Beirut, Lebanon
  • Jarrah, Hala Hachem, American University of Beirut, Beirut, Lebanon
  • El-Mallah, Carla, American University of Beirut, Beirut, Lebanon
  • Obeid, Omar, American University of Beirut, Beirut, Lebanon
  • Jaffa, Miran A., American University of Beirut, Beirut, Lebanon
  • Itani, Hana A., American University of Beirut, Beirut, Lebanon

NaCl concentrates in tissues over time and activates immune cells including T H17 cells and dendritic cells, which are known to contribute to hypertension, in a Serum/Glucocorticoid Kinase 1(SGK1)-dependent fashion. In addition to TH17 cells and dendritic cells, memory T cells play a vital role in hypertension genesis. Long-lived memory cells generate a systemic inflammatory response through mobilization to target organs and release of cytokines. To understand the mechanisms by which memory T cells sense salt, we tested the hypothesis that SGK1, an important intracellular sensor of Na+, in T cells is necessary for the formation of memory T cells and their mediation of salt sensitive hypertension and organ damage.


We employed mice with T cell-specific deletion of SGK1, SGK1fl/fl x tgCD4cre mice, and used SGK1fl/fl mice as controls. To mimic repeated exposure to hypertensive stimuli, we treated mice with L-NAME (0.5mg/ml) in drinking water for 2 weeks, allowed a 2-week washout interval, followed by a high salt(HS) diet (4% NaCl) for 3 weeks.


L-NAME/HS significantly increased blood pressure as well as memory T cell infiltration in the kidney, aorta, and bone marrow of SGK1fl/fl mice, as compared to SGK1fl/fl x tgCD4cre mice. SGK1fl/fl mice also demonstrated caused striking albuminuria, cortical fibrosis, cortical ROS generation and increased renal IFN-γ and NGAL expression after L-NAME/HS. Myography studies demonstrated an impaired relaxation in response to acetylcholine but not sodium nitroprusside in mesenteric arterioles from SGK1fl/fl mice, but not SGK1fl/fl x tg CD4cre mice. T cells were sorted and adoptively transferred from the bone marrow of CD45.2 SGK1fl/fl x tgCD4cre mice or SGK1fl/fl controls that had undergone the L-NAME/HS protocol, to recipient CD45.1 mice. Recipient mice were then fed a HS diet for 3 weeks. Strikingly, mice that had received T cells from SGK1fl/fl donors exhibited significantly increased blood pressure and renal memory T cell infiltration, compared to mice that had received cells from SGK1fl/fl x tgCD4cre donors.


Our data suggest a new therapeutic target to reduce the formation of hypertension-specific memory T cells, which will protect against hypertension and end-organ damage in response to repeated hypertensive stimuli.


  • Other NIH Support