LIVIVO - Search results -

Search results

Result 1 - 10 of total 39

Search options

Article ; Online: American Society of Nephrology Kidney TREKS Program.

Rubin, Molly / Lecker, Stewart H / Ramkumar, Nirupama / Sozio, Stephen M / Hoover, Robert S / Zeidel, Mark L / Ko, Benjamin S

Journal of the American Society of Nephrology : JASN

2024

Abstract: In response to decreasing numbers of individuals entering into nephrology fellowships, the American Society of Nephrology launched Kidney TREKS (Tutored Research and Education for Kidney Scholars) to stimulate interest in nephrology among medical ... ...

Abstract	In response to decreasing numbers of individuals entering into nephrology fellowships, the American Society of Nephrology launched Kidney TREKS (Tutored Research and Education for Kidney Scholars) to stimulate interest in nephrology among medical students, graduate students, and postdoctoral fellows. The program combines a one-week intensive exposure to kidney physiology with a longitudinal mentorship program at the participants' home institutions. Ten years in, an analysis was conducted to assess its effectiveness. We surveyed participants to assess their opinions regarding nephrology before and after the course and followed them longitudinally to determine their career choices. TREKS applicants who were not selected to participate were used as a comparison group. 381 people participated in the program and 242 completed the survey. After TREKS, both medical students and graduate students showed increased interest in nephrology, with rank scores of 5.6±0.2 pre- to 7.5±0.1 post-course for medical students (mean ± standard deviation, n=189, p=0.001) and 7.3±0.3 to 8.7±0.3 (n=53, p=0.001) for graduate students. In long term follow-up, TREKS medical students chose a nephrology pipeline residency at a higher rate than medical students overall (57% vs. 31%, p=0.01) and TREKS applicants who did not participate (47% vs. 31%, p=0.04). Nephrology fellowship rates for these groups exceeded the general population but did not significantly differ between TREKS participants and applicants. PhD students and postdoctoral TREKS participants had a higher rate of participating in nephrology research compared to TREKS applicants (66% vs. 30%, p=0.01). In summary, the ASN Kidney TREKS program has demonstrated that it can improve interest in nephrology in the short term and increase the number of individuals going into nephrology careers. This long-term effect is most evident in PhD students and postdoctoral participants. Further study is needed to assess the impact of TREKS on enrollment in nephrology fellowship programs.
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.0000000000000384
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3344: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article: The Pharmacological Inhibition of CaMKII Regulates Sodium Chloride Cotransporter Activity in mDCT15 Cells

Gholam, Mohammed F. / Ko, Benjamin / Ghazi, Zinah M. / Hoover, Robert S. / Alli, Abdel A.

Biology. 2021 Dec. 16, v. 10, no. 12

2021

Abstract: The thiazide-sensitive sodium chloride cotransporter (NCC) in the distal convoluted tubule is responsible for reabsorbing up to one-tenth of the total filtered load of sodium in the kidney. The actin cytoskeleton is thought to regulate various transport ... ...

Abstract	The thiazide-sensitive sodium chloride cotransporter (NCC) in the distal convoluted tubule is responsible for reabsorbing up to one-tenth of the total filtered load of sodium in the kidney. The actin cytoskeleton is thought to regulate various transport proteins in the kidney but the regulation of the NCC by the actin cytoskeleton is largely unknown. Here, we identify a direct interaction between the NCC and the cytoskeletal protein filamin A in mouse distal convoluted tubule (mDCT15) cells and in the native kidney. We show that the disruption of the actin cytoskeleton by two different mechanisms downregulates NCC activity. As filamin A is a substrate of the Ca²⁺/calmodulin-dependent protein kinase II (CaMKII), we investigate the physiological significance of CaMKII inhibition on NCC luminal membrane protein expression and NCC activity in mDCT15 cells. The pharmacological inhibition of CaMKII with the compound KN93 increases the active form of the NCC (phospho-NCC) at the luminal membrane and also increases NCC activity in mDCT15 cells. These data suggest that the interaction between the NCC and filamin A is dependent on CaMKII activity, which may serve as a feedback mechanism to maintain basal levels of NCC activity in the distal nephron.
Keywords	calcium-calmodulin-dependent protein kinase ; filamin ; kidneys ; mice ; microfilaments ; protein synthesis ; sodium ; sodium chloride symporters
Language	English
Dates of publication	2021-1216
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology10121335
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: P2X7

Benson, Lance N / Deck, Katherine S / Mora, Christoph J / Guo, Yunping / Rafferty, Tonya M / Li, Lin-Xi / Huang, Lu / Andrews, J Tucker / Qin, Zhiqiang / Trott, Daniel W / Hoover, Robert S / Liu, Yunmeng / Mu, Shengyu

Hypertension (Dallas, Tex. : 1979)

2024 Volume 81, Issue 3, Page(s) 530–540

Abstract: Background: CD8: Methods: We used mouse models of hypertension. Wild type were used as genetic controls, OT1 and Rag2/OT1 mice were utilized to determine antigen dependency, and P2X7-knockout mice were studied to define the role of P2X7 in activating ...

Abstract	Background: CD8 Methods: We used mouse models of hypertension. Wild type were used as genetic controls, OT1 and Rag2/OT1 mice were utilized to determine antigen dependency, and P2X7-knockout mice were studied to define the role of P2X7 in activating CD8Ts and promoting hypertension. Blood pressure was monitored continuously and kidneys were obtained at different experimental end points. Freshly isolated CD8Ts from mice for activation assays and ATP stimulation. CD8T activation-induced promotion of sodium retention was explored in cocultures of CD8Ts and mouse DCTs. Results: We found that OT1 and Rag2/OT1 mice, which are nonresponsive to common antigens, still developed hypertension and CD8T-activation in response to deoxycorticosterone acetate/salt treatment, similar to wild-type mice. Further studies identified the P2X7 receptor on CD8Ts as a possible mediator of this antigen-independent activation of CD8Ts in hypertension. Knockout of the P2X7 receptor prevented calcium influx and cytokine production in CD8Ts. This finding was associated with reduced CD8T-DCT stimulation, reversal of excessive salt retention in DCTs, and attenuated development of salt-sensitive hypertension. Conclusions: Our findings suggest a novel mechanism by which CD8Ts are activated in hypertension to exacerbate salt retention and infer that the P2X7 receptor on CD8Ts may represent a new therapeutic target to attenuate T-cell-mediated immunopathology in hypertension.
MeSH term(s)	Mice ; Animals ; CD8-Positive T-Lymphocytes ; Receptors, Purinergic P2X7/genetics ; Mice, Knockout ; Hypertension ; Sodium Chloride, Dietary ; Sodium ; Adenosine Triphosphate ; Mice, Inbred C57BL
Chemical Substances	Receptors, Purinergic P2X7 ; Sodium Chloride, Dietary ; Sodium (9NEZ333N27) ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2024-01-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.123.21819
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1488: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Angiotensin II: a candidate for an aldosterone-independent mediator of potassium preservation during volume depletion.

Hoover, Robert S

Kidney international

2011 Volume 79, Issue 4, Page(s) 377–379

Abstract: Two different stimulators of aldosterone secretion, high-potassium diet and low-sodium diet, have disparate effects on potassium secretion in the distal nephron. The mechanism by which the kidney preserves potassium in the face of a high-aldosterone, ... ...

Abstract	Two different stimulators of aldosterone secretion, high-potassium diet and low-sodium diet, have disparate effects on potassium secretion in the distal nephron. The mechanism by which the kidney preserves potassium in the face of a high-aldosterone, volume-depleted state has engendered much thought. Yue et al. now propose that angiotensin II inhibits the renal outer medullary potassium channel (ROMK1) through stimulation of the protein tyrosine kinase c-Src, perhaps acting as a signal to differentiate volume depletion from a high-potassium diet.
MeSH term(s)	Aldosterone/metabolism ; Angiotensin II/metabolism ; Animals ; Diet, Sodium-Restricted ; Humans ; Hypovolemia/metabolism ; Kidney/metabolism ; Models, Biological ; Potassium/metabolism ; Potassium Channels, Inwardly Rectifying ; Potassium, Dietary/administration & dosage ; Protein-Tyrosine Kinases/metabolism ; src-Family Kinases
Chemical Substances	Potassium Channels, Inwardly Rectifying ; Potassium, Dietary ; Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; CSK tyrosine-protein kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2011-02
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2010.476
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 797: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: The Pharmacological Inhibition of CaMKII Regulates Sodium Chloride Cotransporter Activity in mDCT15 Cells.

Gholam, Mohammed F / Ko, Benjamin / Ghazi, Zinah M / Hoover, Robert S / Alli, Abdel A

Biology

2021 Volume 10, Issue 12

Abstract	The thiazide-sensitive sodium chloride cotransporter (NCC) in the distal convoluted tubule is responsible for reabsorbing up to one-tenth of the total filtered load of sodium in the kidney. The actin cytoskeleton is thought to regulate various transport proteins in the kidney but the regulation of the NCC by the actin cytoskeleton is largely unknown. Here, we identify a direct interaction between the NCC and the cytoskeletal protein filamin A in mouse distal convoluted tubule (mDCT15) cells and in the native kidney. We show that the disruption of the actin cytoskeleton by two different mechanisms downregulates NCC activity. As filamin A is a substrate of the Ca
Language	English
Publishing date	2021-12-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology10121335
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Reimagining Nephrology Fellowship Education to Meet the Future Needs of Nephrology: A Report of the American Society of Nephrology Task Force on the Future of Nephrology.

Rosenberg, Mark E / Anderson, Sharon / Farouk, Samira S / Gibson, Keisha L / Hoover, Robert S / Humphreys, Benjamin D / Orlowski, Janis M / Udani, Suneel M / Waitzman, Joshua S / West, Melissa / Ibrahim, Tod

Clinical journal of the American Society of Nephrology : CJASN

2023 Volume 18, Issue 6, Page(s) 816–825

Abstract: The American Society of Nephrology (ASN) Task Force on the Future of Nephrology was established in April 2022 in response to requests from the American Board of Internal Medicine and the Accreditation Council for Graduate Medical Education regarding ... ...

Abstract	The American Society of Nephrology (ASN) Task Force on the Future of Nephrology was established in April 2022 in response to requests from the American Board of Internal Medicine and the Accreditation Council for Graduate Medical Education regarding training requirements in nephrology. Given recent changes in kidney care, ASN also charged the task force with reconsidering all aspects of the specialty's future to ensure that nephrologists are prepared to provide high-quality care for people with kidney diseases. The task force engaged multiple stakeholders to develop 10 recommendations focused on strategies needed to promote: ( 1 ) just, equitable, and high-quality care for people living with kidney diseases; ( 2 ) the value of nephrology as a specialty to nephrologists, the future nephrology workforce, the health care system, the public, and government; and ( 3 ) innovation and personalization of nephrology education across the scope of medical training. This report reviews the process, rationale, and details (the "why" and the "what") of these recommendations. In the future, ASN will summarize the "how" of implementing the final report and its 10 recommendations.
MeSH term(s)	Humans ; United States ; Nephrology/education ; Fellowships and Scholarships ; Education, Medical, Graduate ; Internal Medicine/education ; Nephrologists
Language	English
Publishing date	2023-02-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.0000000000000133
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6584: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron.

Wynne, Brandi M / Samson, Trinity K / Moyer, Hayley C / van Elst, Henrieke J / Moseley, Auriel S / Hecht, Gillian / Paul, Oishi / Al-Khalili, Otor / Gomez-Sanchez, Celso / Ko, Benjamin / Eaton, Douglas C / Hoover, Robert S

American journal of physiology. Cell physiology

2022 Volume 323, Issue 5, Page(s) C1512–C1523

Abstract: Hypertension is characterized by increased sodium ( ... ...

Abstract	Hypertension is characterized by increased sodium (Na
MeSH term(s)	Receptors, Mineralocorticoid ; Aldosterone/pharmacology ; Interleukin-6 ; Reactive Oxygen Species ; Kidney Tubules, Distal ; Nephrons ; Sodium ; Thiazides
Chemical Substances	Receptors, Mineralocorticoid ; Aldosterone (4964P6T9RB) ; Interleukin-6 ; Reactive Oxygen Species ; Sodium (9NEZ333N27) ; Thiazides
Language	English
Publishing date	2022-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00272.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Calcineurin A-α suppression drives nuclear factor-κB-mediated NADPH oxidase-2 upregulation.

Cheriyan, Aswathy M / Ume, Adaku C / Francis, Cynthia E / King, Keyona N / Linck, Valerie A / Bai, Yun / Cai, Hui / Hoover, Robert S / Ma, Heping P / Gooch, Jennifer L / Williams, Clintoria R

American journal of physiology. Renal physiology

2021 Volume 320, Issue 5, Page(s) F789–F798

Abstract: Calcineurin inhibitors (CNIs) are vital immunosuppressive therapies in the management of inflammatory conditions. A long-term consequence is nephrotoxicity. In the kidneys, the primary, catalytic calcineurin (CnA) isoforms are CnAα and CnAβ. Although the ...

Abstract	Calcineurin inhibitors (CNIs) are vital immunosuppressive therapies in the management of inflammatory conditions. A long-term consequence is nephrotoxicity. In the kidneys, the primary, catalytic calcineurin (CnA) isoforms are CnAα and CnAβ. Although the renal phenotype of CnAα
MeSH term(s)	Animals ; Calcineurin/deficiency ; Calcineurin/genetics ; Calcineurin/metabolism ; Calcineurin Inhibitors/toxicity ; Cell Line ; Cyclosporine/toxicity ; Fibrosis ; Immunosuppressive Agents/toxicity ; Kidney/drug effects ; Kidney/enzymology ; Kidney/pathology ; Kidney Diseases/chemically induced ; Kidney Diseases/enzymology ; Kidney Diseases/genetics ; Kidney Diseases/pathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; NADPH Oxidase 2/genetics ; NADPH Oxidase 2/metabolism ; NF-kappa B/metabolism ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Up-Regulation ; Mice
Chemical Substances	Calcineurin Inhibitors ; Immunosuppressive Agents ; NF-kappa B ; Reactive Oxygen Species ; Cyclosporine (83HN0GTJ6D) ; Cybb protein, mouse (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; Calcineurin (EC 3.1.3.16)
Language	English
Publishing date	2021-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00254.2020
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Molecular physiology of the thiazide-sensitive sodium-chloride cotransporter.

Ko, Benjamin / Hoover, Robert S

Current opinion in nephrology and hypertension

2009 Volume 18, Issue 5, Page(s) 421–427

Abstract: Purpose of review: This review summarizes recent advances in the understanding of the molecular physiology and regulation of the thiazide-sensitive sodium-chloride cotransporter (NCC).: Recent findings: Mutations of with-no-lysine (WNK) kinases 1 and ...

Abstract	Purpose of review: This review summarizes recent advances in the understanding of the molecular physiology and regulation of the thiazide-sensitive sodium-chloride cotransporter (NCC). Recent findings: Mutations of with-no-lysine (WNK) kinases 1 and 4 result in hyperactivity of NCC and familial hyperkalemic hypertension, a genetic syndrome of hypertension. Recent studies have shown that WNK1 and WNK4 activate the STE20 family protein kinases Ste20-related proline/alanine-rich kinase and odd-skipped-related 1, resulting in phosphorylation and activation of NCC. Additionally, a mouse knock-in model for a WNK4 familial hyperkalemic hypertension mutant demonstrated increased Ste20-related proline/alanine-rich kinase/odd-skipped-related 1 and NCC phosphorylation. It is unclear how these studies fit with the data indicating that WNK4 inhibits NCC, and the familial hyperkalemic hypertension mutations of WNK4 are loss-of-function mutations. Another WNK kinase, WNK3, also regulates NCC, activating NCC and antagonizing the effect of WNK4. Extracellular signal-related kinase 1/2 mitogen-activated protein kinase activation by Ras guanyl nucleotide-releasing protein 1 is another kinase pathway that appears to be a potent regulator of NCC. Other studies have described a role for angiotensin II in pressure natriuresis via actions on NCC. Recent studies examining the hormonal regulation of NCC have implicated angiotensin II and aldosterone in regulation of the WNK4-Ste20-related proline/alanine-rich kinase-NCC pathway. Summary: NCC is subject to a complex regulatory network of kinases, which appear quite sensitive to alterations of the hormonal and physiologic milieu.
MeSH term(s)	Animals ; Diuretics/pharmacology ; Hormones/physiology ; Humans ; Mice ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Sodium Chloride Symporters/drug effects ; Sodium Chloride Symporters/genetics ; Sodium Chloride Symporters/physiology ; Thiazides/pharmacology
Chemical Substances	Diuretics ; Hormones ; Sodium Chloride Symporters ; Thiazides ; Protein Kinases (EC 2.7.-)
Language	English
Publishing date	2009-07-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0b013e32832f2fcb
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3686: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The IFNγ-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension.

Benson, Lance N / Liu, Yunmeng / Wang, Xiangting / Xiong, Yunzhao / Rhee, Sung W / Guo, Yunping / Deck, Katherine S / Mora, Christoph J / Li, Lin-Xi / Huang, Lu / Andrews, J Tucker / Qin, Zhiqiang / Hoover, Robert S / Ko, Benjamin / Williams, Ryan M / Heller, Daniel A / Jaimes, Edgar A / Mu, Shengyu

Circulation research

2022 Volume 130, Issue 10, Page(s) 1550–1564

Abstract: Background: Renal T cells contribute importantly to hypertension, but the underlying mechanism is incompletely understood. We reported that CD8Ts directly stimulate distal convoluted tubule cells (DCTs) to increase NCC (sodium chloride co-transporter) ... ...

Abstract	Background: Renal T cells contribute importantly to hypertension, but the underlying mechanism is incompletely understood. We reported that CD8Ts directly stimulate distal convoluted tubule cells (DCTs) to increase NCC (sodium chloride co-transporter) expression and salt reabsorption. However, the mechanistic basis of this pathogenic pathway that promotes hypertension remains to be elucidated. Methods: We used mouse models of DOCA+salt (DOCA) treatment and adoptive transfer of CD8 Results: We identified critical molecular players and demonstrated their roles in augmenting the CD8T-DCT interaction leading to salt-sensitive hypertension. We found that activated CD8Ts exhibit enhanced interaction with DCTs via IFN-γ-induced upregulation of MHC-I and PDL1 in DCTs, thereby stimulating higher expression of NCC in DCTs to cause excessive salt retention and progressive elevation of blood pressure. Eliminating IFN-γ or renal tubule-specific knockdown of PDL1 prevented T cell homing into the kidney, thereby attenuating hypertension in 2 different mouse models. Conclusions: Our results identified the role of activated CD8Ts in contributing to increased sodium retention in DCTS through the IFNγ-PDL1 pathway. These findings provide a new mechanism for T cell involvement in the pathogenesis of hypertension and reveal novel therapeutic targets.
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/metabolism ; Desoxycorticosterone Acetate/metabolism ; Desoxycorticosterone Acetate/pharmacology ; Disease Models, Animal ; Hypertension/metabolism ; Kidney Tubules, Distal/metabolism ; Kidney Tubules, Distal/pathology ; Mice ; Sodium/metabolism ; Sodium Chloride Symporters/metabolism ; Sodium Chloride, Dietary
Chemical Substances	Sodium Chloride Symporters ; Sodium Chloride, Dietary ; Desoxycorticosterone Acetate (6E0A168OB8) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2022-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.121.320373
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.70: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito