دورية أكاديمية
Male kidney-specific BMAL1 knockout mice are protected from K + -deficient, high-salt diet-induced blood pressure increases.
| العنوان: | Male kidney-specific BMAL1 knockout mice are protected from K + -deficient, high-salt diet-induced blood pressure increases. |
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| المؤلفون: | Crislip GR; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States.; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Center for Integrative Cardiovascular and Metabolic Disease, University of Florida, Gainesville, Florida, United States., Costello HM; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States.; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Center for Integrative Cardiovascular and Metabolic Disease, University of Florida, Gainesville, Florida, United States., Juffre A; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States.; Center for Integrative Cardiovascular and Metabolic Disease, University of Florida, Gainesville, Florida, United States.; Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida, United States., Cheng KY; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States., Lynch IJ; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Department of Research, North Florida/South Georgia Veterans Health System, Gainesville, Florida, United States., Johnston JG; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Center for Integrative Cardiovascular and Metabolic Disease, University of Florida, Gainesville, Florida, United States.; Department of Research, North Florida/South Georgia Veterans Health System, Gainesville, Florida, United States., Drucker CB; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States., Bratanatawira P; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States., Agarwal A; Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida, United States., Mendez VM; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States., Thelwell RS; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States., Douma LG; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida, United States., Wingo CS; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States.; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Department of Research, North Florida/South Georgia Veterans Health System, Gainesville, Florida, United States., Alli AA; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States.; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Center for Integrative Cardiovascular and Metabolic Disease, University of Florida, Gainesville, Florida, United States., Scindia YM; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Florida, Gainesville, Florida, United States., Gumz ML; Department of Physiology and Aging, University of Florida, Gainesville, Florida, United States.; Division of Nephrology, Hypertension, and Renal Transplantation, Department of Medicine, University of Florida, Gainesville, Florida, United States.; Center for Integrative Cardiovascular and Metabolic Disease, University of Florida, Gainesville, Florida, United States.; Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida, United States. |
| المصدر: | American journal of physiology. Renal physiology [Am J Physiol Renal Physiol] 2023 Nov 01; Vol. 325 (5), pp. F656-F668. Date of Electronic Publication: 2023 Sep 14. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Physiological Society Country of Publication: United States NLM ID: 100901990 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1522-1466 (Electronic) Linking ISSN: 15221466 NLM ISO Abbreviation: Am J Physiol Renal Physiol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Bethesda, Md. : American Physiological Society, c1997- |
| مواضيع طبية MeSH: | ARNTL Transcription Factors*/metabolism , Hypertension*/genetics , Hypertension*/prevention & control, Animals ; Male ; Mice ; Blood Pressure/physiology ; Circadian Rhythm/physiology ; Cytokines ; Diet ; Kidney/metabolism ; Mice, Knockout ; Sodium Chloride, Dietary |
| مستخلص: | The circadian clock protein basic helix-loop-helix aryl hydrocarbon receptor nuclear translocator-like protein 1 (BMAL1) is a transcription factor that impacts kidney function, including blood pressure (BP) control. Previously, we have shown that male, but not female, kidney-specific cadherin Cre-positive BMAL1 knockout (KS-BMAL1 KO) mice exhibit lower BP compared with littermate controls. The goal of this study was to determine the BP phenotype and immune response in male KS-BMAL1 KO mice in response to a low-K + high-salt (LKHS) diet. BP, renal inflammatory markers, and immune cells were measured in male mice following an LKHS diet. Male KS-BMAL1 KO mice had lower BP following the LKHS diet compared with control mice, yet their circadian rhythm in pressure remained unchanged. Additionally, KS-BMAL1 KO mice exhibited lower levels of renal proinflammatory cytokines and immune cells following the LKHS diet compared with control mice. KS-BMAL1 KO mice were protected from the salt-sensitive hypertension observed in control mice and displayed an attenuated immune response following the LKHS diet. These data suggest that BMAL1 plays a role in driving the BP increase and proinflammatory environment that occurs in response to an LKHS diet. NEW & NOTEWORTHY We show here, for the first time, that kidney-specific BMAL1 knockout mice are protected from blood pressure (BP) increases and immune responses to a salt-sensitive diet. Other kidney-specific BMAL1 knockout models exhibit lower BP phenotypes under basal conditions. A salt-sensitive diet exacerbates this genotype-specific BP response, leading to fewer proinflammatory cytokines and immune cells in knockout mice. These data demonstrate the importance of distal segment BMAL1 in BP and immune responses to a salt-sensitive environment. |
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| معلومات مُعتمدة: | R01 DK109570 United States DK NIDDK NIH HHS; F32 DK121424 United States DK NIDDK NIH HHS; R01 DK123078 United States DK NIDDK NIH HHS; T32 HL083810 United States HL NHLBI NIH HHS; P30 AG028740 United States AG NIA NIH HHS |
| فهرسة مساهمة: | Keywords: circadian rhythm; clock; hypertension; immune cells; inflammation |
| المشرفين على المادة: | 0 (ARNTL Transcription Factors) 0 (Cytokines) 0 (Sodium Chloride, Dietary) 0 (Bmal1 protein, mouse) |
| تواريخ الأحداث: | Date Created: 20230914 Date Completed: 20231114 Latest Revision: 20240220 |
| رمز التحديث: | 20240220 |
| مُعرف محوري في PubMed: | PMC10874679 |
| DOI: | 10.1152/ajprenal.00126.2023 |
| PMID: | 37706232 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1522-1466 |
|---|---|
| DOI: | 10.1152/ajprenal.00126.2023 |