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MAY 10 th  Key Note LectureS




奈良女子大学 生活環境学部教授 吉本光佐




2005年 奈良女子大学大学院 人間文化研究科 博士後期課程修了博士

2005年 奈良女子大学 大学院人間文化研究科 博士研究員

2006年 ミネソタ大学医学部生理学講座 ポストドクトタルフェロー

208年 カリフォルニア州 サンノゼ 在住

2010年 奈良女子大学 大学院人間文化研究科 博士研究員

2010年 国立循環器病研究センター 研究員

2014年 奈良女子大学研究院 生活環境科学系 助教

2015年 奈良女子大学研究院 生活環境科学系 准教授

2022年 奈良女子大学研究院 生活環境科学系  教授

IMG - Mu 2022.jpeg

Non-antigen-dependent CD8T-activation promotes salt-sensitive hypertension

Department of Pharmacology and Toxicology University of Arkansas for Medical Sciences  Shengyu Mu

Background: Hypertension is a significant public health problem worldwide, but the pathophysiologic mechanisms are only partially understood. CD8+ T cells (CD8Ts) have been implicated recently in the development of salt-sensitive hypertension. However, the specific mechanisms and key players involved in this process still need to be fully understood. In this study, we used in-vivo models of hypertension and ex-vivo assays of CD8T signaling to investigate the contribution of the P2X7 receptor to CD8T activation and subsequent promotion of sodium retention by the sodium chloride cotransporter (NCC) in the kidney.

Methods: We employed the DOCA/salt and CD8T-adoptive transfer mouse models of hypertension. Wild-type (WT) were used as genetic controls, OT-1 mice were utilized to determine antigen dependency of CD8T-activation, and P2X7-KO mice were studied to define the role of P2X7 in activating CD8Ts and promoting hypertension. Blood pressure was monitored continuously using biotelemetry, and kidneys were obtained at different experimental endpoints for analysis. For activation assays and ATP stimulation, freshly isolated CD8Ts were obtained from sham and hypertensive mice. The role of P2X7 in CD8T activation and promotion of NCC-mediated sodium retention was explored in CD8Ts and mouse distal convoluted tubule cells (DCTs) co-cultures.

Results: We found that OT-1 mice, nonresponsive to common antigens, still developed hypertension and CD8T-activation in response to DOCA/salt treatment, similar to WT 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.

Conclusion: Collectively, our findings suggest a novel mechanism by which CD8Ts are activated in hypertension to exacerbate salt retention. We infer that the P2X7 receptor on CD8Ts may represent a new therapeutic target to attenuate T cell-mediated immunopathology in hypertension.



Ph.D. (Dr. of Medical Science) University of Tokyo, Tokyo, Japan 2006 - 2011

M.D. TianJin Medical University, TianJin, China 1999 - 2004

Academic Appointments

Associate Professor (with tenure) Department of Pharmacology & Toxicology University of Arkansas for Medical Sciences (UAMS) Little Rock, AR 2022 - Present

Assistant Professor (tenure track) Department of Pharmacology & Toxicology UAMS Little Rock, AR2017 - 2022

Graduate Faculty (GPIBS) UAMS Little Rock, AR 2016 - Present

Assistant Professor (research track) Department of Pharmacology & Toxicology UAMS Little Rock, AR 2013 - 2017

Project Assistant Professor Division of Clinical Epigenetics Research Center for Advanced Science and Technology University of Tokyo, Tokyo, Japan 2012 - 2013

Postdoctoral Fellow Department of Nephrology and Endocrinology School of Medicine, University of Tokyo, Tokyo, Japan 2011 - 2012

Graduate Research Assistant Department of Nephrology and Endocrinology School of Medicine, University of Tokyo, Tokyo, Japan 2007 - 2011

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