Brown-Norway chromosome 1 mitigates the upregulation of proinflammatory pathways in mTAL cells and subsequent age-related CKD in Dahl SS/JrHsdMcwi rats-Reference-Cited by-同舟云学术

Brown-Norway chromosome 1 mitigates the upregulation of proinflammatory pathways in mTAL cells and subsequent age-related CKD in Dahl SS/JrHsdMcwi rats

Published:2023-02-01 Issue:2 Volume:324 Page:F193-F210
ISSN:1931-857X
Container-title:American Journal of Physiology-Renal Physiology
language:en
Short-container-title:American Journal of Physiology-Renal Physiology

Author:

Chivers Jacqueline M.¹^ORCID,Whiles Shannon A.¹^ORCID,Miles Conor B.¹,Biederman Brianna E.¹,Ellison Megan F.¹,Lovingood Connor W.¹,Wright Marie H.¹,Hoover Donald B.¹²^ORCID,Raafey Muhammad A.³,Youngberg George A.³,Venkatachalam Manjeri A.⁴,Zheleznova Nadezhda N.⁵,Yang Chun⁵,Liu Pengyuan⁵,Kriegel Alison J.⁵^ORCID,Cowley Allen W.⁵,O’Connor Paul M.⁶,Picken Maria M.⁷^ORCID,Polichnowski Aaron J.¹²^ORCID

Affiliation:

1. Department of Biomedical Sciences, East Tennessee State University, Johnson City, Tennessee

2. Center of Excellence in Inflammation, Infectious Disease and Immunity, East Tennessee State University, Johnson City, Tennessee

3. Department of Pathology, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee

4. Department of Pathology, University of Texas Health Science Center, San Antonio, Texas

5. Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin

6. Department of Physiology, Augusta University, Augusta, Georgia

7. Department of Pathology, Loyola University Medical Center, Maywood, Illinois

Abstract

This study shows that the robust age-related progression of kidney disease in Dahl SS/JrHsdMcw rats maintained on a normal-salt diet is abolished in consomic SS.BN1 rats. Evidence that medullary thick ascending limb segments of SS/JrHsdMcw rats are structurally abnormal and enriched in proinflammatory pathways before the development of protein casts provides new insights into the pathogenesis of kidney disease in this model.

Funder

American Heart Association

American Physiological Society

American Society of Nephrology

East Tennessee State University

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | National Institutes of Health

Publisher

American Physiological Society

Subject

Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajprenal.00145.2022

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