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Leukocytic Thy‐1 Expression Differs in Kidney Cortex and Medulla in Spontaneously Hypertensive Rats
Author(s) -
Meariman Jacob K.,
Sutphen Jane,
Denys Ian,
Harrison David G.,
Kapusta Daniel R.,
Gao Juan
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.08989
Subject(s) - medulla , renal cortex , immune system , cortex (anatomy) , denervation , inflammation , kidney , medicine , endocrinology , renal medulla , biology , immunology , neuroscience
Sympathoexcitation and increased inflammation are both involved in mediating hypertension, and decreasing sympathetic nerve activity is vital for reducing inflammation in this disease. However, the mechanism(s) by which the nervous system communicates with the immune system in hypertension is still largely unknown. To examine this interaction in this study, twenty‐week‐old spontaneously hypertensive rats (SHR) underwent renal denervation (RDN) via radiofrequency ablation of the renal artery. After two months, kidneys were harvested and separated into cortex and medulla, and lymphocytes were detected by flow cytometry. RDN significantly decreased CD4 + T cells, CD8 + T cells, and B cells in the renal medulla but had no effect on these immune cells in the cortex. In a separate group of intact SHR, Thy‐1, a reported activator of T cells, was measured in leukocytes isolated from the renal cortex and medulla. Thy‐1 mRNA expression was significantly increased in T cells, non‐T cells, CD45 + cells, and CD45 − cells from the leukocytes isolated from the cortex compared to those isolated from the medulla. These findings suggest that Thy‐1 in cortical leukocytes might activate the immune system in the renal cortex independent of the renal nerves. Downregulation of Thy‐1 in the renal cortex could increase the benefit of RDN and decrease renal inflammation in hypertension. Support or Funding Information NIH NIGMS P30 GM106392

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