ICHIHARA Atsuhiro
   Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine
   Position   Professor and Division head
Article types Original article
Language English
Peer review Peer reviewed
Title A functional (pro)renin receptor is expressed in human lymphocytes and monocytes.
Journal Formal name:American journal of physiology. Renal physiology
Abbreviation:Am J Physiol Renal Physiol
ISSN code:15221466/15221466
Volume, Issue, Page 308(5),pp.F487-99
Author and coauthor NARUMI Kaori†, HIROSE Takuo†, SATO Emiko, MORI Takefumi, KISU Kiyomi, ISHIKAWA Mayuko, TOTSUNE Kazuhito, ISHII Tomonori, ICHIHARA Atsuhiro, Genevieve Nguyen, SATO Hiroshi, ITO Sadayoshi
Publication date 2015/03
Summary The renin-angiotensin system (RAS) is involved in inflammation. The signaling via the ANG II type 1 receptor in human lymphocytes and monocytes, which play key roles in pathophysiology of glomerulonephritis (GN), can enhance inflammation. However, the role of the (pro)renin receptor [(P)RR], a component of the RAS, in inflammatory reactions is unknown. We assessed whether (P)RR is expressed in human lymphocytes and monocytes by RT-PCR, Western blotting, flow cytometry, and immunohistochemistry, and whether (P)RR functions in inflammation. (P)RR mRNA and protein were expressed in human peripheral blood mononuclear cells (PBMCs). Flow cytometric analysis revealed high expression of (P)RR on monocytes. (P)RR was present on PBMCs, infiltrating lymphocytes, and macrophages around glomeruli with a crescent in anti-neutrophil cytoplasmic antibody (ANCA)-associated GN. Renin stimulation of PBMCs from healthy subjects in the presence of the ANG II type 1 receptor and ANG II type 2 receptor blockers induced ERK1/2 phosphorylation and release of IL-6 and expression of cyclooxygenase-2 (COX-2). The increases in cytokine release and COX-2 expression were inhibited in the presence of an ERK1/2 inhibitor. (P)RR knockdown by small interfering RNA inU937 cells, a human leukemic monocyte lymphoma cell line, significantly decreased ERK1/2 phosphorylation after renin stimulation. Thus (P)RR expressed in human inflammatory cells might contribute to inflammation in ANCA-associated GN.
DOI 10.1152/ajprenal.00206.2014
PMID 25503726