Protective Roles of Xenotropic and Polytropic Retrovirus Receptor 1 (XPR1) in Uremic Vascular Calcification.

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Tytuł:: Protective Roles of Xenotropic and Polytropic Retrovirus Receptor 1 (XPR1) in Uremic Vascular Calcification.
Autorzy:: Arase H; Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 8128582, Japan.
Yamada S; Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 8128582, Japan.
Torisu K; Department of Integrated Therapy for Chronic Kidney Disease, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 8128582, Japan.
Tokumoto M; Department of Internal Medicine, Fukuoka Dental College, 2-15-1 Tamura, Sawara-Ku, Fukuoka, 8140193, Japan.
Taniguchi M; Fukuoka Renal Clinic, 4-6-20 Watanabe-Dori, Chuo-Ku, Fukuoka, 8100004, Japan.
Tsuruya K; Department of Nephrology, Nara Medical University, 840 Shijo-Cho, Kashihara, Nara, 6348521, Japan.
Nakano T; Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 8128582, Japan. .
Kitazono T; Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 8128582, Japan.
Źródło:: Calcified tissue international [Calcif Tissue Int] 2022 Jun; Vol. 110 (6), pp. 685-697. Date of Electronic Publication: 2022 Feb 02.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: New York Ny : Springer Verlag
Original Publication: Berlin, New York, Springer International.
MeSH Terms:: Renal Insufficiency, Chronic*/metabolism
Renal Insufficiency, Chronic*/pathology
Vascular Calcification*/metabolism
Xenotropic and Polytropic Retrovirus Receptor*/metabolism
Animals ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Myocytes, Smooth Muscle ; Phosphates/metabolism ; RNA, Messenger/metabolism
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Contributed Indexing:: Keywords: Mouse model; Phosphate transporter; Vascular calcification; Vascular smooth muscle cell; XPR1
Substance Nomenclature:: 0 (Phosphates)
0 (RNA, Messenger)
0 (Xenotropic and Polytropic Retrovirus Receptor)
0 (Xpr1 protein, mouse)
Entry Date(s):: Date Created: 20220203 Date Completed: 20220517 Latest Revision: 20220615
Update Code:: 20240104
DOI:: 10.1007/s00223-022-00947-3
PMID:: 35112184
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Cellular phosphate transporters play critical roles in the pathogenesis of vascular calcification (VC) in chronic kidney disease (CKD). However, the mechanistic link between VC and xenotropic and polytropic receptor 1 (XPR1), a newly identified phosphate exporter, remains unknown. We developed a new mouse model with rapidly progressive uremic VC in C57BL/6 mice and examined the roles of XPR1. The combination of surgical heminephrectomy and 8 weeks of feeding a customized warfarin and adenine-based diet induced extensive aortic VC in almost all mice. The XPR1 mRNA level in the aorta of CKD mice was significantly lower than those in control mice as early as week 2, when there was no apparent VC, which progressively declined thereafter. Dietary phosphate restriction increased XPR1 mRNA expression in the aorta but reduced aortic VC in CKD mice. In cultured vascular smooth muscle cells (VSMCs), a calcifying medium supplemented with high phosphate and calcium did not affect XPR1 mRNA expression. The XPR1 mRNA expression in cultured VCMCs was also unaffected by administration of indoxyl sulfate or calcitriol deficiency but was decreased by 1-34 parathyroid hormone or fibroblast growth factor 23 supplementation. Furthermore, XPR1 deletion in the cultured VSMCs exacerbated calcification of the extracellular matrix as well as the osteogenic phenotypic switch under the condition of calcifying medium. Our data suggest that XPR1 plays protective roles in the pathogenesis of VC and its decrease in the aorta may contribute to the progression of VC in CKD.
(© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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