ArticleArteriosclerosis, thrombosis, and vascular biology2013
Sodium-dependent phosphate cotransporters and phosphate-induced calcification of vascular smooth muscle cells: redundant roles for PiT-1 and PiT-2.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 125 citations in OpenAlex.
- Review
- Whole-genome sequencing GWAS reveals bovine genomic effects on enteric methane emissions in beef cattle.Scientific reports · 2025Article
- Calciphylaxis diagnosis, management and future directions: a comprehensive update on behalf of the European Renal Association CKD-MBD Working Group.Clinical kidney journal · 2025Review
- La Ribonucleoprotein 7 Protects Vascular Smooth Muscle Cell Contractile Phenotype in CKD by Coupling with P300.Journal of the American Society of Nephrology : JASN · 2025Article
- Review
- Phosphate overload via the type III Na-dependent Pi transporter represses aortic wall elastic fiber formation.Fujita medical journal · 2024Article
- In Vitro Models of Cardiovascular Calcification.Biomedicines · 2024Review
- Zinc Action in Vascular Calcification.Preventive nutrition and food science · 2024Review
- SGK3 promotes vascular calcification via Pit-1 in chronic kidney disease.Theranostics · 2024Article
- Phosphate Control in Peritoneal Dialysis Patients: Issues, Solutions, and Open Questions.Nutrients · 2023Review
- Role of the extracellular ATP/pyrophosphate metabolism cycle in vascular calcification.Purinergic signalling · 2023Review
- SLC20a1/PiT-1 is required for chorioallantoic placental morphogenesis.Vascular biology (Bristol, England) · 2023Article
- Role of transporters in regulating mammalian intracellular inorganic phosphate.Frontiers in pharmacology · 2023Review
- MiR-708-5p/Pit-1 axis mediates high phosphate-induced calcification in vascular smooth muscle cells via Wnt8b/β-catenin pathway.The Kaohsiung journal of medical sciences · 2022Article
- Review
- Oxidative Stress Related to Plasmalemmal and Mitochondrial Phosphate Transporters in Vascular Calcification.Antioxidants (Basel, Switzerland) · 2022Review
- Magnesium to prevent kidney disease-associated vascular calcification: crystal clear?Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022Article
- Insights Into the Role of Mitochondria in Vascular Calcification.Frontiers in cardiovascular medicine · 2022Review
- Klotho deficiency-induced arterial calcification involves osteoblastic transition of VSMCs and activation of BMP signaling.Journal of cellular physiology · 2022Article
- Phosphate and Cellular Senescence.Advances in experimental medicine and biology · 2022Article
12 more citing papers are in PubMed but not listed here.
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11 authors at 2 institutions in 1 country.
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Abstract
objectiveElevated serum phosphate has emerged as a major risk factor for vascular calcification. The sodium-dependent phosphate cotransporter, PiT-1, was previously shown to be required for phosphate-induced osteogenic differentiation and calcification of cultured human vascular smooth muscle cells (VSMCs), but its importance in vascular calcification in vivo and the potential role of its homologue, PiT-2, have not been determined. We investigated the in vivo requirement for PiT-1 in vascular calcification using a mouse model of chronic kidney disease and the potential compensatory role of PiT-2 using in vitro knockdown and overexpression strategies. APPROACH AND
resultsMice with targeted deletion of PiT-1 in VSMCs were generated (PiT-1(Δsm)). PiT-1 mRNA levels were undetectable, whereas PiT-2 mRNA levels were increased 2-fold in the vascular aortic media of PiT-1(Δsm) compared with PiT-1(flox/flox) control. When arterial medial calcification was induced in PiT-1(Δsm) and PiT-1(flox/flox) by chronic kidney disease followed by dietary phosphate loading, the degree of aortic calcification was not different between genotypes, suggesting compensation by PiT-2. Consistent with this possibility, VSMCs isolated from PiT-1(Δsm) mice had no PiT-1 mRNA expression, increased PiT-2 mRNA levels, and no difference in sodium-dependent phosphate uptake or phosphate-induced matrix calcification compared with PiT-1(flox/flox) VSMCs. Knockdown of PiT-2 decreased phosphate uptake and phosphate-induced calcification of PiT-1(Δsm) VSMCs. Furthermore, overexpression of PiT-2 restored these parameters in human PiT-1-deficient VSMCs.
conclusionsPiT-2 can mediate phosphate uptake and calcification of VSMCs in the absence of PiT-1. Mechanistically, PiT-1 and PiT-2 seem to serve redundant roles in phosphate-induced calcification of VSMCs.
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