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Abstract: SA-PO870

The Mechanism of Sodium-Dependent Phosphate Cotransporter Pit-1 in Phosphate-Induced Vascular Calcification in HASMCs

Session Information

  • Vascular Calcification
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Mineral Disease

  • 1205 Vascular Calcification


  • Ding, Minwen, Huashan Hosopital, Fudan Univeristy, Shanghai, China
  • Jiang, Xinxin, Huashan Hosopital, Fudan Univeristy, Shanghai, China
  • Wang, Mengjing, Huashan Hosopital, Fudan Univeristy, Shanghai, China
  • Zhang, Minmin, Huashan Hosopital, Fudan Univeristy, Shanghai, China
  • Chen, Jing, Huashan Hosopital, Fudan Univeristy, Shanghai, China

Vascular calcification (VC) is an important risk factor for cardiovascular disease in maintenance hemodialysis (MHD) patients. Hyperphosphatemia and micro-inflammatory state are known to be the prevalent conditions in MHD patients, which contribute greatly to the development of VC. The aims of this study were to explore the effects of hyperphosphate on peripheral blood mononuclear cells (PBMCs) and then the direct effects of hyperphosphate and TNF-αon human aortic smooth muscle cells (HASMCs).


Low concentration TNF-α(10pg/ml) and supernatants of monocytes (isolated from healthy donors’ PBMCs) were used to evaluate the effects of micro-inflammatory on HASMCs. Cells were divided into five groups: NP, HP, TNF-α, supernatants and PFA group. The antagonist of Pit-1 (PFA) was used to explore the possible effects of Pit-1 on monocytes and the further effects on HASMCs. We used Alizarin red staining to determine the vascular calcification extent. The gene expressions of TNF-α, Pit-1 and osteochondrogenic factors (OCF) were tested by Realtime PCR. The excretion of TNF-α in monocytes was evaluated by ELISA. The protein expression of Pit-1 was tested by Western Blot.


1. After exposure of human monocytes to HP (4M), the concentration and mRNA expression of TNF-α was increased (p<0.05 vs. NP). HP also increased the protein and mRNA expression of Pit-1 (p<0.05 vs. NP). Incubation in the presence of PFA (2M) partially prevented the effects of HP (p<0.05 vs. HP).
2. The presence of low concentration TNF-α(10pg/ml) alone or supernatants of monocytes alone had no effect of OCF gene expression or mineralization (p>0.05 vs.NP) on HASMCs. HP increased the mRNA and protein expression of OPN and Runx2 (p<0.05 vs. NP) and caused mineralization in HASMCs.
3. After exposure to both HP(4M) and TNF-α(10pg/ml) or supernatants, the mineralization and OCF gene expression were markedly increased in HASMCs (p<0.05 vs.HP). Incubation in the presence of PFA (2M) also partially prevented the aforementioned effects (p<0.05 vs.HP) in HASMCs.


We conclude that via Pit-1, hyperphosphate could increase the synthesis and secretion of TNF-α in human monocytes, furthermore accelerating the vascular calcification in HASMCs, which may be the therapeutic target in preventing vascular calcification in MHD patients.