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Neuromedin B modulates phosphate-induced vascular calcification

김형준|배수경|Hyun-Joo Park|Yeon Kim|배문경|Mi-Kyoung Kim
생화학분자생물학회 (Korean Society Of Biochemistry And Molecular Biology)|2021.11|BMB Reports|제54권 제11호|pp. 569-574

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참고문헌

키워드

Vascular calcificationVascular smooth muscle cellsBombesin-like peptidesNeuromedin BNeuromedin B receptor
주제분류화학

초록

Vascular calcification is the heterotopic accumulation of calciumphosphate salts in the vascular tissue and is highly correlatedwith increased cardiovascular morbidity and mortality. In thisstudy, we found that the expression of neuromedin B (NMB)and NMB receptor is upregulated in phosphate-induced calcificationof vascular smooth muscle cells (VSMCs). Silencing ofNMB or treatment with NMB receptor antagonist, PD168368,inhibited the phosphate-induced osteogenic differentiation ofVSMCs by inhibiting Wnt/β-catenin signaling and VSMC apoptosis. PD168368 also attenuated the arterial calcification in culturedaortic rings and in a rat model of chronic kidney disease. Theresults of this study suggest that NMB–NMB receptor axis mayhave potential therapeutic value in the diagnosis and treatmentof vascular calcification.

Abstract

Vascular calcification is the heterotopic accumulation of calciumphosphate salts in the vascular tissue and is highly correlatedwith increased cardiovascular morbidity and mortality. In thisstudy, we found that the expression of neuromedin B (NMB)and NMB receptor is upregulated in phosphate-induced calcificationof vascular smooth muscle cells (VSMCs). Silencing ofNMB or treatment with NMB receptor antagonist, PD168368,inhibited the phosphate-induced osteogenic differentiation ofVSMCs by inhibiting Wnt/β-catenin signaling and VSMC apoptosis. PD168368 also attenuated the arterial calcification in culturedaortic rings and in a rat model of chronic kidney disease. Theresults of this study suggest that NMB–NMB receptor axis mayhave potential therapeutic value in the diagnosis and treatmentof vascular calcification.

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