Wnt1 inhibits vascular smooth muscle cell calcification by promoting ANKH expression
Wnt signaling plays a critical role in vascular calcification (VC). Wnt factors induce different physiological and pathological effects on cardiovascular functions. Wnt1, a ligand of Wnt/β-catenin signaling, promotes pro-angiogenesis and reduces myocardial infarction. The role of Wnt1 on VC in chron...
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| Published in | Journal of molecular and cellular cardiology Vol. 135; pp. 10 - 21 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.10.2019
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| Abstract | Wnt signaling plays a critical role in vascular calcification (VC). Wnt factors induce different physiological and pathological effects on cardiovascular functions. Wnt1, a ligand of Wnt/β-catenin signaling, promotes pro-angiogenesis and reduces myocardial infarction. The role of Wnt1 on VC in chronic kidney disease (CKD) is not fully understood.
We used human vascular smooth muscle cells (VSMCs) and a rat model of chronic renal failure (CRF), and observed a native protective mechanism by which VC is reduced via the activation of Wnt1 and its transcriptional target ANKH inorganic pyrophosphate transport regulator (ANKH) gene. ANKH is an essential calcification inhibitor that effluxes inorganic pyrophosphate (PPi) from VSMCs to play an inhibitory role in VC. Vascular ANKH and plasma PPi were significantly downregulated in the rat model of CRF. The knockdown or inhibition of ANKH reversed the effect of Wnt1 on VC in VSMCs. Clinical analysis revealed low plasma levels of Wnt1 and PPi were associated with CKD in patients. Applying a Wnt/β-catenin signaling agonist can alleviate the progression of VC.
This work reveals the ANKH regulation of Wnt1 in VSMCs is essential for blocking VC. Our findings may contribute to the development of medications that target Wnt signaling and/or ANKH to inhibit VC.
•Novel mechanism of Wnt1 protects against vascular calcification.•ANKH, a vascular calcification inhibitor, is a target gene of Wnt1/β-catenin signal.•Agonist of Wnt/β-catenin signal is a potential medicine for vascular calcification. |
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| AbstractList | Wnt signaling plays a critical role in vascular calcification (VC). Wnt factors induce different physiological and pathological effects on cardiovascular functions. Wnt1, a ligand of Wnt/β-catenin signaling, promotes pro-angiogenesis and reduces myocardial infarction. The role of Wnt1 on VC in chronic kidney disease (CKD) is not fully understood.
We used human vascular smooth muscle cells (VSMCs) and a rat model of chronic renal failure (CRF), and observed a native protective mechanism by which VC is reduced via the activation of Wnt1 and its transcriptional target ANKH inorganic pyrophosphate transport regulator (ANKH) gene. ANKH is an essential calcification inhibitor that effluxes inorganic pyrophosphate (PPi) from VSMCs to play an inhibitory role in VC. Vascular ANKH and plasma PPi were significantly downregulated in the rat model of CRF. The knockdown or inhibition of ANKH reversed the effect of Wnt1 on VC in VSMCs. Clinical analysis revealed low plasma levels of Wnt1 and PPi were associated with CKD in patients. Applying a Wnt/β-catenin signaling agonist can alleviate the progression of VC.
This work reveals the ANKH regulation of Wnt1 in VSMCs is essential for blocking VC. Our findings may contribute to the development of medications that target Wnt signaling and/or ANKH to inhibit VC.
•Novel mechanism of Wnt1 protects against vascular calcification.•ANKH, a vascular calcification inhibitor, is a target gene of Wnt1/β-catenin signal.•Agonist of Wnt/β-catenin signal is a potential medicine for vascular calcification. Wnt signaling plays a critical role in vascular calcification (VC). Wnt factors induce different physiological and pathological effects on cardiovascular functions. Wnt1, a ligand of Wnt/β-catenin signaling, promotes pro-angiogenesis and reduces myocardial infarction. The role of Wnt1 on VC in chronic kidney disease (CKD) is not fully understood. We used human vascular smooth muscle cells (VSMCs) and a rat model of chronic renal failure (CRF), and observed a native protective mechanism by which VC is reduced via the activation of Wnt1 and its transcriptional target ANKH inorganic pyrophosphate transport regulator (ANKH) gene. ANKH is an essential calcification inhibitor that effluxes inorganic pyrophosphate (PPi) from VSMCs to play an inhibitory role in VC. Vascular ANKH and plasma PPi were significantly downregulated in the rat model of CRF. The knockdown or inhibition of ANKH reversed the effect of Wnt1 on VC in VSMCs. Clinical analysis revealed low plasma levels of Wnt1 and PPi were associated with CKD in patients. Applying a Wnt/β-catenin signaling agonist can alleviate the progression of VC. This work reveals the ANKH regulation of Wnt1 in VSMCs is essential for blocking VC. Our findings may contribute to the development of medications that target Wnt signaling and/or ANKH to inhibit VC. Wnt signaling plays a critical role in vascular calcification (VC). Wnt factors induce different physiological and pathological effects on cardiovascular functions. Wnt1, a ligand of Wnt/β-catenin signaling, promotes pro-angiogenesis and reduces myocardial infarction. The role of Wnt1 on VC in chronic kidney disease (CKD) is not fully understood.AIMSWnt signaling plays a critical role in vascular calcification (VC). Wnt factors induce different physiological and pathological effects on cardiovascular functions. Wnt1, a ligand of Wnt/β-catenin signaling, promotes pro-angiogenesis and reduces myocardial infarction. The role of Wnt1 on VC in chronic kidney disease (CKD) is not fully understood.We used human vascular smooth muscle cells (VSMCs) and a rat model of chronic renal failure (CRF), and observed a native protective mechanism by which VC is reduced via the activation of Wnt1 and its transcriptional target ANKH inorganic pyrophosphate transport regulator (ANKH) gene. ANKH is an essential calcification inhibitor that effluxes inorganic pyrophosphate (PPi) from VSMCs to play an inhibitory role in VC. Vascular ANKH and plasma PPi were significantly downregulated in the rat model of CRF. The knockdown or inhibition of ANKH reversed the effect of Wnt1 on VC in VSMCs. Clinical analysis revealed low plasma levels of Wnt1 and PPi were associated with CKD in patients. Applying a Wnt/β-catenin signaling agonist can alleviate the progression of VC.METHODS AND RESULTSWe used human vascular smooth muscle cells (VSMCs) and a rat model of chronic renal failure (CRF), and observed a native protective mechanism by which VC is reduced via the activation of Wnt1 and its transcriptional target ANKH inorganic pyrophosphate transport regulator (ANKH) gene. ANKH is an essential calcification inhibitor that effluxes inorganic pyrophosphate (PPi) from VSMCs to play an inhibitory role in VC. Vascular ANKH and plasma PPi were significantly downregulated in the rat model of CRF. The knockdown or inhibition of ANKH reversed the effect of Wnt1 on VC in VSMCs. Clinical analysis revealed low plasma levels of Wnt1 and PPi were associated with CKD in patients. Applying a Wnt/β-catenin signaling agonist can alleviate the progression of VC.This work reveals the ANKH regulation of Wnt1 in VSMCs is essential for blocking VC. Our findings may contribute to the development of medications that target Wnt signaling and/or ANKH to inhibit VC.CONCLUSIONThis work reveals the ANKH regulation of Wnt1 in VSMCs is essential for blocking VC. Our findings may contribute to the development of medications that target Wnt signaling and/or ANKH to inhibit VC. |
| Author | Xu, Ming-Jiang Feng, Lu Yin, Sen Cui, Zhong-Kai Chu, Yun-Chin Zhao, Ban Mao, Yonghui Wang, Cun-Yu Zhao, Yang Han, Duanyang Chen, Beidong Wang, Xian Zhao, Gexin |
| Author_xml | – sequence: 1 givenname: Beidong orcidid: 0000-0002-0561-7873 surname: Chen fullname: Chen, Beidong organization: MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing, China – sequence: 2 givenname: Yang surname: Zhao fullname: Zhao, Yang organization: Department of Laboratory Medicine, Peking University Third Hospital, Beijing, China – sequence: 3 givenname: Duanyang surname: Han fullname: Han, Duanyang organization: Shenzhen Key Laboratory of Spine Surgery, Department of Spine Surgery, Peking University Shenzhen Hospital, Shenzhen, China – sequence: 4 givenname: Ban surname: Zhao fullname: Zhao, Ban organization: Department of Nephrology, Beijing Hospital, Beijing, China – sequence: 5 givenname: Yonghui surname: Mao fullname: Mao, Yonghui organization: Department of Nephrology, Beijing Hospital, Beijing, China – sequence: 6 givenname: Zhong-Kai orcidid: 0000-0003-3112-9379 surname: Cui fullname: Cui, Zhong-Kai organization: Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China – sequence: 7 givenname: Yun-Chin surname: Chu fullname: Chu, Yun-Chin organization: Department of Statistics, North Carolina State University, USA – sequence: 8 givenname: Lu surname: Feng fullname: Feng, Lu organization: MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing, China – sequence: 9 givenname: Sen surname: Yin fullname: Yin, Sen organization: MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing, China – sequence: 10 givenname: Cun-Yu surname: Wang fullname: Wang, Cun-Yu organization: School of Dentistry, University of California, Los Angeles, USA – sequence: 11 givenname: Xian surname: Wang fullname: Wang, Xian organization: Department of Physiology and Pathophysiology, School of Basic Medical Science, Peking University Health Science Center, Beijing, China – sequence: 12 givenname: Ming-Jiang surname: Xu fullname: Xu, Ming-Jiang email: mingjiangxu@bjmu.edu.cn organization: Department of Physiology and Pathophysiology, School of Basic Medical Science, Peking University Health Science Center, Beijing, China – sequence: 13 givenname: Gexin orcidid: 0000-0003-2278-3432 surname: Zhao fullname: Zhao, Gexin email: zhaogexin@ucla.edu organization: Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, USA |
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| CitedBy_id | crossref_primary_10_1038_s41598_020_77732_5 crossref_primary_10_3389_fcell_2020_586831 crossref_primary_10_1016_j_bone_2020_115243 crossref_primary_10_1016_j_lfs_2023_122309 crossref_primary_10_12677_ACM_2022_132169 crossref_primary_10_1016_j_acthis_2020_151551 crossref_primary_10_1080_0886022X_2022_2072337 crossref_primary_10_14336_AD_2021_1024 crossref_primary_10_2147_VHRM_S242685 crossref_primary_10_1016_j_bone_2020_115656 crossref_primary_10_3389_fgene_2022_838220 crossref_primary_10_1016_j_jacc_2023_01_044 crossref_primary_10_2139_ssrn_3894903 crossref_primary_10_2174_1567202619666220316115425 crossref_primary_10_1080_0886022X_2022_2114370 crossref_primary_10_1016_j_bone_2022_116525 |
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| Keywords | Vascular calcification Chronic kidney disease ANKH Wnt1 Vascular smooth muscle cells |
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| Title | Wnt1 inhibits vascular smooth muscle cell calcification by promoting ANKH expression |
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