ArticleActa pharmacologica Sinica2010
Adrenomedullin up-regulates osteopontin and attenuates vascular calcification via the cAMP/PKA signaling pathway.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Hydrogen Sulfide Deficiency Contributes to Tubular Damage and Calcium Oxalate Crystal Formation in Hyperoxaluria Nephropathy: Role of Osteopontin and Tamm-Horsfall Protein.Antioxidants (Basel, Switzerland) · 2025Article
- Isoforskolin modulates AQP4-SPP1-PIK3C3 related pathway for chronic obstructive pulmonary disease via cAMP signaling.Chinese medicine · 2023Article
- Flavocoxid Ameliorates Aortic Calcification Induced by Hypervitaminosis DCardiovascular drugs and therapy · 2022Article
- Osteopontin - The stirring multifunctional regulatory factor in multisystem aging.Frontiers in endocrinology · 2022Review
- Adrenomedullin Attenuates Inflammation in White Adipose Tissue of Obese Rats Through Receptor-Mediated PKA Pathway.Obesity (Silver Spring, Md.) · 2021Article
- Review
- Regulation of Vascular Calcification by Growth Hormone-Releasing Hormone and Its Agonists.Circulation research · 2018Article
- Hydrogen Sulfide Facilitates the Impaired Sensitivity of Carotid Sinus Baroreflex in Rats with Vascular Calcification.Frontiers in pharmacology · 2017Article
- Magnesium modulates the expression levels of calcification-associated factors to inhibit calcification in a time-dependent manner.Experimental and therapeutic medicine · 2015Article
- A Lindera obtusiloba Extract Blocks Calcium-/Phosphate-Induced Transdifferentiation and Calcification of Vascular Smooth Muscle Cells and Interferes with Matrix Metalloproteinase-2 and Metalloproteinase-9 and NF-κB.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- C-type natriuretic peptide inhibiting vascular calcification might involve decreasing bone morphogenic protein 2 and osteopontin levels.Molecular and cellular biochemistry · 2014Article
- Inhibition of vascular smooth muscle growth via signaling crosstalk between AMP-activated protein kinase and cAMP-dependent protein kinase.Frontiers in physiology · 2012Article
- Article
- Frontiers of vascular biology and disease research.Acta pharmacologica Sinica · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo determine whether adrenomedullin (ADM) attenuates vascular calcification (VC) by inducing osteopontin (OPN) expression.
methodsA VC model of rat aorta was induced with vitamin D3 plus nicotine (VDN), and vascular smooth muscle cell (VSMC) calcification was induced with beta-glycerophosphate. Von Kossa staining and alizarin red staining were assessed. Alkaline phosphatase (ALP) activity was measured. Immunohistochemical analysis was used to detect alpha-actin, while RT-PCR and Western blot analysis were used to quantify OPN expression.
resultsAdministration of ADM greatly reduced VC in VDN-treated aortas compared with controls, which was confirmed in calcified VSMCs. The decrease in alpha-actin expression was ameliorated by ADM both in vivo and in vitro. Moreover, mRNA and protein expression levels of OPN were significantly up-regulated in calcified aortas, and ADM increased OPN expression in calcified aortas. Furthermore, ADM up-regulated OPN expression in normal aortas and VSMCs. The ADM-mediated effects were similar to that of forskolin, which activates adenylyl cyclase; additionally, while the PKA inhibitor H89 and Ca²(+) chelator Fura-2 blocked the effect of ADM. However, the MEK/ERK inhibitor PD98509 had no effect on ADM induction of OPN mRNA expression. An OPN polyclonal antibody inhibited ADM-mediated attenuation of VC.
conclusionADM up-regulates OPN expression and thus attenuates VC via PKA. ADM appears to be an endogenous cardiovascular protective peptide and may represent a new therapeutic target for VC treatment.
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