Next Article in Journal
Antiangiogenic Potential of Microbial Metabolite Elaiophylin for Targeting Tumor Angiogenesis
Next Article in Special Issue
New Terpenoids from Chamaecyparis formosensis (Cupressaceae) Leaves with Modulatory Activity on Matrix Metalloproteases 2 and 9
Previous Article in Journal
Isolation and Purification of Two Isoflavones from Hericium erinaceum Mycelium by High-Speed Counter-Current Chromatography
Previous Article in Special Issue
Persicaline, A New Antioxidant Sulphur-Containing Imidazoline Alkaloid from Salvadora persica Roots
Article Menu
Issue 3 (March) cover image

Export Article

Open AccessArticle
Molecules 2018, 23(3), 561;

Wedelolactone Enhances Osteoblastogenesis through ERK- and JNK-mediated BMP2 Expression and Smad/1/5/8 Phosphorylation

Institute (College) of Integrative Medicine, Dalian Medical University, Dalian 116044, China
Glucose and Lipid Metabolism Laboratory of Liaoning Province, College of Life Science and Technology, Dalian University, Dalian 116622, China
Author to whom correspondence should be addressed.
Received: 2 February 2018 / Revised: 16 February 2018 / Accepted: 28 February 2018 / Published: 2 March 2018
(This article belongs to the Collection Bioactive Compounds)
Full-Text   |   PDF [7297 KB, uploaded 2 March 2018]   |  


Our previous study showed that wedelolactone, a compound isolated from Ecliptae herba, has the potential to enhance osteoblastogenesis. However, the molecular mechanisms by which wedelolactone promoted osteoblastogenesis from bone marrow mesenchymal stem cells (BMSCs) remain largely unknown. In this study, treatment with wedelolactone (2 μg/mL) for 3, 6, and 9 days resulted in an increase in phosphorylation of extracellular signal-regulated kinases (ERKs), c-Jun N-terminal protein kinase (JNK), and p38. Phosphorylation of mitogen-activated protein kinases (MAPKs), ERK and JNK started to increase on day 3 of treatment, and p38 phosphorylation was increased by day 6 of treatment. Expression of bone morphogenetic protein (BMP2) mRNA and phosphorylation of Smad1/5/8 was enhanced after treatment of cells with wedelolactone for 6 and 9 days. The addition of the JNK inhibitor SP600125, ERK inhibitor PD98059, and p38 inhibitor SB203580 suppressed wedelolactone-induced alkaline-phosphatase activity, bone mineralization, and osteoblastogenesis-related marker genes including Runx2, Bglap, and Sp7. Increased expression of BMP2 mRNA and Smad1/5/8 phosphorylation was blocked by SP600125 and PD98059, but not by SB203580. These results suggested that wedelolactone enhanced osteoblastogenesis through induction of JNK- and ERK-mediated BMP2 expression and Smad1/5/8 phosphorylation. View Full-Text
Keywords: BMP2; MAPK; osteoblastogenesis; Smad; wedelolactone BMP2; MAPK; osteoblastogenesis; Smad; wedelolactone

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Zhu, D.; Deng, X.; Han, X.-F.; Sun, X.-X.; Pan, T.-W.; Zheng, L.-P.; Liu, Y.-Q. Wedelolactone Enhances Osteoblastogenesis through ERK- and JNK-mediated BMP2 Expression and Smad/1/5/8 Phosphorylation. Molecules 2018, 23, 561.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top