ArticleMolecular medicine reports2018
Crocin prevents platelet‑derived growth factor BB‑induced vascular smooth muscle cells proliferation and phenotypic switch.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Tiaozhi Tongmai Formula attenuates atherosclerosis by modulating the JAK1/STAT3 pathway to inhibit phenotypic transformation of vascular smooth muscle cells.Cardiovascular diagnosis and therapy · 2026Article
- miR-567 indicates atherosclerosis development and regulates inflammation, phenotype switch, proliferation, and migration of platelet-derived growth factor (PDGF)-BB-induced vascular smooth muscle cells (VSMCs) via CSF1R.Journal of molecular histology · 2026Article
- Pharmacological and toxicological roles of Kruppel-like factors (KLFs) in the cardiovascular system: a review.Molecular biology reports · 2025Review
- Hsa_circ_0007765 Promotes Platelet-Derived Growth Factor-BB-Induced Proliferation and Migration of Human Aortic Vascular Smooth Muscle Cells in Atherosclerosis.Cardiovascular toxicology · 2024Article
- Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Activation of the GTPase ARF6 regulates invasion of human vascular smooth muscle cells by stimulating MMP14 activity.Scientific reports · 2022Article
- Ginsenoside Rh1 Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cell Migration and Proliferation through Suppression of the ROS-Mediated ERK1/2/p90RSK/KLF4 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- Kahweol, a Diterpenoid Molecule, Inhibits CTGF-Dependent Synthetic Phenotype Switching and Migration in Vascular Smooth Muscle Cells.Molecules (Basel, Switzerland) · 2021Article
- Role of activin receptor-like kinase 1 in vascular development and cerebrovascular diseases.Neural regeneration research · 2020Review
- Reduced Platelet miR-223 Induction in Kawasaki Disease Leads to Severe Coronary Artery Pathology Through a miR-223/PDGFRβ Vascular Smooth Muscle Cell Axis.Circulation research · 2020Article
- Differential Responsiveness of the Platelet Biomarkers, Systemic CD40 Ligand, CD62P, and Platelet-Derived Growth Factor-BB, to Virally-Suppressive Antiretroviral Therapy.Frontiers in immunology · 2020Article
- Recent advance in treatment of atherosclerosis: Key targets and plaque-positioned delivery strategies.Journal of tissue engineeringReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phenotypic switch of vascular smooth muscle cells (VSMCs) is a major initiating factor for atherosclerotic cardiovascular diseases. Platelet‑derived growth factor‑BB (PDGF‑BB) initiates a number of biological processes that contribute to VSMC proliferation and phenotypic switch. Crocin, a component of saffron, has been reported to inhibit atheromatous plaque formation. However, the effects of crocin on PDGF‑BB‑induced VSMC proliferation and phenotypic switch remain unclear. The aim of the present study was to investigate the role of crocin on PDGF‑BB‑induced VSMCs proliferation and phenotypic switch and its underlying mechanisms. Cell proliferation and markers of VSMCs phenotypic switch were measured using a Cell Counting Kit‑8 assay and western blot analysis, respectively. The signaling pathways involved in the effects of crocin on VSMCs were validated by western blot analysis with or without the use of specific pathway inhibitors. Crocin significantly inhibited PDGF‑BB‑induced VSMCs proliferation compared with the PDGF‑BB only group (P<0.05). In addition, crocin significantly abrogated the PDGF‑BB‑induced increase in contractile protein α‑smooth muscle actin, calponin and decrease in synthetic proteins osteopontin (OPN) in a concentration dependent manner (P<0.05). In addition, crocin slowed PDGF‑BB‑induced Janus kinase (JAK)‑signal transducer and activator of transcription 3 (STAT3) and extracellular signal‑regulated kinase (ERK)/Kruppel‑like factor 4 (KLF4) signaling activation in VSMCs. By applying the JAK inhibitor (AG490) and ERK1/2 inhibitor (U0126), the results suggested that the crocin inhibited PDGF‑BB‑induced VSMCs phenotypic switch through the JAK/STAT3 and ERK/KLF4 signaling pathways. These results suggested that crocin may effectively prevent PDGF‑BB‑induced VSMCs proliferation and phenotypic switch and may be a promising candidate for the therapy of atherosclerotic cardiovascular diseases.
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