ArticleScientific reports2015
Heat shock protein 60 stimulates the migration of vascular smooth muscle cells via Toll-like receptor 4 and ERK MAPK activation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Inhibition of PHB1/PHB2 suppresses atherosclerotic plaque formation by interrupting PI3K/AKT/mTOR signaling.PloS one · 2025Article
- IgA Vasculitis (Henoch-Schönlein Purpura): An Update on Treatment.Journal of clinical medicine · 2024Review
- Heat Shock Response and Heat Shock Proteins: Current Understanding and Future Opportunities in Human Diseases.International journal of molecular sciences · 2024Review
- Toll-like receptor 4 in pancreatic damage and immune infiltration in acute pancreatitis.Frontiers in immunology · 2024Review
- Rutin Ameliorates Cadmium-Induced Necroptosis in the Chicken Liver via Inhibiting Oxidative Stress and MAPK/NF-κB Pathway.Biological trace element research · 2022Article
- Endothelial Function in Postmenopausal Women: The Possible Role of Heat Shock Protein 60 and Serum Androgens.Frontiers in molecular medicine · 2022Article
- Review
- Mitochondrial DAMPs and altered mitochondrial dynamics in OxLDL burden in atherosclerosis.Molecular and cellular biochemistry · 2021Review
- HSP60 knockdown exerts differential response in endothelial cells and monocyte derived macrophages during atherogenic transformation.Scientific reports · 2021Article
- The Role of Toll-like Receptors in Atherothrombotic Cardiovascular Disease.ACS pharmacology & translational science · 2020Review
- TLR4 (Toll-Like Receptor 4) Mediates the Development of Intracranial Aneurysm Rupture.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Immunologic and Non-Immunologic Mechanisms Leading to Airway Remodeling in Asthma.International journal of molecular sciences · 2020Review
- Heat Shock Protein 60 in Cardiovascular Physiology and Diseases.Frontiers in molecular biosciences · 2020Review
- Complex Destabilization in the Mitochondrial Chaperonin Hsp60 Leads to Disease.Frontiers in molecular biosciences · 2020Review
- Targeting toll-like receptor 4 signalling pathways: can therapeutics pay the toll for hypertension?British journal of pharmacology · 2019Review
- Damage-Associated Molecular Patterns in Inflammatory Diseases.Immune network · 2018Review
- Endothelial TNF-α induction by Hsp60 secreted from THP-1 monocytes exposed to hyperglycaemic conditions.Cell stress & chaperones · 2018Article
- Lactoferrin promotes murine C2C12 myoblast proliferation and differentiation and myotube hypertrophy.Molecular medicine reports · 2018Article
- Adiponectin and its receptors are involved in hypertensive vascular injury.Molecular medicine reports · 2018Article
- Heat Shock Proteins in Vascular Diabetic Complications: Review and Future Perspective.International journal of molecular sciences · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates that heat shock protein (HSP) 60 is strongly associated with the pathology of atherosclerosis (AS). However, the precise mechanisms by which HSP60 promotes atherosclerosis remain unclear. In the present study, we found that HSP60 mRNA and protein expression levels in the thoracic aorta are enhanced not only in a mouse model of AS but also in high-fat diet (HFD) mice. HSP60 expression and secretion was activated by platelet-derived growth factor-BB (PDGF-BB) and interleukin (IL)-8 in both human umbilical vein endothelial cells (HUVECs) and vascular smooth muscle cells (VSMCs). HSP60 was found to induce VSMC migration, and exposure to HSP60 activated ERK MAPK signaling. U0126, an inhibitor of ERK, reduced VSMC migration. The HSP60-stimulated VSMCs were found to express TLR4 mRNA but not TLR2 mRNA. Knockdown of TLR4 by siRNA reduced HSP60-induced VSMC migration and HSP60-induced ERK activation. Finally, HSP60 induced IL-8 secretion in VSMCs. Together these results suggest that HSP60 is involved in the stimulation of VSMC migration, via TLR4 and ERK MAPK activation. Meanwhile, activation of HSP60 is one of the most powerful methods of sending a 'danger signal' to the immune system to generate IL-8, which assists in the management of an infection or disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.