ArticleInternational journal of molecular sciences2020
Norepinephrine Inhibits the Proliferation of
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- A Biomimetic Norepinephrine-Loaded Aligned Mineralized Collagen Scaffold for Coordinated Neurovascular, Osteogenic, and Immunomodulatory Repair of Critical-Sized Bone Defects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Sympathetic regulation of bone homeostasis and remodeling: molecular mechanisms, pathophysiological roles, and therapeutic implications.Frontiers in immunology · 2026Review
- G protein-coupled receptor signaling in osteogenic bone mesenchymal stem/stromal cells.Frontiers in cell and developmental biology · 2026Review
- From nerve to bone: a tale of autonomic nervous system, bone cells, and beyond.Military Medical Research · 2026Review
- New Insight into Bone Immunity in Marrow Cavity and Cancellous Bone Microenvironments and Their Regulation.Biomedicines · 2025Review
- The influence of adrenoceptor blocker treatment on fracture healing in osteoporotic and non-osteoporotic bone.Frontiers in physiology · 2025Article
- The function of GPCRs in different bone cells.International journal of biological sciences · 2025Review
- Coordination between circadian neural circuit and intracellular molecular clock ensures rhythmic activation of adult neural stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Neuro-bone tissue engineering: emerging mechanisms, potential strategies, and current challenges.Bone research · 2023Review
- The effect of local sympatholysis on bone-tendon interface healing in a murine rotator cuff repair model.Journal of orthopaedic translation · 2023Article
- The Sympathetic Nervous System in Dental Implantology.Journal of clinical medicine · 2023Review
- Intervention effects of traditional Chinese medicine on stem cell therapy of myocardial infarction.Frontiers in pharmacology · 2022Review
- Myeloid cell-derived catecholamines influence bone turnover and regeneration in mice.Frontiers in endocrinology · 2022Article
- Review
- Driving βFrontiers in immunology · 2021Article
- How Long Are Reperfusion Therapies Beneficial for Patients after Stroke Onset? Lessons from Lethal Ischemia Following Early Reperfusion in a Mouse Model of Stroke.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Bone marrow-derived mesenchymal stem cells (BMSCs) represent an alternative to chondrocytes to support cartilage regeneration in osteoarthritis (OA). The sympathetic neurotransmitter norepinephrine (NE) has been shown to inhibit their chondrogenic potential; however, their proliferation capacity under NE influence has not been studied yet. Therefore, we used BMSCs obtained from trauma and OA donors and compared the expression of adrenergic receptors (AR). Then, BMSCs from both donor groups were treated with NE, as well as with combinations of NE and α1-, α2- or β1/2-AR antagonists (doxazosin, yohimbine or propranolol). Activation of AR-coupled signaling was investigated by analyzing ERK1/2 and protein kinase A (PKA) phosphorylation. A similar but not identical subset of ARs was expressed in trauma (α2B-, α2C- and β2-AR) and OA BMSCs (α2A-, α2B-, and β2-AR). NE in high concentrations inhibited the proliferation of both trauma and OA BMCSs significantly. NE in low concentrations did not influence proliferation. ERK1/2 as well as PKA were activated after NE treatment in both BMSC types. These effects were abolished only by propranolol. Our results demonstrate that NE inhibits the proliferation and accordingly lowers the regenerative capacity of human BMSCs likely via β2-AR-mediated ERK1/2 and PKA phosphorylation. Therefore, targeting β2-AR-signaling might provide novel OA therapeutic options.
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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.