ArticleArthritis research & therapy2014
Neurotrophins are expressed in giant cell arteritis lesions and may contribute to vascular remodeling.
Article in Arthritis research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Review
- Vascular-adhesion protein 1 in giant cell arteritis and polymyalgia rheumatica.Frontiers in medicine · 2024Review
- ProBDNF and its receptors in immune-mediated inflammatory diseases: novel insights into the regulation of metabolism and mitochondria.Frontiers in immunology · 2023Review
- New Insights into the Pathogenesis of Giant Cell Arteritis: Mechanisms Involved in Maintaining Vascular Inflammation.Journal of clinical medicine · 2022Review
- The innate face of Giant Cell Arteritis: Insight into cellular and molecular innate immunity pathways to unravel new possible biomarkers of disease.Frontiers in molecular medicine · 2022Review
- Pleiotropic activity of nerve growth factor in regulating cardiac functions and counteracting pathogenesis.ESC heart failure · 2021Review
- The immunoinhibitory PD-1/PD-L1 pathway in inflammatory blood vessel disease.Journal of leukocyte biology · 2018Review
- Giant cell arteritis and polymyalgia rheumatica: current challenges and opportunities.Nature reviews. Rheumatology · 2017Review
- Giant Cell Arteritis: From Pathogenesis to Therapeutic Management.Current treatment options in rheumatology · 2016Article
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Authors and funding
16 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionGiant cell arteritis (GCA) is characterized by intimal hyperplasia leading to ischaemic manifestations that involve large vessels. Neurotrophins (NTs) and their receptors (NTRs) are protein factors for growth, differentiation and survival of neurons. They are also involved in the migration of vascular smooth muscle cells (VSMCs). Our aim was to investigate whether NTs and NTRs are involved in vascular remodelling of GCA.
methodsWe included consecutive patients who underwent a temporal artery biopsy for suspected GCA. We developed an enzymatic digestion method to obtain VSMCs from smooth muscle cells in GCA patients and controls. Neurotrophin protein and gene expression and functional assays were studied from these VSMCs. Neurotrophin expression was also analysed by immunohistochemistry in GCA patients and controls.
resultsWhereas temporal arteries of both GCA patients (n = 22) and controls (n = 21) expressed nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB) and sortilin, immunostaining was more intense in GCA patients, especially in the media and intima, while neurotrophin-3 (NT-3) and P75 receptor (P75NTR) were only detected in TA from GCA patients. Expression of TrkB, a BDNF receptor, was higher in GCA patients with ischaemic complications. Serum NGF was significantly higher in GCA patients (n = 28) vs. controls (n = 48), whereas no significant difference was found for BDNF and NT-3. NGF and BDNF enhanced GCA-derived temporal artery VSMC proliferation and BDNF facilitated migration of temporal artery VSMCs in patients with GCA compared to controls.
conclusionsOur results suggest that NTs and NTRs are involved in vascular remodelling of GCA. In GCA-derived temporal artery VSMC, NGF promoted proliferation and BDNF enhanced migration by binding to TrkB and p75NTR receptors. Further experiments are needed on a larger number of VSMC samples to confirm these results.
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