2014
DOI: 10.1186/s13075-014-0487-z
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Neurotrophins are expressed in giant cell arteritis lesions and may contribute to vascular remodeling

Abstract: Introduction: Giant 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. Methods: We included consecutive patients who underwent a temporal artery bi… Show more

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Cited by 21 publications
(10 citation statements)
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“…147 Chaldakov et al 138 were the first to demonstrate that the level of NGF was significantly reduced in human coronary arteries with advanced atherosclerotic lesions. These results also revealed that the coronary adventitia of atherosclerotic subjects displayed an overexpression of p75NTR immunoreactivity 67,93 and a significantly greater number of MCs and vasa vasorum than those of The role of NGF in regulating cardiac functions controls. 138,139,148 There is a possibility that the secretion of NGF in pathological tissues is reduced because VSMCs, which are the main vascular source of NGF, 138,149 undergo atrophy in atherosclerosis and/or the NGF turnover is higher in atherosclerotic arteries than in normal arteries.…”
Section: Congestive Heart Failurementioning
confidence: 80%
See 1 more Smart Citation
“…147 Chaldakov et al 138 were the first to demonstrate that the level of NGF was significantly reduced in human coronary arteries with advanced atherosclerotic lesions. These results also revealed that the coronary adventitia of atherosclerotic subjects displayed an overexpression of p75NTR immunoreactivity 67,93 and a significantly greater number of MCs and vasa vasorum than those of The role of NGF in regulating cardiac functions controls. 138,139,148 There is a possibility that the secretion of NGF in pathological tissues is reduced because VSMCs, which are the main vascular source of NGF, 138,149 undergo atrophy in atherosclerosis and/or the NGF turnover is higher in atherosclerotic arteries than in normal arteries.…”
Section: Congestive Heart Failurementioning
confidence: 80%
“…Moreover, type 1 diabetes down-regulates the levels of NGF and TrkA in ischaemic skeletal muscles and concomitantly induces p75NTR expression in capillary ECs, 17,20 suggesting that p75NTR is responsible for diabetes-induced impairment in neovascularization of ischaemic limb muscles. 7 In contrast to Trk actions, ligand (NGF and pro-NGF)-dependent activation of p75NTR, which is increased following vascular injury (in pathological conditions such as diabetes or atherosclerosis 17,67,93 ), reportedly induces EC 7,9,36,73,94 and neointimal smooth muscle cell death. 1,7,95 Interestingly, rather than initiating apoptosis of diabetic ECs via p75NTR, NGF supplementation down-regulates p75NTR expression by a mechanism that has not yet been clarified and promotes EC survival and vascular regeneration.…”
Section: Cardiac Sympathetic Nerve Activitymentioning
confidence: 99%
“…31 Myofibroblast differentiation and extracellular matrix deposition in the intima lead to vascular remodeling and possible vessel occlusion. [31][32][33][34][35] The microenvironment created by this inflammatory process weakens the vessel media and internal elastic lamina and leads to hyperplasia of the vessel intima. 32 Compared with AAV, the pathogenesis of ILD in GCA does not include pulmonary capillaritis with alveolar hemorrhage or oxidative stress from ANCA.…”
Section: Discussionmentioning
confidence: 99%
“…In GCA, VSMCs are injured by mediators released by mononuclear cells, which have accumulated in the media, and acquire pro-inflammatory properties [ 121 ]. Activated macrophages and VSMCs themselves produce several growth factors (PDGF, TGF-β, endothelin-1 [ET-1], NGF and BDNF neutrophins [ 98 , 121 , 122 , 123 ]), thus inducing the migration of VSMCs into the intima and their differentiation into myofibroblasts, which synthesize matrix proteins. This process finally leads to intimal hyperplasia and vascular occlusion.…”
Section: Immunopathological Model Of Gcamentioning
confidence: 99%