PMID- 25418464
OWN - NLM
STAT- MEDLINE
DCOM- 20151030
LR  - 20181113
IS  - 1478-6362 (Electronic)
IS  - 1478-6354 (Print)
IS  - 1478-6354 (Linking)
VI  - 16
IP  - 6
DP  - 2014 Nov 24
TI  - Neurotrophins are expressed in giant cell arteritis lesions and may contribute to 
      vascular remodeling.
PG  - 487
LID - 10.1186/s13075-014-0487-z [doi]
LID - 487
AB  - 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 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. RESULTS: Whereas 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. 
      CONCLUSIONS: Our 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.
FAU - Ly, Kim Heang
AU  - Ly KH
FAU - Regent, Alexis
AU  - Regent A
FAU - Molina, Elsa
AU  - Molina E
FAU - Saada, Sofiane
AU  - Saada S
FAU - Sindou, Philippe
AU  - Sindou P
FAU - Le-Jeunne, Claire
AU  - Le-Jeunne C
FAU - Brezin, Antoine
AU  - Brezin A
FAU - Witko-Sarsat, Veronique
AU  - Witko-Sarsat V
FAU - Labrousse, Francois
AU  - Labrousse F
FAU - Robert, Pierre-Yves
AU  - Robert PY
FAU - Bertin, Philippe
AU  - Bertin P
FAU - Bourges, Jean-Louis
AU  - Bourges JL
FAU - Fauchais, Anne-Laure
AU  - Fauchais AL
FAU - Vidal, Elisabeth
AU  - Vidal E
FAU - Mouthon, Luc
AU  - Mouthon L
FAU - Jauberteau, Marie-Odile
AU  - Jauberteau MO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141124
PL  - England
TA  - Arthritis Res Ther
JT  - Arthritis research & therapy
JID - 101154438
RN  - 0 (Nerve Growth Factors)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Cells, Cultured
MH  - Cohort Studies
MH  - Female
MH  - Gene Expression Regulation
MH  - Giant Cell Arteritis/*metabolism/pathology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nerve Growth Factors/*biosynthesis
MH  - Prospective Studies
MH  - Temporal Arteries/*metabolism/pathology
MH  - Vascular Remodeling/*physiology
PMC - PMC4274683
EDAT- 2014/11/25 06:00
MHDA- 2015/10/31 06:00
PMCR- 2014/11/24
CRDT- 2014/11/25 06:00
PHST- 2014/03/24 00:00 [received]
PHST- 2014/11/10 00:00 [accepted]
PHST- 2014/11/25 06:00 [entrez]
PHST- 2014/11/25 06:00 [pubmed]
PHST- 2015/10/31 06:00 [medline]
PHST- 2014/11/24 00:00 [pmc-release]
AID - s13075-014-0487-z [pii]
AID - 487 [pii]
AID - 10.1186/s13075-014-0487-z [doi]
PST - epublish
SO  - Arthritis Res Ther. 2014 Nov 24;16(6):487. doi: 10.1186/s13075-014-0487-z.