PMID- 16441896
OWN - NLM
STAT- MEDLINE
DCOM- 20060327
LR  - 20181113
IS  - 1465-993X (Electronic)
IS  - 1465-9921 (Print)
IS  - 1465-9921 (Linking)
VI  - 7
IP  - 1
DP  - 2006 Jan 29
TI  - Differential regulation of neurotrophin expression in human bronchial smooth 
      muscle cells.
PG  - 18
AB  - BACKGROUND: Human bronchial smooth muscle cells (HBSMC) may regulate airway 
      inflammation by secreting cytokines, chemokines and growth factors. The 
      neurotrophins, including nerve growth factor (NGF), brain-derived neurotrophic 
      factor (BDNF) and neurotrophin-3 (NT-3), have been shown to be elevated during 
      airway inflammation and evoke airway hyperresponsiveness. We studied if HBSMC may 
      be a source of NGF, BDNF and NT-3, and if so, how inflammatory cytokines may 
      influence their production. METHODS: Basal and cytokine (IL-1beta, IFN-gamma, 
      IL-4)-stimulated neurotrophin expression in HBSMC cultured in vitro was 
      quantified. The mRNA expression was quantified by real-time RT-PCR and the 
      protein secretion into the cell culture medium by ELISA. RESULTS: We observed a 
      constitutive NGF, BDNF and NT-3 expression. IL-1beta stimulated a transient 
      increase of NGF, while the increase of BDNF had a later onset and was more 
      sustained. COX-inhibitors (indomethacin and NS-398) markedly decreased 
      IL-1beta-stimulated secretion of BDNF, but not IL-1beta-stimulated NGF secretion. 
      IFN-gamma increased NGF expression, down-regulated BDNF expression and 
      synergistically enhanced IL-1beta-stimulated NGF expression. In contrast, IL-4 
      had no effect on basal NGF and BDNF expression, but decreased IL-1beta-stimulated 
      NGF expression. NT-3 was not altered by the tested cytokines. CONCLUSION: Taken 
      together, our data indicate that, in addition to the contractile capacity, HBSMC 
      can express NGF, BDNF and NT-3. The expression of these neurotrophins may be 
      differently regulated by inflammatory cytokines, suggesting a dynamic interplay 
      that might have a potential role in airway inflammation.
FAU - Kemi, Cecilia
AU  - Kemi C
AD  - Division of Respiratory Medicine, Department of Medicine, Karolinska Institutet, 
      Karolinska University Hospital Solna, 171 76 Stockholm, Sweden. 
      Cecilia.Kemi@ki.se
FAU - Grunewald, Johan
AU  - Grunewald J
FAU - Eklund, Anders
AU  - Eklund A
FAU - Hoglund, Caroline Olgart
AU  - Hoglund CO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060129
PL  - England
TA  - Respir Res
JT  - Respiratory research
JID - 101090633
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclooxygenase Inhibitors)
RN  - 0 (Drug Combinations)
RN  - 0 (Interleukin-1)
RN  - 0 (Neurotrophin 3)
RN  - 0 (RNA, Messenger)
RN  - 207137-56-2 (Interleukin-4)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Bronchi/cytology/drug effects/*metabolism
MH  - Cells, Cultured
MH  - Cyclooxygenase Inhibitors/pharmacology
MH  - Drug Combinations
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-1/pharmacology
MH  - Interleukin-4/pharmacology
MH  - Myocytes, Smooth Muscle/drug effects/*metabolism
MH  - Nerve Growth Factor/genetics/*metabolism
MH  - Neurotrophin 3/genetics/*metabolism
MH  - RNA, Messenger/metabolism
PMC - PMC1386667
EDAT- 2006/01/31 09:00
MHDA- 2006/03/28 09:00
PMCR- 2006/01/29
CRDT- 2006/01/31 09:00
PHST- 2005/09/22 00:00 [received]
PHST- 2006/01/29 00:00 [accepted]
PHST- 2006/01/31 09:00 [pubmed]
PHST- 2006/03/28 09:00 [medline]
PHST- 2006/01/31 09:00 [entrez]
PHST- 2006/01/29 00:00 [pmc-release]
AID - 1465-9921-7-18 [pii]
AID - 10.1186/1465-9921-7-18 [doi]
PST - epublish
SO  - Respir Res. 2006 Jan 29;7(1):18. doi: 10.1186/1465-9921-7-18.