PMID- 18037433
OWN - NLM
STAT- MEDLINE
DCOM- 20080403
LR  - 20220331
IS  - 1095-8584 (Electronic)
IS  - 0022-2828 (Linking)
VI  - 44
IP  - 2
DP  - 2008 Feb
TI  - Differential expression of cardiac neurotrophic factors and sympathetic nerve 
      ending abnormalities within the failing heart.
PG  - 380-7
AB  - In congestive heart failure (CHF), cardiac sympathetic nerve endings 
      transdifferentiate from a balanced norepinephrine (NE) storage/release/uptake 
      apparatus to a nerve that predominantly releases NE. Little is known about the 
      neurotrophic factors that may trigger this process. In the present study, we 
      evaluated the cardiac expression pattern of nerve growth factor (NGF), 
      neurotrophin-3 (NT-3), brain-derived neurotrophic factor (BDNF) and ciliary 
      neurotrophic factor (CNTF) in salt-sensitive Dahl rats (DS), which are 
      characterized by profound alterations of the cardiac sympathetic nervous system. 
      Experiments were performed in male DS and salt-resistant Dahl rats (DR) 30, 40 
      and 50 days after onset of high-salt intake. The sympathetic nerve density was 
      measured by glyoxylic acid-induced histofluorescence. Cardiac NE re-uptake was 
      assessed by isolated heart perfusion with [(3)H]-NE and norepinephrine 
      transporter (NET) mRNA by real-time PCR. Cardiac expression of neurotrophic 
      factors was determined by ribonuclease protection assay and Western blot 
      analysis. DS rats displayed reduced left ventricular sympathetic nerve endings 40 
      days after onset of high-salt intake, which was preceded by an impaired cardiac 
      [(3)H]-NE uptake. NGF, a positive regulator of NE re-uptake, and NT-3 were 
      down-regulated already 30 days after onset of high-salt intake, whereas BDNF and 
      CNTF protein expression were increased not before 40 days after onset of 
      high-salt intake. In conclusion, during the development of CHF, a dysregulated NE 
      storage/release/uptake apparatus within the sympathetic nerve endings might be 
      triggered by differential expression of cardiac neurotrophic factors.
FAU - Kreusser, Michael M
AU  - Kreusser MM
AD  - Department of Cardiology, University of Heidelberg, Im Neuenheimer Feld 410, 
      69120 Heidelberg, Germany.
FAU - Buss, Sebastian J
AU  - Buss SJ
FAU - Krebs, Jutta
AU  - Krebs J
FAU - Kinscherf, Ralf
AU  - Kinscherf R
FAU - Metz, Jurgen
AU  - Metz J
FAU - Katus, Hugo A
AU  - Katus HA
FAU - Haass, Markus
AU  - Haass M
FAU - Backs, Johannes
AU  - Backs J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071126
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Norepinephrine Plasma Membrane Transport Proteins)
RN  - 0 (RNA, Messenger)
RN  - 10028-17-8 (Tritium)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Animals
MH  - Body Weight
MH  - *Gene Expression Profiling
MH  - Gene Expression Regulation
MH  - Heart Failure/*genetics
MH  - Heart Ventricles/metabolism
MH  - Myocardium/*metabolism/*pathology
MH  - Nerve Endings/*abnormalities
MH  - Nerve Growth Factors/*genetics/metabolism
MH  - Norepinephrine/metabolism
MH  - Norepinephrine Plasma Membrane Transport Proteins/genetics/metabolism
MH  - Organ Size
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Inbred Dahl
MH  - Sympathetic Nervous System/*abnormalities
MH  - Tritium
EDAT- 2007/11/27 09:00
MHDA- 2008/04/04 09:00
CRDT- 2007/11/27 09:00
PHST- 2006/10/15 00:00 [received]
PHST- 2007/09/27 00:00 [revised]
PHST- 2007/10/18 00:00 [accepted]
PHST- 2007/11/27 09:00 [pubmed]
PHST- 2008/04/04 09:00 [medline]
PHST- 2007/11/27 09:00 [entrez]
AID - S0022-2828(07)01285-0 [pii]
AID - 10.1016/j.yjmcc.2007.10.019 [doi]
PST - ppublish
SO  - J Mol Cell Cardiol. 2008 Feb;44(2):380-7. doi: 10.1016/j.yjmcc.2007.10.019. Epub 
      2007 Nov 26.