PMID- 9242179
OWN - NLM
STAT- MEDLINE
DCOM- 19970826
LR  - 20190706
IS  - 0009-7330 (Print)
IS  - 0009-7330 (Linking)
VI  - 81
IP  - 2
DP  - 1997 Aug
TI  - Hemodynamic regulation of tumor necrosis factor-alpha gene and protein expression 
      in adult feline myocardium.
PG  - 187-95
AB  - Tumor necrosis factor-alpha (TNF-alpha) mRNA and protein biosynthesis were 
      examined in adult feline myocardium in the presence and absence of superimposed 
      hemodynamic pressure overloading. A brief period of hemodynamic pressure 
      overloading ex vivo resulted in de novo TNF-alpha mRNA expression within 30 
      minutes and de novo TNF-alpha protein production within 60 minutes; neither 
      TNF-alpha mRNA nor protein was detected in hearts perfused at normal perfusion 
      pressures. Moreover, TNF-alpha mRNA and protein biosynthesis were observed in 
      myocyte and nonmyocyte cell types in the pressure-overloaded hearts. To determine 
      whether a simple passive stretch of the myocardium was a sufficient stimulus for 
      TNF-alpha biosynthesis, we examined TNF-alpha mRNA expression in stretched and 
      unstretched papillary muscles. This study showed that myocardial stretch was a 
      sufficient stimulus for the induction of TNF-alpha mRNA biosynthesis. The 
      functional significance of the intramyocardial production of TNF-alpha was 
      determined by examining cell motion in isolated contracting cardiac myocytes 
      treated with superfusates from pressure-overloaded and control hearts. These 
      studies showed that cell motion was depressed in myocytes treated with 
      superfusates from the pressure-overloaded hearts but was normal with the 
      superfusates from the control hearts. Finally, hemodynamic pressure overloading 
      in vivo under physiological conditions was also shown to result in de novo 
      intramyocardial TNF-alpha mRNA biosynthesis. In conclusion, this study 
      constitutes the initial demonstration that the adult mammalian myocardium 
      elaborates biologically active TNF-alpha, both ex vivo and in vivo, in response 
      to hemodynamic pressure overloading.
FAU - Kapadia, S R
AU  - Kapadia SR
AD  - Department of Medicine, Veterans Administration Medical Center, Houston, TX 
      77030, USA.
FAU - Oral, H
AU  - Oral H
FAU - Lee, J
AU  - Lee J
FAU - Nakano, M
AU  - Nakano M
FAU - Taffet, G E
AU  - Taffet GE
FAU - Mann, D L
AU  - Mann DL
LA  - eng
GR  - P50 HL-O6H/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cats
MH  - Female
MH  - Gene Expression Regulation/*physiology
MH  - Heart/*physiology
MH  - Hemodynamics/*physiology
MH  - In Vitro Techniques
MH  - Male
MH  - RNA, Messenger/analysis
MH  - Tumor Necrosis Factor-alpha/*physiology
EDAT- 1997/08/01 00:00
MHDA- 1997/08/01 00:01
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 1997/08/01 00:01 [medline]
PHST- 1997/08/01 00:00 [entrez]
AID - 10.1161/01.res.81.2.187 [doi]
PST - ppublish
SO  - Circ Res. 1997 Aug;81(2):187-95. doi: 10.1161/01.res.81.2.187.