PMID- 17051337
OWN - NLM
STAT- MEDLINE
DCOM- 20070313
LR  - 20220317
IS  - 1360-8185 (Print)
IS  - 1573-675X (Electronic)
IS  - 1360-8185 (Linking)
VI  - 11
IP  - 12
DP  - 2006 Dec
TI  - Death receptor-associated pro-apoptotic signaling in aged skeletal muscle.
PG  - 2115-26
AB  - Tumor necrosis factor-alpha (TNF-alpha) is elevated in the serum as a result of 
      aging and it promotes pro-apoptotic signaling upon binding to the type I TNF 
      receptor. It is not known if activation of this apoptotic pathway contributes to 
      the well-documented age-associated decline in muscle mass (i.e. sarcopenia). We 
      tested the hypothesis that skeletal muscles from aged rodents would exhibit 
      elevations in markers involved in the extrinsic apoptotic pathway when compared 
      to muscles from young adult rodents, thereby contributing to an increased 
      incidence of nuclear apoptosis in these muscles. The plantaris (fast) and soleus 
      (slow) muscles were studied in young adult (5-7 mo, n=8) and aged (33 mo, n=8) 
      Fischer(344) x Brown Norway rats. Muscles from aged rats were significantly 
      smaller while exhibiting a greater incidence of apoptosis. Furthermore, muscles 
      from aged rats had higher type I TNF receptor and Fas associated death domain 
      protein (FADD) mRNA, protein contents for FADD, BCL-2 Interacting Domain (Bid), 
      FLICE-inhibitory protein (FLIP), and enzymatic activities of caspase-8 and 
      caspase-3 than muscles from young adult rats. Significant correlations were 
      observed in the plantaris muscle between caspase activity and muscle weight and 
      the apoptotic index, while similar relationships were not found in the soleus. 
      These data demonstrate that pro-apoptotic signaling downstream of the TNF 
      receptor is active in aged muscles. Furthermore, our data extend the previous 
      demonstration that type II fibers are preferentially affected by aging and 
      support the hypothesis that type II fiber containing skeletal muscles may be more 
      susceptible to muscle mass loses via the extrinsic apoptotic pathway.
FAU - Pistilli, Emidio E
AU  - Pistilli EE
AD  - Laboratory of Muscle Biology and Sarcopenia, Division of Exercise Physiology, 
      West Virginia University School of Medicine, Morgantown, West Virginia 26506, 
      USA.
FAU - Jackson, Janna R
AU  - Jackson JR
FAU - Alway, Stephen E
AU  - Alway SE
LA  - eng
GR  - R01 AG021530/AG/NIA NIH HHS/United States
GR  - R01 AG021530-02/AG/NIA NIH HHS/United States
GR  - R01 AGO21530/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Apoptosis
JT  - Apoptosis : an international journal on programmed cell death
JID - 9712129
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Death Domain)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - *Aging
MH  - Animals
MH  - *Apoptosis
MH  - Body Weight
MH  - Caspase 3/metabolism
MH  - Caspase 8/metabolism
MH  - Gene Expression Regulation
MH  - Male
MH  - Models, Biological
MH  - Muscle, Skeletal/*cytology/*metabolism
MH  - Organ Size
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Inbred BN
MH  - Rats, Inbred F344
MH  - Receptors, Death Domain/genetics/*metabolism
MH  - *Signal Transduction
PMC - PMC5271588
MID - NIHMS142298
EDAT- 2006/10/20 09:00
MHDA- 2007/03/14 09:00
PMCR- 2017/01/27
CRDT- 2006/10/20 09:00
PHST- 2006/10/20 09:00 [pubmed]
PHST- 2007/03/14 09:00 [medline]
PHST- 2006/10/20 09:00 [entrez]
PHST- 2017/01/27 00:00 [pmc-release]
AID - 10.1007/s10495-006-0194-6 [doi]
PST - ppublish
SO  - Apoptosis. 2006 Dec;11(12):2115-26. doi: 10.1007/s10495-006-0194-6.