Dual mechanisms governing muscle cell death in tadpole tail during amphibian metamorphosis

2003 ◽  
Vol 227 (2) ◽  
pp. 246-255 ◽  
Author(s):  
Keisuke Nakajima ◽  
Yoshio Yaoita
Keyword(s):  
Cell Death ◽  
Muscle Cell ◽  
Amphibian Metamorphosis ◽  
Tadpole Tail

Hormonal regulation of programmed cell death during amphibian metamorphosis

1994 ◽  
Vol 72 (11-12) ◽  
pp. 581-588 ◽  
Author(s):  
Jamshed R. Tata
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Hormonal Regulation ◽  
Hormone Receptors ◽  
Amphibian Metamorphosis ◽  
Early Genes ◽  
Tadpole Tail ◽  
Inducible Genes ◽  
Promote Cell Death

Extensive programmed cell death (PCD) is initiated at the onset of amphibian metamorphosis, resulting in 100% of cells dying in some larval tissues, as during total regression of tail and gills. All cell death during metamorphosis is under the control of thyroid hormone (TH), which can initiate the process precociously in whole tadpoles or in individual tissues in culture. The hormone prolactin (PRL), given exogenously, prevents natural and TH-induced metamorphosis. We have exploited this dual hormonal regulation in premetamorphic Xenopus tails in organ culture to identify and characterize early genes that are TH-induced and considered important for initiating cell death. Among the earliest genes activated by TH are those encoding the two thyroid hormone receptors TRα and TRβ. This autoinduction of TR genes is considered important since, in blocking this process, PRL also inhibited the expression of other TH-inducible genes and prevented cell death. The expression of early genes other than TR genes, which are known to promote cell death or survival, is also considered to be important for the initiation of PCD during amphibian metamorphosis. We are, therefore, working on the identification, characterization, and expression of members of the Xenopus bcl-2-like gene family, as well as other genes, such as nur-77 and ICE, which may act as early genes during tadpole tail regression.Key words: cell death, thyroid hormones, Xenopus, metamorphosis, gene expression.

Mitochondria in muscle cell death

1999 ◽  
Vol 20 (6) ◽  
pp. 395-400 ◽  
Author(s):  
P. Bernardi
Keyword(s):  
Cell Death ◽  
Muscle Cell

scholarly journals A link between smooth muscle cell death and extracellular matrix degradation during vascular atrophy

2011 ◽  
Vol 54 (1) ◽  
pp. 182-191.e24 ◽  
Author(s):  
Richard D. Kenagy ◽  
Seung-Kee Min ◽  
Eileen Mulvihill ◽  
Alexander W. Clowes
Keyword(s):  
Extracellular Matrix ◽  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

scholarly journals Targeting necroptosis in muscle fibers ameliorates inflammatory myopathies

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Mari Kamiya ◽  
Fumitaka Mizoguchi ◽  
Kimito Kawahata ◽  
Dengli Wang ◽  
Masahiro Nishibori ◽  
...  
Keyword(s):  
Cell Death ◽  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Muscle Cell ◽  
Muscle Injury ◽  
Fas Ligand ◽  
Muscle Fibers ◽  
Inflammatory Molecules

AbstractMuscle cell death in polymyositis is induced by CD8+ cytotoxic T lymphocytes. We hypothesized that the injured muscle fibers release pro-inflammatory molecules, which would further accelerate CD8+ cytotoxic T lymphocytes-induced muscle injury, and inhibition of the cell death of muscle fibers could be a novel therapeutic strategy to suppress both muscle injury and inflammation in polymyositis. Here, we show that the pattern of cell death of muscle fibers in polymyositis is FAS ligand-dependent necroptosis, while that of satellite cells and myoblasts is perforin 1/granzyme B-dependent apoptosis, using human muscle biopsy specimens of polymyositis patients and models of polymyositis in vitro and in vivo. Inhibition of necroptosis suppresses not only CD8+ cytotoxic T lymphocytes-induced cell death of myotubes but also the release of inflammatory molecules including HMGB1. Treatment with a necroptosis inhibitor or anti-HMGB1 antibodies ameliorates myositis-induced muscle weakness as well as muscle cell death and inflammation in the muscles. Thus, targeting necroptosis in muscle cells is a promising strategy for treating polymyositis providing an alternative to current therapies directed at leukocytes.

scholarly journals Maduramicin induces cardiac muscle cell death by the ROS‐dependent PTEN/Akt–Erk1/2 signaling pathway

2018 ◽  
Vol 234 (7) ◽  
pp. 10964-10976 ◽  
Author(s):  
Xin Chen ◽  
Yue Li ◽  
Meng Feng ◽  
Xiaoyu Hu ◽  
Hai Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiac Muscle ◽  
Signaling Pathway ◽  
Muscle Cell ◽  
Cardiac Muscle Cell

scholarly journals Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis

2018 ◽  
Vol 114 (4) ◽  
pp. 622-634 ◽  
Author(s):  
Mandy O J Grootaert ◽  
Manon Moulis ◽  
Lynn Roth ◽  
Wim Martinet ◽  
Cécile Vindis ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell

scholarly journals Muscle cell death during the development of head and neck muscles in the chick embryo

1995 ◽  
Vol 202 (4) ◽  
pp. 365-377 ◽  
Author(s):  
Deedra McClearn ◽  
Richard Medville ◽  
Drew Noden
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Head And Neck ◽  
Muscle Cell ◽  
Neck Muscles
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