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Printable Handouts
Navigable Slide Index
- Introduction
- Apoptosis occurs in skeletal muscle
- Nuclear apoptosis
- Muscle fibers are multinucleated
- Nuclear apoptosis in muscle loading
- Apoptosis and overload-induced hypertrophy
- Overload in aging rats
- Stretch-overload in aged quail
- Loading causing hypertrophy decreases apoptosis
- Hypertrophied muscle from old quails
- Mitochondrial apoptosis signal transduction
- Quail loading – Bax and Bcl2 protein
- Loading-induced regulators of apoptosis (1)
- Loading-induced regulators of apoptosis (2)
- Apoptotic signaling during muscle wasting
- Models of muscle wasting
- Sarcopenia
- Sarcopenia & apoptosis
- Bax/Bcl-2
- Denervation-induced muscle wasting
- Apoptosis is activated during muscle denervation
- Response to apoptotic stimulus
- Cytochrome c levels post denervation
- Caspase-3 and caspase-9 levels post denervation
- PARP levels post denervation
- Smac levels post denervation
- AIF levels post denervation
- p53 levels post denervation
- Effects of aging on apoptosis
- Unloading/disuse -associated muscle wasting
- Apoptosis is activated during hindlimb suspension
- Apoptotis in hindlimb suspension (mitochondria)
- Apoptosis is activated during muscle regression
- BrdU-positive nuclei under lamina
- Percent of BrdU-positive nuclei
- TUNEL under lamina
- TUNEL-positive/BrdU-positive nucleus
- Mitochondria-apoptosis in unloading
- Nuclear apoptosis and muscle regression
- Id2 signaling in apoptosis
- Id2 in aging muscles
- Hindlimb suspension increases cytoplasmic Id2
- Id2 levels in unloaded quail muscles
- Relationship of Id2 and apoptosis
- Will overexpression of Id2 increase apoptosis?
- Annexin V as an early marker of apoptosis
- Muscle wasting/unloading
- Unloading followed by reloading and apoptosis
- XIAP protein
- Apoptotic index after hindlimb suspension
- Apoptosis signaling in aging-induced sarcopenia
- Mitochondrial regulated sarcopenia
- Potential model for apoptosis induction
- Cross-talk between signaling pathways
- Extrinsic and intrinsic signaling pathways
- Cross-talk – cell death to mitochondria pathways
Topics Covered
- Introduction to apoptosis in skeletal muscle
- Nuclear apoptosis
- Apoptotic signaling during muscle wasting
- Denervation-induced muscle wasting
- Unloading/disuse -associated muscle wasting
- Id2 signaling in apoptosis; aging and muscle disuse
- Unloading followed by reloading and apoptosis
- Apoptosis signaling pathways in aging-induced sarcopenia
- Cross-talk between extrinsic and mitochondrial signaling pathways
Talk Citation
Alway, S.E. (2018, December 2). Pathways of apoptosis in muscle 1 [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 9, 2024, from https://doi.org/10.69645/OUQR4660.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Stephen E. Alway has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Pathways of apoptosis in muscle 1
Published on December 2, 2018
47 min
A selection of talks on Cell Biology
Transcript
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0:00
In this talk, I will focus on apoptotic pathways that have been
shown to be active in skeletal muscle during periods of muscle loss.
0:09
Apoptosis in skeletal muscle occurs under
various conditions and in pathological and non-pathological perturbations.
This include but are not limited to muscle loading,
aging, muscle disuse, and denervation.
Conditions of extreme muscle loading and bulky apoptotic signaling,
perhaps in part, a result of
muscle damage or increases in oxidative stress to the muscle.
Although resistance exercise has been used to offset muscle loss with aging,
sarcopenia or muscle wasting with age is inevitable.
Apoptosis has a role in regulating sarcopenic loss of muscle fiber number,
controlling atrophy of the existing muscle fibers,
and regulating at least in part the degree
to which hypertrophy can occur in loaded muscles.
Unloading and disuse, whether by prolonged bed rest or experimentally
in animals reduces muscle mass and invokes apoptotic signaling.
Denervation by loss of the motor nerve to the muscle,
whether by directly severing the nerve or by
spinal cord injury results in massive muscle loss,
and this is accompanied by increased apoptotic signaling in the muscle.
1:14
Apoptosis in skeletal muscle is more precisely described as nuclear apoptosis.
1:22
Why this distinction for nuclear apoptosis?
Muscle fibers are multinucleated and consisted both post-mitotic myonuclei,
and Dorman's satellite cells,
so they're capable of proliferation.
Unlike single-cell systems, which die if the nucleus is eliminated by apoptosis,
the elimination of a single nucleus may make muscle fiber a little bit smaller,
but it will not result in the death of the multinucleated muscle fiber.
Many nuclei must die and be eliminated before the entire muscle cell dies.