scholarly journals Iron accumulation in skeletal muscles of old mice is associated with impaired regeneration after ischaemia–reperfusion damage

2021 ◽  
Author(s):  
Francesca M. Alves ◽  
Kai Kysenius ◽  
Marissa K. Caldow ◽  
Justin P. Hardee ◽  
Peter J. Crouch ◽  
...  
Keyword(s):  
Skeletal Muscles ◽  
Iron Accumulation ◽  
Ischaemia Reperfusion ◽  
Reperfusion Damage ◽  
Old Mice

scholarly journals Deletion of small ankyrin 1 (sAnk1) isoforms results in structural and functional alterations in aging skeletal muscle fibers

2015 ◽  
Vol 308 (2) ◽  
pp. C123-C138 ◽  
Author(s):  
E. Giacomello ◽  
M. Quarta ◽  
C. Paolini ◽  
R. Squecco ◽  
P. Fusco ◽  
...  
Keyword(s):  
Structural Damage ◽  
Skeletal Muscles ◽  
Functional Characterization ◽  
Sr Proteins ◽  
Endurance Test ◽  
Tubular Aggregates ◽  
Functional Studies ◽  
Old Mice ◽  
Contractile Performance

Muscle-specific ankyrins 1 (sAnk1) are a group of small ankyrin 1 isoforms, of which sAnk1.5 is the most abundant. sAnk1 are localized in the sarcoplasmic reticulum (SR) membrane from where they interact with obscurin, a myofibrillar protein. This interaction appears to contribute to stabilize the SR close to the myofibrils. Here we report the structural and functional characterization of skeletal muscles from sAnk1 knockout mice (KO). Deletion of sAnk1 did not change the expression and localization of SR proteins in 4- to 6-mo-old sAnk1 KO mice. Structurally, the main modification observed in skeletal muscles of adult sAnk1 KO mice (4–6 mo of age) was the reduction of SR volume at the sarcomere A band level. With increasing age (at 12–15 mo of age) extensor digitorum longus (EDL) skeletal muscles of sAnk1 KO mice develop prematurely large tubular aggregates, whereas diaphragm undergoes significant structural damage. Parallel functional studies revealed specific changes in the contractile performance of muscles from sAnk1 KO mice and a reduced exercise tolerance in an endurance test on treadmill compared with control mice. Moreover, reduced Qγcharge and L-type Ca2+current, which are indexes of affected excitation-contraction coupling, were observed in diaphragm fibers from 12- to 15-mo-old mice, but not in other skeletal muscles from sAnk1 KO mice. Altogether, these findings show that the ablation of sAnk1, by altering the organization of the SR, renders skeletal muscles susceptible to undergo structural and functional alterations more evident with age, and point to an important contribution of sAnk1 to the maintenance of the longitudinal SR architecture.

scholarly journals Protein of youth (adventure of a sensation)

2018 ◽  
pp. 78-83
Author(s):  
А.А. Пальцын
Keyword(s):  
Growth Factors ◽  
Old Age ◽  
Skeletal Muscles ◽  
Scientific Community ◽  
Harvard University ◽  
Transforming Growth Factors ◽  
Tissue Concentrations ◽  
Mammalian Blood ◽  
Old Mice ◽  
Reliable Methods

Группа исследователей из Гарвардского университета в 2013 и последующих годах опубликовала серию статей об одном из трансформирующих факторов роста b - GDF-11. По данным этого коллектива, концентрация GDF-11 в крови и тканях млекопитающих с возрастом снижается. Искусственное повышение содержания GDF-11 у старых мышей путем ежедневных инъекций рекомбинантного GDF-11 или парабиоза в течение месяца с молодыми мышами существенно снижало и даже устраняло свойственные старости неблагоприятные изменения сердца, скелетных мышц, мозга. Статьи Гарвардской группы привлекли большое внимание научного сообщества, были комментированы в сотнях публикаций, и в них GDF-11 стали часто называть белком молодости. Капитальность заявки Гарварда стимулировала капитальность проверочных экспериментов с привлечением максимально надежных методик. Эти эксперименты расширили знания о GDF-11, но не подтвердили его права называться белком молодости. A research group at the Harvard University in 2013 and the next years has published a series of articles focusing on one of transforming growth factors b, GDF-11. According to these reports mammalian blood and tissue concentrations of GDF-11 decrease with age. Increasing the GDF-11 content in old mice using daily injections of recombinant GDF-11 or one-month parabiosis induced in young mice significantly reduced and even eliminated adverse, old age-specific changes in the heart, skeletal muscles, and brain. The reports of the Harvard group have attracted much attention of the scientific community, and were cited in hundreds of publications where GDF-11 was often called the protein of youth. The solidity of the Harvard team statement warranted solidity of test experiments, which used the most reliable methods. These experiments have expanded the knowledge of GDF-11 but did not confirm its right to be called a protein of youth.

Selective portal clamping to minimize hepatic ischaemia–reperfusion damage and avoid accelerated outgrowth of experimental colorectal liver metastases

2006 ◽  
Vol 93 (8) ◽  
pp. 1015-1022 ◽  
Author(s):  
J. D. W. van der Bilt ◽  
O. Kranenburg ◽  
A. Verheem ◽  
R. van Hillegersberg ◽  
I. H. M. Borel Rinkes
Keyword(s):  
Liver Metastases ◽  
Colorectal Liver Metastases ◽  
Ischaemia Reperfusion ◽  
Reperfusion Damage

scholarly journals The NLRP3 inflammasome contributes to sarcopenia and lower muscle glycolytic potential in old mice

2017 ◽  
Vol 313 (2) ◽  
pp. E222-E232 ◽  
Author(s):  
Marin Jane McBride ◽  
Kevin P. Foley ◽  
Donna M. D’Souza ◽  
Yujin E. Li ◽  
Trevor C. Lau ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Strength ◽  
Nlrp3 Inflammasome ◽  
Skeletal Muscles ◽  
Metabolic Flux ◽  
Caspase 1 ◽  
Gapdh Activity ◽  
Age Related ◽  
Glycolytic Potential ◽  
Old Mice

The mechanisms underpinning decreased skeletal muscle strength and slowing of movement during aging are ill-defined. “Inflammaging,” increased inflammation with advancing age, may contribute to aspects of sarcopenia, but little is known about the participatory immune components. We discovered that aging was associated with increased caspase-1 activity in mouse skeletal muscle. We hypothesized that the caspase-1-containing NLRP3 inflammasome contributes to sarcopenia in mice. Male C57BL/6J wild-type (WT) and NLRP3−/− mice were aged to 10 (adult) and 24 mo (old). NLRP3−/− mice were protected from decreased muscle mass (relative to body mass) and decreased size of type IIB and IIA myofibers, which occurred between 10 and 24 mo of age in WT mice. Old NLRP3−/− mice also had increased relative muscle strength and endurance and were protected from age-related increases in the number of myopathic fibers. We found no evidence of age-related or NLRP3-dependent changes in markers of systemic inflammation. Increased caspase-1 activity was associated with GAPDH proteolysis and reduced GAPDH enzymatic activity in skeletal muscles from old WT mice. Aging did not alter caspase-1 activity, GAPDH proteolysis, or GAPDH activity in skeletal muscles of NLRP3−/− mice. Our results show that the NLRP3 inflammasome participates in age-related loss of muscle glycolytic potential. Deletion of NLRP3 mitigates both the decline in glycolytic myofiber size and the reduced activity of glycolytic enzymes in muscle during aging. We propose that the etiology of sarcopenia involves direct communication between immune responses and metabolic flux in skeletal muscle.

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