scholarly journals Protein of youth (adventure of a sensation)

Author(s):  
А.А. Пальцын

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.

1997 ◽  
Vol 75 (12) ◽  
pp. 1753-1760 ◽  
Author(s):  
IE Eder ◽  
A Stenzl ◽  
A Hobisch ◽  
MV Cronauer ◽  
G Bartsch ◽  
...  

2015 ◽  
Vol 308 (2) ◽  
pp. C123-C138 ◽  
Author(s):  
E. Giacomello ◽  
M. Quarta ◽  
C. Paolini ◽  
R. Squecco ◽  
P. Fusco ◽  
...  

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.


2000 ◽  
pp. 213-226 ◽  
Author(s):  
Mamta Shah ◽  
Patricia Rorison ◽  
Mark Ferguson

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