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Evidence That The Overexpression Of The Inducible Heat Shock Protein 70 In Mouse Improves Recovery Of Skeletal Muscle From Atrophy
Author(s) -
Miyabara Elen Haruka,
Rodrigues Debora C.,
Nascimento Tabata L.,
Davilla Fernando W.,
Mou Younss A.,
De Tombe Pieter,
Mestril Ruben
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1050.3
Subject(s) - skeletal muscle , atrophy , muscle atrophy , heat shock protein , genetically modified mouse , hindlimb , extensor digitorum longus muscle , transgene , myocyte , medicine , endocrinology , sarcopenia , contraction (grammar) , chemistry , biology , andrology , biochemistry , gene
This work aimed to investigate the effect of the overexpression of the inducible heat shock protein 70 (HSP70i) in mouse on skeletal muscle atrophy and subsequent recovery. Wild type (WT) and HSP70i‐overexpressing transgenic mice were subjected to hindlimb immobilization for 7 days or for immobilization (7 days) and subsequent recovery (7 days). The muscle weight and the myofiber cross sectional area of extensor digitorum longus (EDL) from atrophied HSP70i mice were unaltered; however they were increased in atrophied + recovered HSP70i mice when compared to those from WT mice. The maximal tetanic contraction of EDL muscle was decreased in atrophied WT mice but not in atrophied HSP70i mice. EDL muscles from all groups of HSP70i mice subjected to a fatigue protocol showed an increased force production when compared to those from WT mice. The preliminary results suggest that HSP70i improves skeletal muscle recovery from atrophy. Financial support: FAPESP (2009/53528‐7).