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Titolo:
Desmin cytoskeleton linked to muscle mitochondrial distribution and respiratory function
Autore:
Milner, DJ; Mavroidis, M; Weisleder, N; Capetanaki, Y;
Indirizzi:
Baylor Coll Med, Dept Mol & Cell Biol, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 l & Cell Biol, Houston, TX 77030 USA
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 6, volume: 150, anno: 2000,
pagine: 1283 - 1297
SICI:
0021-9525(20000918)150:6<1283:DCLTMM>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERMEDIATE FILAMENT ORGANIZATION; CHICKEN SKELETAL-MUSCLE; MICE LACKING DESMIN; CREATINE-KINASE; DEFICIENT MICE; OUTER-MEMBRANE; BINDING-SITE; IN-VIVO; IDENTIFICATION; ASSOCIATION;
Keywords:
intermediate filaments; mitochondrial proliferation; cardiomyopathy; respiration; desmin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Capetanaki, Y Baylor Coll Med, Dept Mol & Cell Biol, Houston, TX 77030 USABaylor Coll Med Houston TX USA 77030 Houston, TX 77030 USA
Citazione:
D.J. Milner et al., "Desmin cytoskeleton linked to muscle mitochondrial distribution and respiratory function", J CELL BIOL, 150(6), 2000, pp. 1283-1297

Abstract

Ultrastructural studies have previously suggested potential association ofintermediate filaments (IFs) with mitochondria. Thus, we have investigatedmitochondrial distribution and function in muscle lacking the IF protein desmin, Immunostaining of skeletal muscle tissue sections. as well as histochemical staining for the mitochondrial marker enzymes cytochrome C oxidase and succinate dehydrogenase, demonstrate abnormal accumulation of subsarcolemmal clumps of mitochondria in predominantly slow twitch skeletal muscle of desmin-null mice. Ultrastructural observation of desmin-null cardiac muscle demonstrates in addition to clumping, extensive mitochondrial proliferation in a significant fraction of the myocytes, particularly after work overload. These alterations are frequently associated with swelling and degeneration of the mitochondrial matrix. Mitochondrial abnormalities can be detected very early before other structural defects become obvious. To investigate related changes in mitochondrial function, we have analyzed ADP-stimulated respiration of isolated muscle mitochondria, and ADP-stimulated mitochondrial respiration in situ using saponin skinned muscle fibers. The in vitromaximal rates of respiration in isolated cardiac mitochondria from desmin-null and wild-type mice were similar. However, mitochondrial respiration insitu is significantly altered in desmin-null muscle. Both the maximal rateof ADP-stimulated oxygen consumption and the dissociation constant (K-m) for ADP are significantly reduced in desmin-null cardiac and soleus muscle compared with controls. Respiratory parameters for desmin-null fast twitch gastrocnemius muscle were unaffected. Additionally, respiratory measurementsin the presence of creatine indicate that coupling of creatine kinase and the adenine translocator is lost in desmin-null soleus muscle. This coupling is unaffected in cardiac muscle from desmin-null animals. All of these studies indicate that desmin IFs play a significant role in mitochondrial positioning and respiratory function in cardiac and skeletal muscle.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 07:40:04