Myofibrillar myopathy: No evidence of apoptosis by TUNEL

被引：10

作者：

Amato, AA

Jackson, CE

Lampkin, S

Kagan-Hallet, K

机构：

[1] Univ Texas, Hlth Sci Ctr, Dept Med Neurol, San Antonio, TX 78284 USA

[2] Univ Texas, Hlth Sci Ctr, Dept Pathol Neuropathol, San Antonio, TX 78284 USA

来源：

NEUROLOGY | 1999年 / 52卷 / 04期

关键词：

D O I：

10.1212/WNL.52.4.861

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The pathogenesis of myofibrillar myopathy (MFM) is not known. Muscle biopsy specimens demonstrate increased expression of cell cycle regulatory proteins as well as the ectopic expression of lamin B and nuclear matrix protein in the cytoplasm, suggesting the possibility of apoptosis. The authors investigated for apoptosis using the TUNEL method in six muscle biopsy specimens from patients with MFM. There was no evidence of apoptotic myonuclei in any of the MFM muscle biopsies. Further studies regarding the pathogenesis of MFM and the possible role of mitotic catastrophe are needed.

引用

收藏

页码：861 / 863

页数：3

相关论文

共 10 条

[1] The wide spectrum of myofibrillar myopathy suggests a multifactorial etiology and pathogenesis [J].

Amato, AA ;

Kagan-Hallet, K ;

Jackson, CE ;

Lampkin, S ;

Wolfe, GI ;

Ferrante, M ;

Bigio, EH ;

Barohn, RJ .

NEUROLOGY, 1998, 51 (06) :1646-1655

[2] Myofibrillar myopathy with abnormal foci of desmin positivity .2. Immunocytochemical analysis reveals accumulation of multiple other proteins [J].

DeBleecker, JL ;

Engel, AG ;

Ertl, BB .

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1996, 55 (05) :563-577

[3] IDENTIFICATION OF PROGRAMMED CELL-DEATH INSITU VIA SPECIFIC LABELING OF NUCLEAR-DNA FRAGMENTATION [J].

GAVRIELI, Y ;

SHERMAN, Y ;

BENSASSON, SA .

JOURNAL OF CELL BIOLOGY, 1992, 119 (03) :493-501

[4] Missense mutations in desmin associated with familial cardiac and skeletal myopathy [J].

Goldfarb, LG ;

Park, KY ;

Cervenáková, L ;

Gorokhova, S ;

Lee, HS ;

Vasconcelos, O ;

Nagle, JW ;

Semino-Mora, C ;

Sivakumar, K ;

Dalakas, MC .

NATURE GENETICS, 1998, 19 (04) :402-403

[5] CELL BIOLOGY - CELL-CYCLE INHIBITORS MAY HELP BRAKE GROWTH AS CELLS DEVELOP [J].

MARX, J .

SCIENCE, 1995, 267 (5200) :963-964

[6] APOPTOSIS AND THE CELL-CYCLE [J].

MEIKRANTZ, W ;

SCHLEGEL, R .

JOURNAL OF CELLULAR BIOCHEMISTRY, 1995, 58 (02) :160-174

[7] A dysfunctional desmin mutation in a patient with severe generalized myopathy [J].

Muñoz-Mármol, AM ;

Strasser, G ;

Isamat, M ;

Coulombe, PA ;

Yang, YM ;

Roca, X ;

Vela, E ;

Mate, JL ;

Coll, J ;

Fernández-Figueras, MT ;

Navas-Palacios, JJ ;

Ariza, A ;

Fuchs, E .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (19) :11312-11317

[8] Myofibrillar myopathy .3. Abnormal expression of cyclin-dependent kinases and nuclear proteins [J].

Nakano, S ;

Engel, AG ;

Akiguchi, I ;

Kimura, J .

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1997, 56 (08) :850-856

[9] Myofibrillar myopathy with abnormal pool of desmin positivity .1. Light and electron microscopy analysis of 10 cases [J].

Nakano, S ;

Engel, AG ;

Waclawik, AJ ;

EmslieSmith, AM ;

Busis, NA .

JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1996, 55 (05) :549-562

[10] A missense mutation in the αB-crystallin chaperone gene causes a desmin-related myopathy [J].

Vicart, P ;

Caron, A ;

Guicheney, P ;

Li, ZL ;

Prévost, MC ;

Faure, A ;

Chateau, D ;

Chapon, F ;

Tomé, F ;

Dupret, JM ;

Paulin, D ;

Fardeau, M .

NATURE GENETICS, 1998, 20 (01) :92-95