Glucocorticoid-Induced Autophagy in Osteocytes

被引：180

作者：

Xia, Xuechun ^{[1
]}

Kar, Rekha ^{[1
]}

Gluhak-Heinrich, Jelica ^{[2
]}

Yao, Wei ^{[3
]}

Lane, Nancy E. ^{[3
]}

Bonewald, Lynda F. ^{[4
]}

Biswas, Sondip K. ^{[5
]}

Lo, Woo-Kuen ^{[5
]}

Jiang, Jean X. ^{[1
]}

机构：

[1] Univ Texas Hlth Sci Ctr San Antonio, Dept Biochem, San Antonio, TX 78229 USA

[2] Univ Texas Hlth Sci Ctr San Antonio, Dept Orthodont, San Antonio, TX 78229 USA

[3] Univ Calif Davis, Med Ctr, Ctr Healthy Aging Internal Med, Sacramento, CA 95817 USA

[4] Univ Missouri, Sch Dent, Dept Oral Biol, Kansas City, MO USA

[5] Morehouse Sch Med, Dept Neurobiol, Atlanta, GA 30310 USA

来源：

JOURNAL OF BONE AND MINERAL RESEARCH | 2010年 / 25卷 / 11期

基金：

美国国家卫生研究院;

关键词：

GLUCOCORTICOID; OSTEOCYTE; AUTOPHAGY; VIABILITY; IN-VIVO; INDUCED APOPTOSIS; OSTEOBLASTS; MECHANISMS; MICE; YEAST; VITRO; LC3;

D O I：

10.1002/jbmr.160

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Glucocorticoid (GC) therapy is the most frequent cause of secondary osteoporosis In this study we have demonstrated that GC treatment induced the development of autophagy preserving osteocyte viability GC treatment resulted in an increase in autophagy markers and the accumulation of autophagosome vacuoles in vitro and in vivo promoted the onset of the osteocyte autophagy as determined by expression of autophagy markers in an animal model of GC induced osteoporosis An autophagy inhibitor reversed the protective effects of GCs The effects of GCs on osteocytes were in contrast to tumor necrosis factor alpha (TNF alpha) which induced apoptosis but not autophagy Together this study reveals a novel mechanism for the effect of GC on osteocytes shedding new insight into mechanisms responsible for bone loss in patients receiving GC therapy (C) 2010 American Society for Bone and Mineral Research

引用

页码：2479 / 2488

页数：10

共 30 条

[1] Evidence that curcumin suppresses the growth of malignant gliomas in vitro and in vivo through induction of autophagy: Role of Akt and extracellular signal-regulated kinase signaling pathways [J].

Aoki, Hiroshi ;

Takada, Yasunari ;

Kondo, Seiji ;

Sawaya, Raymond ;

Aggarwal, Bharat B. ;

Kondo, Yasuko .

MOLECULAR PHARMACOLOGY, 2007, 72 (01) :29-39

[2]

BIEDERBICK A, 1995, EUR J CELL BIOL, V66, P3

[3] Mechanisms of glucocorticoid action in bone [J].

Canalis, E ;

Delany, AM .

NEUROENDOCRINE IMMUNE BASIS OF THE RHEUMATIC DISEASES II, PROCEEDINGS, 2002, 966 :73-81

[4] Mechanical strain opens connexin 43 hemichannels in osteocytes: A novel mechanism for the release of prostaglandin [J].

Cherian, PP ;

Siller-Jackson, AJ ;

Gu, SM ;

Wang, X ;

Bonewald, LF ;

Sprague, E ;

Jiang, JX .

MOLECULAR BIOLOGY OF THE CELL, 2005, 16 (07) :3100-3106

[5] Vanadate prevents glucocorticoid-induced apoptosis of osteoblasts in vitro and osteocytes in vivo [J].

Conradie, M. M. ;

de Wet, H. ;

Kotze, D. D. R. ;

Burrin, J. M. ;

Hough, F. S. ;

Hulley, P. A. .

JOURNAL OF ENDOCRINOLOGY, 2007, 195 (02) :229-240

[6] Estrogen prevents glucocorticoid-induced apoptosis in osteoblasts in vivo and in vitro [J].

Gohel, A ;

McCarthy, MB ;

Gronowicz, G .

ENDOCRINOLOGY, 1999, 140 (11) :5339-5347

[7] Estrogen protects primary osteocytes against glucocorticoid-induced apoptosis [J].

Gu, G ;

Hentunen, TA ;

Nars, M ;

Härkönen, PL ;

Väänänen, HK .

APOPTOSIS, 2005, 10 (03) :583-595

[8] Is autophagy a double-edged sword for the heart? [J].

Gurusamy, N. ;

Das, D. K. .

ACTA PHYSIOLOGICA HUNGARICA, 2009, 96 (03) :267-276

[9] THE MOLECULAR-BIOLOGY OF RU486 - IS THERE A ROLE FOR ANTIPROGESTINS IN THE TREATMENT OF BREAST-CANCER [J].

HORWITZ, KB .

ENDOCRINE REVIEWS, 1992, 13 (02) :146-163

[10]

Hunter AL, 2005, METH MOLEC MED, V112, P277

← 1 2 3 →