کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8269704 | 1534965 | 2014 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Oxidative damage to osteoblasts can be alleviated by early autophagy through the endoplasmic reticulum stress pathway-Implications for the treatment of osteoporosis
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کلمات کلیدی
E64dBAF-A1MMP(2S,3S)-trans-Epoxysuccinyl-l-leucylamido-3-methylbutane ethyl ester5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolcarbocyanine iodideRAP7-aminoactinomycin D7-AADJC-1CATPARP3-MADCFH-DAMDC3-methyladenine - 3-متیل آدنینROS - ROSAutophagy - اتوفاژیOsteoblast - استئوبلاست Endoplasmic reticulum stress - استرس شبکه آندوپلاسمیOxidative stress - تنش اکسیداتیوApoptosis - خزان یاختهایRapamycin - راپامایسینendoplasmic reticulum - شبکه آندوپلاسمی phycoerythrin - فایکوئیریدینlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Mitochondrial membrane potential - پتانسیل غشای میتوکندریPoly(ADP-ribose) polymerase - پلیمر (ADP-ribose) پلیمرازCatalase - کاتالازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Oxidative stress can damage various cellular components of osteoblasts, and is regarded as a pivotal pathogenic factor for bone loss. Increasing evidence indicates a significant role of cell autophagy in response to oxidative stress. However, the role of autophagy in the osteoblasts under oxidative stress remains to be clarified. In this study, we verified that hydrogen peroxide induced autophagy and apoptosis in a dose- and time-dependent manner in osteoblastic Mc3T3-E1 cells. Both 3-methyladenine (the early steps of autophagy inhibitor) and bafilomycin A1 (the last steps of autophagy inhibitor) enhanced the cell apoptosis and reactive oxygen species level in the osteoblasts insulted by hydrogen peroxide. However, promotion of autophagy with either a pharmacologic inducer (rapamycin) or the Beclin-1 overexpressing technique rescued the cell apoptosis and reduced the reactive oxygen species level in the cells. Treatment with H2O2 significantly increased the levels of carbonylated proteins, malondialdehyde and 8-hydroxy-2â²-deoxyguanosine, decreased the mitochondrial membrane potential, and increased the mitochondria-mediated apoptosis markers. The damaged mitochondria were cleared by autophagy. Furthermore, the molecular levels of the endoplasmic reticula stress signaling pathway changed in hydrogen peroxide-treated Mc3T3-E1 cells, and blocking this stress signaling pathway by RNA interference against candidates of glucose-regulated protein 78 and protein kinase-like endoplasmic reticulum kinase decreased autophagy while increasing apoptosis in the cells. In conclusion, oxidative damage to osteoblasts could be alleviated by early autophagy through the endoplasmic reticulum stress pathway. Our findings suggested that modulation of osteoblast autophagy could have a potentially therapeutic value for osteoporosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 77, December 2014, Pages 10-20
Journal: Free Radical Biology and Medicine - Volume 77, December 2014, Pages 10-20
نویسندگان
Yue-Hua Yang, Bo Li, Xin-Feng Zheng, Jiang-Wei Chen, Ke Chen, Sheng-Dan Jiang, Lei-Sheng Jiang,