کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8478597 | 1551141 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Release of mitochondrial Opa1 following oxidative stress in HT22 cells
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کلمات کلیدی
OMMHT22cyto cIMSGAPDH3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromideATP synthase - ATP سنتازopa1 - grandpa1MTT - MTTROS - ROSAdenosine Triphosphate - آدنوزین تری فسفاتimm - انحصارOxidative stress - تنش اکسیداتیوNeurodegeneration - تولید نوروژنیکcytochrome c - سیتوکروم سیintermembrane space - فضای بین محوریlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH glutamate - گلوتاماتglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Release of mitochondrial Opa1 following oxidative stress in HT22 cells Release of mitochondrial Opa1 following oxidative stress in HT22 cells](/preview/png/8478597.png)
چکیده انگلیسی
Cellular mechanisms involved in multiple neurodegenerative diseases converge on mitochondria to induce overproduction of reactive oxygen species, damage to mitochondria, and subsequent cytochrome c release. Little is currently known regarding the contribution mitochondrial dynamics play in cytochrome c release following oxidative stress in neurodegenerative disease. Here we induced oxidative stress in the HT22 cell line with glutamate and investigated key mediators of mitochondrial dynamics to determine the role this process may play in oxidative stress induced neuronal death. We report that glutamate treatment in HT22 cells induces increase in reactive oxygen species (ROS), release of the mitochondrial fusion protein Opa1 into the cytosol, with concomitant release of cytochrome c. Furthermore, following the glutamate treatment alterations in cell signaling coincide with mitochondrial fragmentation which culminates in significant cell death in HT22 cells. Finally, we report that treatment with the antioxidant tocopherol attenuates glutamate induced-ROS increase, release of mitochondrial Opa1 and cytochrome c, and prevents cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 64, January 2015, Pages 116-122
Journal: Molecular and Cellular Neuroscience - Volume 64, January 2015, Pages 116-122
نویسندگان
Thomas H. Sanderson, Sarita Raghunayakula, Rita Kumar,