کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5506483 1536767 2016 24 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Lenti-siRNA Hsp60 promote bax in mitochondria and induces apoptosis during heat stress
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Lenti-siRNA Hsp60 promote bax in mitochondria and induces apoptosis during heat stress
چکیده انگلیسی
Hsp60 is a typical mitochondrial protein in eukaryotes, and is involved in facilitating the correction of misfolded protein back into the correct conformation. Previous, we identified aspirin-induced HSPs in response to heat stress [1]. To investigate whether Hsp60 can protect against death under heat stress, we used lenti-siRNA to knock down the expression of Hsp60. When exposed to heat stress, more apoptosis was observed with increasing exposure to heat stress, while necrosis was not affected. Furthermore, heat stress induced the loss of mitochondrial membrane potential (ΔΨm) and a significant increase of reactive oxygen species (ROS) produced in mitochondria as measured by TMRE and MitoSOXTM red. The loss of ΔΨm indicated a change in inner mitochondrial function. Real-time Quantitative PCR was used to investigate the mechanism by detecting mRNA expression profile of the inner mitochondrial membrane, including CypD, ANT, and PIC. Results showed no differences between lenti-siRNA Hsp60 and control. However, bax in the cytoplasm translocated to mitochondrial during heat stress and regulated the permeability of outer mitochondrial membrane. We hypothesize that Hsp60 can protect cardiac myocytes against apoptosis involving in outer mitochondrial membrane not the inner mitochondrial membrane under heat stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 481, Issues 1–2, 2 December 2016, Pages 125-131
نویسندگان
, , , , , ,