نتایج جستجو برای: cigarette smoking extracts cse cytochrome c release isolated mitochondria

تعداد نتایج: 1738220  

Journal: :The Biochemical journal 2000
K Nomura H Imai T Koumura T Kobayashi Y Nakagawa

Cytochrome c (cyt. c) is a proapoptotic factor that binds preferentially to cardiolipin (CL), a mitochondrial lipid, but not to cardiolipin hydroperoxide (CL-OOH). Cyt. c that had bound to CL liposomes was liberated on peroxidation of the liposomes by a radical. The generation of CL-OOH in mitochondria occurred before the release of cyt. c in rat basophile leukaemia (RBL)2H3 cells that had been...

Journal: :American journal of physiology. Lung cellular and molecular physiology 2010
Mirella Profita Angelo Sala Anna Bonanno Loredana Riccobono Maria Ferraro Stefania La Grutta Giusy Daniela Albano Angela Marina Montalbano Mark Gjomarkaj

Cigarette smoke is the main cause of chronic obstructive pulmonary disease (COPD), where it can contribute to the observed airway inflammation. PGE(2) is produced within human airways, and both pro- and anti-inflammatory activities have been reported. We quantitated PGE(2) concentrations in induced sputum supernatants from different groups of subjects and correlated the obtained values to neutr...

Journal: :Oncology reports 2016
Jian Gong Yi Chu Meili Xu Jirong Huo Liang Lv

Cigarette smoke has been implicated as a major risk factor for esophageal squamous cell carcinoma (ESCC). Several lines of evidence have suggested that the promoting effect of cigarette smoking extract (CSE) on ESCC is mediated by upregulation of cyclooxygenase-2 (COX-2) expression. Yet, the underlying molecular and cellular mechanisms of how CSE stimulates COX-2 expression and facilitates ESCC...

2016
Dong Wu Yalian Yuan Zhixiu Lin Tianwen Lai Min Chen Wen Li Quanchao Lv Binfan Yuan Dongmin Li Bin Wu

Etiological evidence demonstrates that there is a significant association between cigarette smoking and chronic airway inflammatory disease. Abnormal expression of placental growth factor (PlGF) has been reported in COPD, and its downstream signaling molecules have been reported to contribute to the pathogenesis of airway epithelial cell apoptosis and emphysema. However, the signaling mechanism...

2017
Mohammad Reza Mirshamsi Ramesh Omranipour Amir Vazirizadeh Amir Fakhri Fatemeh Zangeneh Gholam Hussain Mohebbi Ramin Seyedian Jalal Pourahmad

Objective: This study was conducted to investigate whether fractions of jellyfish Cassiope andromeda venom, could selectively induce toxicity on mitochondria isolated from cancer tissue of patients with breast adenocarcinomas. Methods: Firstly, we extracted two fractions, (f1 and f2) from crude jellyfish venom by gel filtration on Sephadex G-200.Then different dilutions of these extracted fract...

2012
Libera Berghella Elisabetta Ferraro

Cytochrome c is a key molecule in mitochondria-mediated apoptosis. It also plays a pivotal role in cell respiration. The switch between these two functions occurs at the moment of its release from mitochondria. This process is therefore extremely relevant for the fate of the cell. Since cytochrome c mediates respiration, we studied the changes in respiratory chain activity during the early stag...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1999
S Krajewski M Krajewska L M Ellerby K Welsh Z Xie Q L Deveraux G S Salvesen D E Bredesen R E Rosenthal G Fiskum J C Reed

Caspase-9 is critical for cytochrome c (cyto-c)-dependent apoptosis and normal brain development. We determined that this apical protease in the cyto-c pathway for apoptosis resides inside mitochondria in several types of cells, including cardiomyocytes and many neurons. Caspase-9 is released from isolated mitochondria on treatment with Ca2+ or Bax, stimuli implicated in ischemic neuronal cell ...

Journal: :Journal of neurochemistry 2002
Anatoly A Starkov Brian M Polster Gary Fiskum

Abnormal accumulation of Ca2+ and exposure to pro-apoptotic proteins, such as Bax, is believed to stimulate mitochondrial generation of reactive oxygen species (ROS) and contribute to neural cell death during acute ischemic and traumatic brain injury, and in neurodegenerative diseases, e.g. Parkinson's disease. However, the mechanism by which Ca2+ or apoptotic proteins stimulate mitochondrial R...

Journal: :Journal of cell science 2001
W Gao Y Pu K Q Luo D C Chang

During apoptosis, cytochrome c is released from mitochondria to the cytosol to activate a caspase cascade, which commits the cell to the death process. It has been proposed that the release of cytochrome c is caused by a swelling of the mitochondrial matrix triggered by the apoptotic stimuli. To test this theory, we measured directly the dynamic re-distribution of green fluorescence protein (GF...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید