scholarly journals Extracellular cytochrome c, a mitochondrial apoptosis-related protein, induces arthritis

Rheumatology ◽  
2004 ◽  
Vol 44 (1) ◽  
pp. 32-39 ◽  
Author(s):  
R. Pullerits ◽  
M. Bokarewa ◽  
I.-M. Jonsson ◽  
M. Verdrengh ◽  
A. Tarkowski
Keyword(s):  
Cytochrome C ◽  
Mitochondrial Apoptosis ◽  
Related Protein ◽  
Apoptosis Related Protein

scholarly journals Anti-Proliferative and Pro-Apoptotic Effects of Calligonum comosum (L’Her.) Methanolic Extract in Human Triple-Negative MDA-MB-231 Breast Cancer Cells

2020 ◽  
Vol 25 ◽  
pp. 2515690X2097839
Author(s):  
Zeyad Alehaideb ◽  
Saleh AlGhamdi ◽  
Wesam Bin Yahya ◽  
Hamad Al-Eidi ◽  
Mashael Alharbi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cytochrome C ◽  
Cell Viability ◽  
Triple Negative ◽  
Methanolic Extract ◽  
Growth Arrest ◽  
Related Protein ◽  
Cell Growth Arrest ◽  
Apoptosis Related Protein

Triple-negative breast cancer (TNBC), the most aggressive subtype, does not respond to targeted therapy due to the lack of hormone receptors. There is an urgent need for alternative therapies, including natural product-based anti-cancer drugs, at lower cost. We investigated the impact of a Calligonum comosum L’Hér. methanolic extract (CcME) on the TNBC MDA-MB-231 cell line proliferation and related cell death mechanisms performing cell viability and cytotoxicity assays, flow cytometry to detect apoptosis and cell cycle analysis. The apoptosis-related protein array and cellular reactive oxygen species (ROS) assay were also carried out. We showed that the CcME inhibited the TNBC cell viability, in a dose-dependent manner, with low cytotoxic effects. The CcME-treated TNBC cells underwent apoptosis, associated with a concomitant increase of apoptosis-related protein expression, including cytochrome c, cleaved caspase-3, cyclin-dependent kinase inhibitor p21, and the anti-oxidant enzyme catalase, compared with the untreated cells. The CcME also enhanced the mitochondrial transition pore opening activity and induced G0/G1 cell growth arrest, which confirmed the cytochrome c release and the increase of the p21 expression detected in the CcME-treated TNBC cells. The CcME-treated TNBC cells resulted in intracellular ROS production, which, when blocked with a ROS scavenger, did not reduce the CcME-induced apoptosis. In conclusion, CcME exerts anti-proliferative effects against TNBC cells through the induction of apoptosis and cell growth arrest. In vivo studies are justified to verify the CcME anti-proliferative activities and to investigate any potential anti-metastatic activities of CcME against TNBC development and progression.

Effects of cytochrome c on the mitochondrial apoptosis-induced channel MAC

2004 ◽  
Vol 286 (5) ◽  
pp. C1109-C1117 ◽  
Author(s):  
Liang Guo ◽  
Dawn Pietkiewicz ◽  
Evgeny V. Pavlov ◽  
Sergey M. Grigoriev ◽  
John J. Kasianowicz ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Outer Membrane ◽  
Cell Types ◽  
Rnase A ◽  
Mitochondrial Outer Membrane ◽  
Dependent Manner ◽  
Mitochondrial Apoptosis ◽  
Noise Type ◽  
Voltage Dependent

Recent studies indicate that cytochrome c is released early in apoptosis without loss of integrity of the mitochondrial outer membrane in some cell types. The high-conductance mitochondrial apoptosis-induced channel (MAC) forms in the outer membrane early in apoptosis of FL5.12 cells. Physiological (micromolar) levels of cytochrome c alter MAC activity, and these effects are referred to as types 1 and 2. Type 1 effects are consistent with a partitioning of cytochrome c into the pore of MAC and include a modest decrease in conductance that is dose and voltage dependent, reversible, and has an increase in noise. Type 2 effects may correspond to “plugging” of the pore or destabilization of the open state. Type 2 effects are a dose-dependent, voltage-independent, and irreversible decrease in conductance. MAC is a heterogeneous channel with variable conductance. Cytochrome c affects MAC in a pore size-dependent manner, with maximal effects of cytochrome c on MAC with conductance of 1.9–5.4 nS. The effects of cytochrome c, RNase A, and high salt on MAC indicate that size, rather than charge, is crucial. The effects of dextran molecules of various sizes indicate that the pore diameter of MAC is slightly larger than that of 17-kDa dextran, which should be sufficient to allow the passage of 12-kDa cytochrome c. These findings are consistent with the notion that MAC is the pore through which cytochrome c is released from mitochondria during apoptosis.

scholarly journals The Potential Roles of the Apoptosis-Related Protein PDRG1 in Diapause Embryo Restarting of Artemia sinica

2018 ◽  
Vol 19 (1) ◽  
pp. 126 ◽  
Author(s):  
Wan Zhang ◽  
Feng Yao ◽  
Hong Zhang ◽  
Na Li ◽  
Xiangyang Zou ◽  
...  
Keyword(s):  
Related Protein ◽  
Artemia Sinica ◽  
Diapause Embryo ◽  
Apoptosis Related Protein

Protective Effects of Serotonin and its Derivatives, N-Feruloylserotonin and N-(p-Coumaroyl) Serotonin, Against Cisplatin-Induced Renal Damage in Mice

2019 ◽  
Vol 47 (02) ◽  
pp. 369-383 ◽  
Author(s):  
Chan Hum Park ◽  
Ah Young Lee ◽  
Ji Hyun Kim ◽  
Su Hui Seong ◽  
Eun Ju Cho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Renal Damage ◽  
Pleiotropic Effect ◽  
Protective Effects ◽  
Related Protein ◽  
Renoprotective Effect ◽  
Serotonin Derivatives ◽  
Mitogen Activated Protein ◽  
Apoptosis Related Protein

This study examined whether serotonin and two of its derivatives, [Formula: see text]-feruloylserotonin and [Formula: see text]-([Formula: see text]-coumaroyl) serotonin, have a renoprotective effect in a mouse model of cisplatin-induced acute renal failure. Cisplatin (20[Formula: see text]mg/kg body weight) was administered by intraperitoneal injection to male BALB/c mice that had received oral serotonin, [Formula: see text]-feruloylserotonin or [Formula: see text]-([Formula: see text]-coumaroyl) serotonin (7.5[Formula: see text]mg/kg body weight per day) during the preceding 2 days. At 3 days after the cisplatin injection, serum and renal biochemical factors, oxidative stress, inflammation and apoptosis-related protein expression were evaluated, and histological examinations were performed. Cisplatin caused reduction in body weight and an increase in kidney weight; however, [Formula: see text]-([Formula: see text]-coumaroyl) serotonin and [Formula: see text]-feruloylserotonin attenuated these effects. Moreover, the serotonin derivatives significantly decreased serum urea nitrogen and creatinine levels. They also significantly reduced the level of reactive oxygen species and upregulated the expression of glutathione peroxidase in the kidney. Furthermore, the serotonin derivatives improved the abnormal expression of mitogen-activated protein kinases activation-dependent inflammation- and apoptosis-related protein and caused less renal damage. These results provide important evidence that [Formula: see text]-([Formula: see text]-coumaroyl) serotonin and [Formula: see text]-feruloylserotonin exert a pleiotropic effect on several parameters related to oxidative stress, inflammation and apoptosis. The derivatives also have a renoprotective effect in cisplatin-treated mice; however, this effect is higher with [Formula: see text]-([Formula: see text]-coumaroyl) serotonin.

scholarly journals Mitochondrial apoptotic signaling is elevated in cardiac but not skeletal muscle in the obese Zucker rat and is reduced with aerobic exercise

2008 ◽  
Vol 105 (6) ◽  
pp. 1934-1943 ◽  
Author(s):  
Jonathan M. Peterson ◽  
Randall W. Bryner ◽  
Amy Sindler ◽  
Jefferson C. Frisbee ◽  
Stephen E. Alway
Keyword(s):  
Cytochrome C ◽  
Exercise Training ◽  
Protein Expression ◽  
Skeletal Muscles ◽  
Zucker Rats ◽  
Mitochondrial Apoptosis ◽  
Apoptotic Signaling ◽  
Bax Protein ◽  
Cardiac Muscles ◽  
Cytosolic Cytochrome

Mitochondrial apoptosis and apoptotic signaling modulations by aerobic training were studied in cardiac and skeletal muscles of obese Zucker rats (OZR), a rodent model of metabolic syndrome. Comparisons were made between left ventricle, soleus, and gastrocnemius muscles from OZR ( n = 16) and aged-matched lean Zucker rats (LZR; n = 16) that were untrained ( n = 8) or aerobically trained on a treadmill for 9 wk ( n = 8). Cardiac Bcl-2 protein expression levels were ∼50% lower in the OZR compared with the LZR, with no difference in either of the skeletal muscles. Bax protein expression levels were similar in skeletal muscles of the OZR compared with the LZR. Furthermore, mitochondrial apoptotic signaling was not different in skeletal muscles of OZR and LZR groups. However, there was an approximate sevenfold increase in the Bax protein accumulation in the myocardial mitochondrial-rich protein fraction of the OZR compared with the LZR. Additionally, there was an increase in cytosolic cytochrome c released from the mitochondria, caspase-9 and caspase-3 activity, with a corresponding elevation in DNA fragmentation in the cardiac muscles of the OZR compared with the LZR. Exercise training reduced cardiac Bax protein levels, the mitochondrial localization of Bax, cytosolic cytochrome c, caspase activity, and DNA fragmentation in cardiac muscles of the OZR after exercise, with no change in the skeletal muscles. These data show that mitochondrial apoptosis is elevated in the cardiac but not skeletal muscles of the OZR, but aerobic exercise training was effective in reducing cardiac mitochondrial apoptotic signaling.

Sign in / Sign up

Export Citation Format

Share Document