Regulation of UCP3 expression and function in response to hypoxia and oxidative stress in mouse cardiomyocytes

2018 ◽  
Vol 120 ◽  
pp. S32 ◽  
Author(s):  
Patricia Sánchez-Pérez ◽  
Elia López-Bernardo ◽  
Andrea Anedda ◽  
Susana Cadenas
2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Somayeh Keshtkar ◽  
Maryam Kaviani ◽  
Zahra Jabbarpour ◽  
Bita Geramizadeh ◽  
Elahe Motevaseli ◽  
...  

Animals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 1135
Author(s):  
Arth David Sol Valmoria Ortega ◽  
Csaba Szabó

Heat stress (HS) significantly affects the performance of pigs by its induced stressors such as inflammation, hypoxia and oxidative stress (OS), which mightily strain the intestinal integrity and function of pigs. As heat stress progresses, several mechanisms in the intestinal epithelium involved in the absorption of nutrients and its protective functions are altered. Changes in these mechanisms are mainly driven by cellular oxidative stress, which promotes disruption of intestinal homeostasis, leading to intestinal permeability, emphasizing intestinal histology and morphology with little possibility of recovering even after exposure to HS. Identification and understanding of these altered mechanisms are crucial for providing appropriate intervention strategies. Therefore, it is this papers’ objective to review the important components for intestinal integrity that are negatively affected by HS and its induced stressors. With due consideration to the amelioration of such effects through nutritional intervention, this work will also look into the capability of dietary antioxidants in mitigating such adverse effects and maintaining the intestine’s integrity and function upon the pigs’ exposure to high environmental temperature.


Author(s):  
Mo Wang ◽  
Ling-ing Lau ◽  
Parameswaran G. Sreekumar ◽  
Christine Spee ◽  
Lin Liu ◽  
...  

Mitochondrial dysfunction and oxidative stress are thought to be relevant to the pathogenesis of age-related macular degeneration (AMD). Glutathione (GSH) homeostasis fulfills a number of important roles in mitochondria, such as maintenance of mitochondrial DNA and respiratory competency of cells. Although the transport of mitochondrial GSH (mGSH) is not fully understood, increasing evidence from non-ocular tissues suggests that OGC (2-oxoglutarate carrier, SLC25A11) and DIC (dicarboxylate carrier, SLC25A10) are involved in mGSH transport. However, whether OGC and DIC mediate the transfer of GSH into the mitochondria of retinal pigment epithelial cells (RPE) remains unknown. Thus, we investigated the expression, localization, and function of OGC and DIC in human RPE (hRPE) in relation to oxidative stress and GSH. Both OGC and DIC are expressed in hRPE and are localized in mitochondria. We also found a dose and time-dependent decrease of OGC and DIC expression under oxidative stress and increased expression in polarized RPE. Our data show that the downregulation of OGC and DIC resulted in increased apoptosis and mGSH depletion which can be overcome by co-treatment with GSH-MEE. These findings suggest that overexpression of OGC and DIC may be an effective strategy to decrease susceptibility to mitochondrial toxicants by elevation of mGSH.


2020 ◽  
Vol 8 (13) ◽  
Author(s):  
Hannah R. Turbeville ◽  
Ashley C. Johnson ◽  
Michael R. Garrett ◽  
Elena L. Dent ◽  
Jennifer M. Sasser

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Peipei Guo ◽  
Zhao Jin ◽  
Jin Wang ◽  
Aming Sang ◽  
Huisheng Wu

Traumatic brain injury (TBI) has a high incidence, mortality, and morbidity all over the world. One important reason for its poor clinical prognosis is brain edema caused by blood-brain barrier (BBB) dysfunction after TBI. The mechanism may be related to the disorder of mitochondrial morphology and function of neurons in damaged brain tissue, the decrease of uncoupling protein 2 (UCP2) activity, and the increase of inflammatory reaction and oxidative stress. In this study, we aimed to investigate the effects of exogenous irisin on BBB dysfunction after TBI and its role in the neuroprotective effects of endurance exercise (EE) in mice. The concentrations of irisin in cerebrospinal fluid (CSF) and plasma of patients with mild to severe TBI were measured by ELISA. Then, male C57BL/6J mice and UCP2 knockout mice with C57BL/6J background were used to establish the TBI model. The BBB structure and permeability were examined by transmission electron microscopy and Evans blue extravasation, respectively. The protein expressions of irisin, occludin, claudin-5, zonula occludens-1 (ZO-1), nuclear factor E2-related factor 2(Nrf2), quinine oxidoreductase (NQO-1), hemeoxygenase-1 (HO-1), cytochrome C (Cyt-C), cytochrome C oxidase (COX IV), BCL2-associated X protein (Bax), cleaved caspase-3, and UCP2 were detected by western blot. The production of reactive oxygen species (ROS) was evaluated by the dihydroethidium (DHE) staining. The levels of inflammatory factors were detected by ELISA. In this study, we found that the CSF irisin levels were positively correlated with the severity of disease in patients with TBI and both EE and exogenous irisin could reduce BBB damage in a mouse model of TBI. In addition, we used UCP2−/− mice and further found that irisin could improve the dysfunction of BBB after TBI by promoting the expression of UCP2 on the mitochondrial membrane of neurons, reducing the damage of mitochondrial structure and function, thus alleviating the inflammatory response and oxidative stress. In conclusion, the results of this study suggested that irisin might alleviate brain edema after TBI by promoting the expression of UCP2 on the mitochondrial membrane of neurons and contribute to the neuroprotection of EE against TBI.


2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
José L. Reyes ◽  
Eduardo Molina-Jijón ◽  
Rafael Rodríguez-Muñoz ◽  
Pablo Bautista-García ◽  
Yazmin Debray-García ◽  
...  

Kidney is a target organ for heavy metals. They accumulate in several segments of the nephron and cause profound alterations in morphology and function. Acute intoxication frequently causes acute renal failure. The effects of chronic exposure have not been fully disclosed. In recent years increasing awareness of the consequences of their presence in the kidney has evolved. In this review we focus on the alterations induced by heavy metals on the intercellular junctions of the kidney. We describe that in addition to the proximal tubule, which has been recognized as the main site of accumulation and injury, other segments of the nephron, such as glomeruli, vessels, and distal nephron, show also deleterious effects. We also emphasize the participation of oxidative stress as a relevant component of the renal damage induced by heavy metals and the beneficial effect that some antioxidant drugs, such as vitamin A (all-trans-retinoic acid) and vitamin E (α-tocopherol), depict on the morphological and functional alterations induced by heavy metals.


2009 ◽  
Vol 105 (5) ◽  
pp. 811-822 ◽  
Author(s):  
Jean-Francois Briat ◽  
Karl Ravet ◽  
Nicolas Arnaud ◽  
Céline Duc ◽  
Jossia Boucherez ◽  
...  

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