scholarly journals FM19G11-Loaded Gold Nanoparticles Enhance the Proliferation and Self-Renewal of Ependymal Stem Progenitor Cells Derived from ALS Mice

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 279 ◽  
Author(s):  
Stefania Marcuzzo ◽  
Davide Isaia ◽  
Silvia Bonanno ◽  
Claudia Malacarne ◽  
Paola Cavalcante ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Progenitor Cells ◽  
Motor Neurons ◽  
Uncoupling Protein ◽  
Hypoxia Inducible Factor ◽  
Disease Onset ◽  
Mitochondrial Uncoupling ◽  
Self Renewal ◽  
Mitochondrial Uncoupling Protein ◽  
G93a Sod1

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. In ALS mice, neurodegeneration is associated with the proliferative restorative attempts of ependymal stem progenitor cells (epSPCs) that normally lie in a quiescent in the spinal cord. Thus, modulation of the proliferation of epSPCs may represent a potential strategy to counteract neurodegeneration. Recent studies demonstrated that FM19G11, a hypoxia-inducible factor modulator, induces epSPC self-renewal and proliferation. The aim of the study was to investigate whether FM19G11-loaded gold nanoparticles (NPs) can affect self-renewal and proliferation processes in epSPCs isolated from G93A-SOD1 mice at disease onset. We discovered elevated levels of SOX2, OCT4, AKT1, and AKT3, key genes associated with pluripotency, self-renewal, and proliferation, in G93A-SOD1 epSPCs at the transcriptional and protein levels after treatment with FM19G11-loaded NPs. We also observed an increase in the levels of the mitochondrial uncoupling protein (UCP) gene in treated cells. FM19G11-loaded NPs treatment also affected the expression of the cell cycle-related microRNA (miR)-19a, along with its target gene PTEN, in G93A-SOD1 epSPCs. Overall our findings establish the significant impact of FM19G11-loaded NPs on the cellular pathways involved in self-renewal and proliferation in G93A-SOD1 epSPCs, thus providing an impetus to the design of novel tailored approaches to delay ALS disease progression.

scholarly journals Effects of Mitochondrial Uncoupling Protein 2 Inhibition by Genipin in Human Cumulus Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Hongshan Ge ◽  
Fan Zhang ◽  
Dan Shan ◽  
Hua Chen ◽  
Xiaona Wang ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Uncoupling Protein ◽  
Physiological Role ◽  
Cumulus Cells ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Cultural Medium ◽  
Cellular Autophagy ◽  
Significant Difference ◽  
Active Caspase

UCP2 plays a physiological role by regulating mitochondrial biogenesis, maintaining energy balance, ROS elimination, and regulating cellular autophagy in numerous tissues. But the exact roles of UCP2 in cumulus cells are still not clear. Genipin, a special UCP2 inhibitor, was added into the cultural medium to explore the roles of UCP2 in human cumulus cells. There were no significant differences in ATP and mitochondrial membrane potential levels in cumulus cells from UCP2 inhibiting groups as compared with the control. The levels of ROS and Mn-SOD were markedly elevated after UCP2 inhibited Genipin. However, the ratio of reduced GSH to GSSG significantly declined after treatment with Genipin. UCP2 inhibition by Genipin also resulted in obvious increase in the active caspase-3, which accompanied the decline of caspase-3 mRNA. The level of progesterone in culture medium declined obviously after Genipin treatment. But there was no significant difference in estradiol concentrations. This study indicated that UCP2 is expressed in human cumulus cells and plays important roles on mediate ROS production, apoptotic process, and steroidogenesis, suggesting UCP2 may be involved in regulation of follicle development and oocyte maturation and quality.

scholarly journals Mitochondrial Hormesis in PancreaticβCells: Does Uncoupling Protein 2 Play a Role?

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Ning Li ◽  
Suzana Stojanovski ◽  
Pierre Maechler
Keyword(s):  
Stress Responses ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Cell Function ◽  
Uncoupling Protein ◽  
Glucose Sensing ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Cellular Stresses ◽  
Excessive Nutrients

In pancreaticβcells, mitochondrial metabolism translates glucose sensing into signals regulating insulin secretion. Chronic exposure ofβcells to excessive nutrients, namely, glucolipotoxicity, impairsβ-cell function. This is associated with elevated ROS production from overstimulated mitochondria. Mitochondria are not only the major source of cellular ROS, they are also the primary target of ROS attacks. The mitochondrial uncoupling protein UCP2, even though its uncoupling properties are debated, has been associated with protective functions against ROS toxicity. Hormesis, an adaptive response to cellular stresses, might contribute to the protection againstβ-cell death, possibly limiting the development of type 2 diabetes. Mitochondrial hormesis, or mitohormesis, is a defense mechanism observed in ROS-induced stress-responses by mitochondria. Inβcells, mitochondrial damages induced by sublethal exogenous H2O2can induce secondary repair and defense mechanisms. In this context, UCP2 is a marker of mitohormesis, being upregulated following stress conditions. When overexpressed in nonstressed naïve cells, UCP2 confers resistance to oxidative stress. Whether treatment with mitohormetic inducers is sufficient to restore or ameliorate secretory function ofβcells remains to be determined.

scholarly journals Mitochondrial uncoupling protein 2 (UCP2), but not UCP3, is sensitive to oxygen concentration in cells

2020 ◽  
Author(s):  
Karolina E. Hilse ◽  
Anne Rupprecht ◽  
Kristopher Ford ◽  
Olena Andrukhova ◽  
Reinhold Erben ◽  
...  
Keyword(s):  
Stem Cell ◽  
Oxygen Concentration ◽  
Uncoupling Protein ◽  
Ischemia Reperfusion ◽  
Stem Cell Differentiation ◽  
Embryonic Stem Cell Differentiation ◽  
Mitochondrial Uncoupling ◽  
Homologous Proteins ◽  
Mitochondrial Uncoupling Protein ◽  
Pathological Conditions

AbstractOne of the important hallmarks of cardiovascular disease is mitochondrial dysfunction, which results in abnormal energy metabolism and increased ROS production in cardiomyocytes. Members of the mitochondrial uncoupling protein family, UCP2 and UCP3, are thought to be beneficial by reducing ROS due to mild uncoupling. More recent hypotheses suggest the involvement of both proteins in cell metabolism by the transport of yet unknown substrates. The protein expression pattern under physiological and pathological conditions is an important clue for the evaluation of UCP2/UCP3 function, however, there is still no consensus about it. Previously, we demonstrated that only UCP3 is present in the adult murine heart under physiological conditions and correlated it with the predominant use of fatty acids for oxidation. In contrast, UCP2 was found only in very young (stem cell – like) cardiomyocytes, that rely mostly on glycolysis. Here, we employed three different models (ex vivo heart ischemia-reperfusion model, myocardial infarction model, and embryonic stem cell differentiation into cardiomyocytes under hypoxic conditions) to evaluate the abundance of both proteins under ischemia and hypoxia conditions. We found that (i) oxygen shortage or bursts did not influence UCP3 levels in the heart and ii) UCP2 was not present in healthy, ischemic, or re-perfused hearts. However, (iii) UCP2 was sensitive to the oxygen concentration in stem cells, in which UCP2 is normally expressed. These results further support the idea, that two highly homologous proteins – UCP2 and UCP3 – are abundant in different cells and tissues, and differently regulated under physiological and pathological conditions.

scholarly journals Mitochondrial Uncoupling protein‐2 regulates NLRP3 inflammasome

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Rajan babu Venugopal ◽  
Ruan Rollin Cox ◽  
prasanna Tamarappu Parthasarathy ◽  
Richard F Lockey ◽  
Narasaiah Kolliputi
Keyword(s):  
Nlrp3 Inflammasome ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein

Mitochondrial uncoupling protein silence is compromised in photosynthesis and redox poise

2013 ◽  
Vol 35 (8) ◽  
pp. 2547-2558 ◽  
Author(s):  
Shuangchen Chen ◽  
Wenjuan Jin ◽  
Ai-rong Liu ◽  
Zimei Liu ◽  
Dilin Liu ◽  
...  
Keyword(s):  
Uncoupling Protein ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Redox Poise
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