Effects of Different Music on HEK293T Cell Growth and Mitochondrial Functions

EXPLORE ◽  
2022 ◽  
Author(s):  
Qian Feng ◽  
Lin Wang ◽  
Yu Chen ◽  
Mengmei Li ◽  
Jie Teng ◽  
...  
Keyword(s):  
Cell Growth ◽  
Hek293t Cell ◽  
Mitochondrial Functions ◽  
And Mitochondrial Functions

scholarly journals LONP1 and ClpP cooperatively regulate mitochondrial proteostasis for cancer cell survival

Oncogenesis ◽  
2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Yu Geon Lee ◽  
Hui Won Kim ◽  
Yeji Nam ◽  
Kyeong Jin Shin ◽  
Yu Jin Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Cell Survival ◽  
Cancer Cell ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Tca Cycle ◽  
Mitochondrial Matrix ◽  
Mitochondrial Functions ◽  
Cancer Cell Survival

AbstractMitochondrial proteases are key components in mitochondrial stress responses that maintain proteostasis and mitochondrial integrity in harsh environmental conditions, which leads to the acquisition of aggressive phenotypes, including chemoresistance and metastasis. However, the molecular mechanisms and exact role of mitochondrial proteases in cancer remain largely unexplored. Here, we identified functional crosstalk between LONP1 and ClpP, which are two mitochondrial matrix proteases that cooperate to attenuate proteotoxic stress and protect mitochondrial functions for cancer cell survival. LONP1 and ClpP genes closely localized on chromosome 19 and were co-expressed at high levels in most human cancers. Depletion of both genes synergistically attenuated cancer cell growth and induced cell death due to impaired mitochondrial functions and increased oxidative stress. Using mitochondrial matrix proteomic analysis with an engineered peroxidase (APEX)-mediated proximity biotinylation method, we identified the specific target substrates of these proteases, which were crucial components of mitochondrial functions, including oxidative phosphorylation, the TCA cycle, and amino acid and lipid metabolism. Furthermore, we found that LONP1 and ClpP shared many substrates, including serine hydroxymethyltransferase 2 (SHMT2). Inhibition of both LONP1 and ClpP additively increased the amount of unfolded SHMT2 protein and enhanced sensitivity to SHMT2 inhibitor, resulting in significantly reduced cell growth and increased cell death under metabolic stress. Additionally, prostate cancer patients with higher LONP1 and ClpP expression exhibited poorer survival. These results suggest that interventions targeting the mitochondrial proteostasis network via LONP1 and ClpP could be potential therapeutic strategies for cancer.

scholarly journals Neurodevelopmental Disorders: Effect of High-Fat Diet on Synaptic Plasticity and Mitochondrial Functions

2020 ◽  
Vol 10 (11) ◽  
pp. 805 ◽  
Author(s):  
Eduardo Penna ◽  
Amelia Pizzella ◽  
Fabiano Cimmino ◽  
Giovanna Trinchese ◽  
Gina Cavaliere ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neurodevelopmental Disorders ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Low Grade ◽  
High Fat ◽  
Mitochondrial Functions ◽  
Diet Pattern ◽  
Metabolic Dysfunctions ◽  
And Mitochondrial Functions

Neurodevelopmental disorders (NDDs) include diverse neuropathologies characterized by abnormal brain development leading to impaired cognition, communication and social skills. A common feature of NDDs is defective synaptic plasticity, but the underlying molecular mechanisms are only partially known. Several studies have indicated that people’s lifestyles such as diet pattern and physical exercise have significant influence on synaptic plasticity of the brain. Indeed, it has been reported that a high-fat diet (HFD, with 30–50% fat content), which leads to systemic low-grade inflammation, has also a detrimental effect on synaptic efficiency. Interestingly, metabolic alterations associated with obesity in pregnant woman may represent a risk factor for NDDs in the offspring. In this review, we have discussed the potential molecular mechanisms linking the HFD-induced metabolic dysfunctions to altered synaptic plasticity underlying NDDs, with a special emphasis on the roles played by synaptic protein synthesis and mitochondrial functions.

Effects of glucose fluctuations on cellular and mitochondrial functions in HL-1 cardiac cell line

2016 ◽  
Vol 42 (4) ◽  
pp. 295 ◽  
Author(s):  
P. Mordel ◽  
M. Nowoczyn ◽  
M. Joubert ◽  
L. Coulbault ◽  
S. Allouche
Keyword(s):  
Cell Line ◽  
Cardiac Cell ◽  
Mitochondrial Functions ◽  
Glucose Fluctuations ◽  
And Mitochondrial Functions

Stearic Acid Supplementation in High Protein to Carbohydrate (P:C) Ratio Diet Improves Physiological and Mitochondrial Functions of Drosophila melanogaster parkin Null Mutants

2017 ◽  
Vol 74 (10) ◽  
pp. 1564-1572 ◽  
Author(s):  
Rijan Bajracharya ◽  
Sonia Bustamante ◽  
John William O Ballard
Keyword(s):  
Fatty Acids ◽  
Stearic Acid ◽  
High Protein Diet ◽  
High Carbohydrate Diet ◽  
High Protein ◽  
Protein Diet ◽  
Carbohydrate Diet ◽  
High Carbohydrate ◽  
Mitochondrial Functions ◽  
And Mitochondrial Functions

Abstract Optimizing dietary macronutrients benefits the prevention and management of many human diseases but there is conflicting dietary advice for Parkinson’s disease (PD), and no single strategy is universally recommended. Recently, it was shown that dietary stearic acid (C18:0) improves survival and mitochondrial functions in the parkin null Drosophila model of PD. Here, we incorporate stearic acid into high protein and high carbohydrate diets and study survival, climbing ability, mitochondrial membrane potential, respiration, basal reactive oxygen species, and conduct lipidomics assays. We observed that parkin null flies showed improvement in all assays tested when stearic acid was added to the high protein diet but not to the high carbohydrate diet. When lipid proportion was examined, we observed higher levels in flies fed the high protein diet with stearic acid diet and the high carbohydrate diet. Unexpectedly, free levels of fatty acids exhibited opposite trend. Combined, these data suggest that dietary Protein: Carbohydrate ratio and stearic acid influences levels of bound fatty acids. The mechanisms that influence free and bound fatty-acid levels remain to be explored, but one possible explanation is that breakdown products can bind to membranes and improve the mitochondrial functions of parkin null flies.

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