Intracellular mitochondrial membrane potential as an indicator of hepatocyte energy metabolism: Further evidence for thermodynamic control of metabolism

1988 ◽  
Vol 936 (3) ◽  
pp. 294-306 ◽  
Author(s):  
Michael N. Berry ◽  
Roland B. Gregory ◽  
Anthony R. Grivell ◽  
Debra C. Henly ◽  
Catherine D. Nobes ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Energy Metabolism ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Thermodynamic Control

scholarly journals Improvement of the energy metabolism of recombinant CHO cells by cell sorting for reduced mitochondrial membrane potential

2007 ◽  
Vol 129 (4) ◽  
pp. 651-657 ◽  
Author(s):  
Georg Hinterkörner ◽  
Gudrun Brugger ◽  
Dethardt Müller ◽  
Friedemann Hesse ◽  
Renate Kunert ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Energy Metabolism ◽  
Mitochondrial Membrane Potential ◽  
Cell Sorting ◽  
Cho Cells ◽  
Mitochondrial Membrane ◽  
Recombinant Cho Cells

Metformin Collaborates With PINK1/Mfn2 Overexpression Prevented Isoproterenol-Induced Cardiomyocyte Injury By Improving Mitochondrial Function

2021 ◽  
Author(s):  
Zhuang Ma ◽  
Zuheng Liu ◽  
Yuting Xue ◽  
Hao Zhang ◽  
Wenjun Xiong ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Energy Metabolism ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Membrane ◽  
Mitochondrial Morphology ◽  
Dependent Manner ◽  
Combination Strategy ◽  
Mitochondrial Energy Metabolism ◽  
Atp Production

Abstract Background: Both mitochondrial quality control and energy metabolism are critical in maintaining the physiological function of cardiomyocytes. Previous studies indicated that PGC-1α is a transcription co-activator in promoting mitochondrial energy metabolism which would be beneficial for cardiomyocytes. However, PGC-1α overexpression in heart tissues could also result in the development of cardiomyopathy. This discrepancy in vivo and in vitro might be due to neglecting the elimination of damaged mitochondrial. Thus, an integration strategy of mitochondrial biogenesis and mitophagy might be beneficial.Methods: We studied the function of PINK1 in mitophagy in isoproterenol (Iso)-induced cardiomyocyte injury. Adenovirus was used to provoke an overexpression of the PINK1/Mfn2 protein. Mitochondrial morphology was examined via electron microscopy and confocal microscopy. Cardiomyocytes injury were measured by mitochondrial membrane potential (MMP), reactive oxygen species (ROS) and apoptosis. Metformin was used to increase mitochondrial biogenesis, the level of which was detected via immunoblotting. Additionally, mitochondrial respiratory function was measured by ATP production and oxygen consumption rate (OCR). Results: Cardiomyocytes treated with Iso had high levels of PINK1 and low levels of Mfn2 in a time-dependent manner. PINK1 overexpression promoted mitophagy, alleviated Iso-induced reduction in MMP, reduced ROS production and the apoptotic rate. In addition to increasing mitophagy, metformin could promote mitochondrial biogenensis and the overexpression of Mfn2 induce mitochondrial fusion. Moreover, metformin treatment and PINK1/Mfn2 overexpression reduced the mitochondrial dysfunction by inhibiting the generation of ROS, and leading to an increase in both ATP production and mitochondrial membrane potential in Iso-induced cardiomyocytes injury. Conclusion: Our findings indicate that a combination strategy may help ameliorate myocardial injury through mitophagy and mitochondrial biogenesis.

scholarly journals Biocontrol of collar rot on passion fruits via induction of apoptosis in the collar rot pathogen by Bacillus subtilis

2020 ◽  
Author(s):  
Yu-Hsuan Chen ◽  
Pei-Chun Lee ◽  
Tzu-Pi Huang
Keyword(s):  
Cell Death ◽  
Bacillus Subtilis ◽  
Membrane Potential ◽  
Energy Metabolism ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Chromatin Condensation ◽  
Passion Fruit ◽  
Biocontrol Agents ◽  
Collar Rot

The seedlings and fresh fruits of passion fruits are of high value in local and global trade. Fusarium solani is a main disease-causing agents affecting passion fruits. The objectives were to develop Bacillus-based biocontrol agents for the management of fusarium diseases on passion fruits and to investigate their putative control mechanisms. Our studies indicated Bacillus subtilis YBC and 151B1 showed antagonistic activity to F. solani PF7 from passion fruits and inhibited the conidial germination of strain PF7. The application of broth cultures from B. subtilis 151B1 and YBC in SYB medium reduced disease severity of fusarium wilt on the leaves of passion fruits, and enhanced the survival rates of passion fruit seedlings challenged with F. solani PF7. With regard to the putative mechanisms of disease control, the results indicated the treatments consisting of the respective culture filtrates from B. subtilis 151B1 and YBC broths caused aberrant conidial morphology and the loss of cell membrane integrity. Additionally, the treatments caused reductions in mitochondrial membrane potential and interfered with the energy metabolism of F. solani PF7. The treatments also enhanced reactive oxygen species accumulation, and resulted in the externalization of phosphatidylserine, chromatin condensation, and DNA fragmentation, suggesting their functions in triggering apoptotic-like cell death. In conclusion, B. subtilis 151B1 and YBC are potential biocontrol agents for passion fruit disease caused by F. solani. Their control efficacy may result from the produced surfactins to trigger apoptotic-like cell death, reducing the mitochondrial membrane potential and interfering with the energy metabolism of the pathogen.

scholarly journals Selenomethionine Improves Mitochondrial Function by Upregulating Mitochondrial Selenoprotein in a Model of Alzheimer’s Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Chen Chen ◽  
Yao Chen ◽  
Zhong-Hao Zhang ◽  
Shi-Zheng Jia ◽  
Yu-Bin Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Membrane Potential ◽  
Energy Metabolism ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Neurofibrillary Tangles ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Amyloid Plaques

Alzheimer’s disease (AD), the most common neurodegenerative disease in elderly humans, is pathologically characterized by amyloid plaques and neurofibrillary tangles. Mitochondrial dysfunction that occurs in the early stages of AD, which includes dysfunction in mitochondrial generation and energy metabolism, is considered to be closely associated with AD pathology. Selenomethionine (Se-Met) has been reported to improve cognitive impairment and reduce amyloid plaques and neurofibrillary tangles in 3xTg-AD mice. Whether Se-Met can regulate mitochondrial dysfunction in an AD model during this process remains unknown.In this study, the N2a-APP695-Swedish (N2aSW) cell and 8-month-old 3xTg-AD mice were treated with Se-Met in vitro and in vivo. Our study showed that the numbers of mitochondria were increased after treatment with Se-Met. Se-Met treatment also significantly increased the levels of NRF1 and Mfn2, and decreased those of OPA1 and Drp1. In addition, the mitochondrial membrane potential was significantly increased, while the ROS levels and apoptosis rate were significantly decreased, in cells after treatment with Se-Met. The levels of ATP, complex IV, and Cyt c and the activity of complex V were all significantly increased. Furthermore, the expression level of SELENO O was increased after Se-Met treatment. Thus, Se-Met can maintain mitochondrial dynamic balance, promote mitochondrial fusion or division, restore mitochondrial membrane potential, promote mitochondrial energy metabolism, inhibit intracellular ROS generation, and reduce apoptosis. These effects are most likely mediated via upregulation of SELENO O. In summary, Se-Met improves mitochondrial function by upregulating mitochondrial selenoprotein in these AD models.

Study on the effects of Polyphyllin I and Curcumin on liver cancer based on the cross-action of ferroptosis and energy metabolism

2021 ◽  
Author(s):  
Shuxian Yu ◽  
Wenhui Gao ◽  
Puhua Zeng ◽  
Mingxuan Lu ◽  
Xiaoning Tan ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Energy Metabolism ◽  
Liver Cancer ◽  
Mitochondrial Membrane Potential ◽  
Release Rate ◽  
Mitochondrial Membrane ◽  
Liver Cancer Cells ◽  
Ldh Release ◽  
Differential Genes

Abstract Background: To investigate the effect and mechanism of Polyphyllin I(PPI) and Curcumin(Cur) on human liver cancer HepG2 and HepG2.2.15 cells. Methods: Download the hepatocellular carcinoma specimens and normal control specimens from the TCGA database, take the intersection with ferroptosis-related genes, and screen the differentially expressed ferroptosis genes; again, make the intersection with the selected differential genes related to energy metabolism; conduct survival analysis; construct prognosis Risk scoring model and evaluation of model performance; through molecular docking to verify the binding effect of PPI, Cur and Ribonucleoside-diphosphate reductase subunit M2(RRM2), SRC(SRC), Acetyl-CoA carboxylase alpha(ACACA) and other genes. Human hepatocellular carcinoma cells were cultured in vitro, PPI and Cur intervened, and Cell Counting Kit-8(CCK-8) was used to detect cell inhibition rate; FeRhoNox-1 fluorescent probe staining to observe the intracellular Fe 2+ status; lactate dehydrogenase (LDH) release Experiment to detect cell LDH release rate; JC-1 staining to detect mitochondrial membrane potential; reactive oxygen species(ROS) kit to detect ROS level;Western blotting (WB) to detect RRM2 and SRC , ACACA and other genes protein expression levels. Results: Through screening, 25 differential genes related to ferroptosis and energy metabolism in liver cancer were obtained;; through survival analysis, three ferroptosis-related genes, such as RRM2, SRC, and ACACA, were obtained，the results showed that these three genes showed high expression and predicted poor overall survival(OS) and disease-free survival(DFS); molecular docking results showed that PPI, Cur It has good affinity with RRM2, SRC and ACACA. The results of in vitro experiments show that PPI and Cur inhibit cell proliferation in a concentration-dependent manner ( P <0.01). PPI and Cur can significantly increase the intracellular Fe2+ concentration, LDH release rate and intracellular ROS levels of HepG2, HepG2.2.15 ( P <0.01), and the effect on mitochondrial membrane potential was significantly lower than that of the blank group ( P <0.01), and significantly down-regulated the protein expression levels of RRM2, SRC, and ACACA ( P <0.01). Conclusion: The high expression of RRM2, SRC, ACACA and other three genes related to ferroptosis and energy metabolism in liver cancer indicate poor OS and DFS; PPI and Cur can up-regulate the LDH release rate, ROS and Fe 2+ levels of liver cancer cells, and down-regulate the cell mitochondrial membrane potential and other methods to inhibit the proliferation of liver cancer cells; and down-regulate the expression of RRM2, SRC, ACACA and other proteins to affect the prognosis of liver cancer.

Platelets apoptosis in rats after global brain ischemia

2018 ◽  
pp. 27-35
Author(s):  
А.А. Соколовская ◽  
Э.Д. Вирюс ◽  
В.В. Александрин ◽  
А.С. Роткина ◽  
К.А. Никифорова ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Ischemic Stroke ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Brain Ischemia ◽  
Mitochondrial Membrane ◽  
Male Rats ◽  
Global Brain Ischemia ◽  
Platelet Apoptosis ◽  
Global Brain

Цель исследования. Ишемические повреждения головного мозга, являются одной из наиболее частой причин инвалидности и смертности во всем мире. Недавно была установлена роль апоптоза тромбоцитов в патофизиологии инсульта, однако его механизмы до сих пор остаются невыясненными. Несмотря на различные экспериментальные модели, направленные на мониторинг апоптоза тромбоцитов, результаты, относительно изучения и выявления апоптоза тромбоцитов при ишемии головного мозга у крыс, весьма немногочисленны. Цель исследования - анализ апоптоза тромбоцитов с помощью метода проточной цитофлуориметрии на модели глобальной ишемии мозга у крыс. Методика. В экспериментах использовано 6 крыс-самцов Вистар в возрасте от 5 до 6 мес., разделенных на 2 группы: интактный контроль (К) и глобальная ишемия головного мозга. Модель глобальной ишемии головного мозга у крыс воспроизводилась путём билатеральной окклюзии общих сонных артерий на фоне гипотензии. Уровень системного артериального давления снижали посредством кровопотери до 40-45 мм рт. ст. Суспензию тромбоцитов крыс получали методом гельфильтрации с использованием сефарозы 2B. Для анализа экстернализации фосфатидилсерина (ФС) тромбоциты крыс инкубировали с Аннексином V-PE в связывающем буфере. Для оценки митохондриального мембранного потенциала (ММП) тромбоциты инкубировали с катионным красителем JC-1. После инкубации образцы немедленно анализировали на проточном цитофлуориметре FACSCalibur (Becton Dickinson, США). Результаты. Согласно полученным данным, экстернализация ФС на тромбоцитах крыс, перенесших инсульт, была значительно выше (53,45 ± 4,21%), чем в контрольной группе крыс (5,27 ± 2,40%). Данный эффект подтверждается выраженной деполяризацией митохондриальных мембран (DYm). После экспериментальной ишемии мозга почти 40% тромбоцитов было деполяризовано. Заключение. Использованный в работе подбор методов и маркеров обеспечивает понимание механизмов апоптоза тромбоцитов как в экспериментальных, так и в клинических условиях. Полученные данные позволяют сделать заключение, что апоптоз тромбоцитов является одним из факторов развития глобальной ишемии головного мозга у крыс. Результаты могут быть использованы для понимания механизмов, участвующих в развитии ишемического повреждения, что, в свою очередь, может быть использовано при разработке новых терапевтических стратегий. Aim. Stroke is one of the most common causes of disability and mortality worldwide. Multiple experimental models of stroke have focused on monitoring of platelet apoptosis. However, studies on and detection of platelet apoptosis in rats with ischemic stroke are very scarce. We investigated platelet apoptosis in rats with global brain ischemia using flow cytometry. Methods. Experiments were carried out on healthy, adult Wistar male rats weighing 300-350 g. The rats were divided into the following 2 groups: intact rats and rats with global brain ischemia. Global brain ischemia was induced by two-vessel (2-VO) carotid occlusion in combination with hypotension. Systemic blood pressure was reduced by 40-45 mm Hg by inducing haemorrhage. Platelets were isolated by gel filtration on Sepharose 2B. For evaluation of phosphatidylserine (PS) externalization, platelets were incubated with Annexin V-PE and analyzed on FACSCalibur (BD Biosciences). Mitochondrial membrane potential (DY) was measured during platelets apoptosis using JC-1, a mitochondrial membrane potential indicator. Platelets were analyzed by flow cytometry immediately after the incubation. Results. PS externalization on platelets was significantly greater after global brain ischemia (53.45 ± 4.21%) than in the control group (5.27 ± 2.40%). Pronounced depolarization of mitochondrial membrane potential (DYm) confirmed this finding. In the rat group with experimental brain ischemia, almost 40% (35.24 ± 5.21%) of platelets were depolarized. Conclusion. Our results provide insight into mechanisms involved in platelet apoptosis during ischemic stroke and can be used in further development of new therapeutic strategies.

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