Purpose: To develop and evaluate liposomal formulations prepared with an isolated mitochondrial fraction as a mitochondria-specific delivery vehicle.
Methods: Liposomes were prepared with either a crude mitochondrial fraction extracted from cells or lipids extracted from the crude mitochondrial fraction and were then characterized by determining their size and zeta potential. The cell uptake of the liposomes and loaded bioactive was studied using flow cytometry and confocal microscopy. The cytotoxicity of the formulations was tested by MTS cytotoxicity assay.
Results: Liposomes prepared with the mitochondrial extracts were non-toxic and colocalized with mitochondria in F98 cells. Addition of DOTAP to the liposomes facilitated DNA complexation and the DNA delivered intracellularly co-localized with mitochondria.
Conclusion: The results from this study establish the potential of using a mitochondrial fraction isolated from cells to prepare liposomes capable of delivering biologically active molecules to mitochondria of live mammalian cells.
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http://dx.doi.org/10.1007/s11095-011-0531-5 | DOI Listing |
Endocr Metab Immune Disord Drug Targets
January 2025
Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Background: Heart failure with preserved ejection fraction (HFpEF) represents a challenging cardiovascular condition characterized by normal systolic function but impaired diastolic performance. Despite its increasing prevalence, therapeutic options remain limited. This study investigated the metabolic effects of canagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, on cardiac function and energy metabolism in HFpEF.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
Department of Medical Biology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Mitochondria play a fundamental role in energy metabolism, particularly in high-energy-demand tissues such as skeletal muscle. Understanding the proteomic composition of mitochondria in these cells is crucial for elucidating the mechanisms underlying muscle physiology and pathology. However, effective isolation of mitochondria from primary human skeletal muscle cells has been challenging due to the complex cellular architecture and the propensity for contamination with other organelles.
View Article and Find Full Text PDFPhytomedicine
January 2025
Pharmacology and Toxicology Laboratory, Dietetics & Nutrition Technology Division, CSIR-Institute of Himalayan Bioresource Technology, Palampur, Himachal Pradesh 176061, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, Uttar Pradesh 201002, India. Electronic address:
Background: Non-alcoholic steatohepatitis (NASH) has become a serious public health concern with high global prevalence. The lack of safe and efficient treatment for the condition demands exploring new therapeutic solutions.
Purpose: In the present study, we investigated the protective efficacy of picrosides-rich fraction (PF) from Picrorhiza kurroa against steatohepatitis and revealed the molecular mechanism of action.
Free Radic Biol Med
January 2025
Department of Radiation Oncology, Mays Cancer Center at UT Health San Antonio MD Anderson, Joe R. and Teresa Lozano Long School of Medicine, TX, USA. Electronic address:
Manganese superoxide dismutase (MnSOD/SOD2) is an essential mitochondrial enzyme that detoxifies superoxide radicals generated during oxidative respiration. MnSOD/SOD2 lysine 68 acetylation (K68-Ac) is an important post-translational modification (PTM) that regulates enzymatic activity, responding to nutrient status or oxidative stress, and elevated levels have been associated with human illness. To determine the in vivo role of MnSOD-K68 in the heart, we used a whole-body non-acetylation mimic mutant (MnSOD) knock-in mouse.
View Article and Find Full Text PDFJACC Basic Transl Sci
December 2024
Vascular Metabolism Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
Exercise intolerance, a hallmark of heart failure with preserved ejection fraction (HFpEF) exacerbated by obesity, involves unclear mechanisms related to skeletal muscle metabolism. In a "2-hit" model of HFpEF, we investigated the ability of exercise therapy (voluntary wheel running) to reverse skeletal muscle dysfunction and exercise intolerance. Using state-of-the-art metabolic cages and a multiomic approach, we demonstrate exercise can rescue dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restore exercise capacity in mice with cardiometabolic HFpEF.
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