Complexome Profiling of Plant Mitochondrial Fractions

2021 ◽  
pp. 101-110
Author(s):  
Lucie Schröder ◽  
Holger Eubel ◽  
Hans-Peter Braun
Keyword(s):  
Mitochondrial Fractions

Gender dimorphism in rat liver mitochondrial oxidative metabolism and biogenesis

2005 ◽  
Vol 289 (2) ◽  
pp. C372-C378 ◽  
Author(s):  
Roberto Justo ◽  
Jordi Boada ◽  
Margalida Frontera ◽  
Jordi Oliver ◽  
Jordi Bermúdez ◽  
...  
Keyword(s):  
Gender Differences ◽  
Protein Content ◽  
Rat Liver ◽  
Oxidative Metabolism ◽  
Mitochondrial Protein ◽  
Electron Microscopic ◽  
Gender Dimorphism ◽  
Protein Levels ◽  
Mitochondrial Fractions ◽  
Mitochondrial Oxidative Metabolism

In the present study, we have investigated gender differences in rat liver mitochondrial oxidative metabolism. Total mitochondrial population (M) as well as the heavy (M1), medium (M3), and light (M8) mitochondrial fractions obtained by means of differential centrifugation steps at 1,000, 3,000, and 8,000 g, respectively, were isolated. Electron microscopic analysis was performed and mitochondrial protein content and cardiolipin levels, mitochondrial O2 flux, ATP synthase activity, mitochondrial membrane potential, and mitochondrial transcription factor A (TFAM) protein levels were measured in each sample. Our results indicate that mitochondria from females have higher protein content and higher cardiolipin levels, greater respiratory and phosphorylative capacities, and more-energized mitochondria in respiratory state 3. Moreover, protein levels of TFAM were four times greater in females than in males. Gender differences in the aforementioned parameters were more patent in the isolated heavy M1 and M3 mitochondrial fractions. The present study demonstrates that gender-related differences in liver mitochondrial function are due mainly to a higher capacity and efficiency of substrate oxidation, likely related to greater mitochondrial machinery in females than in males, which is in accord with greater mitochondrial differentiation in females.

scholarly journals Studies on the sterols and sterol esters of the intracellular organelles of maize shoots

1968 ◽  
Vol 110 (1) ◽  
pp. 119-125 ◽  
Author(s):  
R. J. Kemp ◽  
E. I. Mercer
Keyword(s):  
Linolenic Acid ◽  
Microsomal Fraction ◽  
The Other ◽  
Nuclear Fraction ◽  
Unesterified Cholesterol ◽  
Sterol Esters ◽  
Mitochondrial Fractions ◽  
Intracellular Organelles

1. The composition of the esterified and unesterified sterols of the nuclear, chloroplastidic, mitochondrial and microsomal fractions of 21-day-old maize shoots was examined. 2. The microsomal and mitochondrial fractions contain the bulk of the sterols of the tissue. 3. Only 1% of the sterol isolated from all the organelles is esterified. 4. The nuclear fraction has the greatest proportion of esterified sterol and the microsomal fraction the least. 5. 4-Demethyl sterols constitute the bulk of both esterified and unesterified sterols in all organelle fractions. 6. Cholesterol is the major esterified 4-demethyl sterol of the nuclear and chloroplastidic fractions, but only the nuclear fraction has an appreciable proportion of unesterified cholesterol. 7. Sterol esters of linolenic acid are more abundant in the mitochondrial and microsomal fractions than in the other two fractions.

scholarly journals Role of mitochondria in paricalcitol-mediated cytoprotection during obstructive nephropathy

2012 ◽  
Vol 302 (12) ◽  
pp. F1595-F1605 ◽  
Author(s):  
Isabel Mercedes García ◽  
Liliana Altamirano ◽  
Luciana Mazzei ◽  
Miguel Fornés ◽  
Marisa Nile Molina ◽  
...  
Keyword(s):  
Vitamin D ◽  
Nadph Oxidase ◽  
Protective Effect ◽  
Renin Angiotensin System ◽  
Obstructive Nephropathy ◽  
Control Group ◽  
Mitochondrial Morphology ◽  
Vitamin D Receptors ◽  
Nadph Oxidase 4 ◽  
Mitochondrial Fractions

Vitamin D slows the progression of chronic kidney disease. Furthermore, activators of vitamin D receptors (VDR) have suppressant effects on the renin-angiotensin system, as well as anti-inflammatory and antifibrotic actions. This study aimed to evaluate the cytoprotective effects of paricalcitol, a VDR activator, at the mitochondrial level using an obstructive nephropathy model [unilateral ureteral obstruction (UUO)]. Rats subjected to UUO and controls were treated daily with vehicle or paricalcitol. The control group underwent a sham surgery. The treatment was done for 15 days (30 ng/kg). The following were determined: biochemical parameters; fibrosis; apoptosis; mitochondrial morphology; VDR, AT1 receptor, and NADPH oxidase 4 expression; and NADPH oxidase activity (in total and in mitochondrial fractions from the renal cortex). VDR activation prevented fibrosis (20 ± 5 vs. 60 ± 10%) and the number of TUNEL-positive apoptotic cells (10 ± 3 vs. 25 ± 4) in UUO. Biochemical, histological, and molecular studies suggest mitochondrial injury. Electron microscopy revealed in UUO electronically luminous material in the nucleus. Some mitochondria were increased in size and contained dilated crests and larger than normal spaces in their interiors. These changes were not present with paricalcitol treatment. Additionally, high AT1-receptor mRNA and NADPH activity was reverted in mitochondrial fractions from obstructed paricalcitol-treated animals (0.58 ± 0.06 vs. 0.95 ± 0.05 relative densitometry units and 9,000 ± 800 vs. 15,000 ± 1,000 relative fluorescence units·μg protein−1·min−1, respectively). These changes were consistent with an improvement in VDR expression (0.75 ± 0.05 vs. 0.35 ± 0.04 relative densitometry units). These results suggest that paricalcitol confers a protective effect and reveal, as well, a possible AT1 receptor-dependent protective effect that occurs at the mitochondrial level.

scholarly journals Localization of transforming growth factor-beta 1 in mitochondria of murine heart and liver.

1991 ◽  
Vol 2 (6) ◽  
pp. 467-477 ◽  
Author(s):  
U I Heine ◽  
J K Burmester ◽  
K C Flanders ◽  
D Danielpour ◽  
E F Munoz ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Polyclonal Antibodies ◽  
Rat Hepatocytes ◽  
Cell Fractionation ◽  
Tgf Beta ◽  
Electron Microscopic ◽  
Mitochondrial Fractions ◽  
Growth Factor Beta

Using both electron microscopic immunohistochemistry and cell fractionation techniques, we show that transforming growth factor-beta 1 (TGF-beta 1) is found in mitochondria of rat and mouse cardiac myocytes and rat hepatocytes. Four different polyclonal antibodies, raised against various epitopes encompassing the mature portion of the TGF-beta 1 molecule as well as the pro-region of its precursor, were used for the electron microscopy studies. The localization of TGF-beta 1 in mitochondria was confirmed by detection of the native peptide in mitochondria isolated from rat heart and liver; the majority of native TGF-beta 1 found in liver homogenates was recovered in highly pure mitochondrial fractions. The functional role of TGF-beta in the mitochondrion is unknown at present.

Abstract 1552: Cardioplegic Arrest And Subsequent Reperfusion Induce Urocortin Expression In Non-apoptotic Cardiac Cells Selectively Associated With Mitochondrial Relocation Of PKCϵ

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Carol Chen-Scarabelli ◽  
Zhaokan Yuan ◽  
Giuseppe Faggian ◽  
Francesco Santini ◽  
Alessio Rungatscher ◽  
...  
Keyword(s):  
Western Blotting ◽  
Internal Control ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Fold Increase ◽  
Cardiac Cells ◽  
Image Analyzer ◽  
Cardioplegic Arrest ◽  
Mitochondrial Fractions

BACKGROUND: Cardioplegic arrest and subsequent reperfusion inevitably expose the heart to an iatrogenic ischemia/reperfusion injury (iIRI). We previously reported that iIRI caused mitochondria-initiated myocyte apoptosis, but also induction of urocortin (Ucn), an endogenous cardioprotective peptide. We also showed that Ucn induced PKCϵ-mediated opening of mitochondrial K ATP channels in isolated heart mitochondria. AIM: To investigate, in patients exposed to iIRI, the cardioprotective role and the mechanism of action of Ucn, with respect to PKCϵ expression, activation and relocation. METHODS AND RESULTS: Two sequential biopsies were obtained from the right atrium of 25 patients undergoing coronary artery bypass grafting at the start of grafting (internal control) and 10 mins after release of the aortic clamp. Mean values of ejection fraction, aortic cross-clamping time and number of grafts were 51±8; 48±8 mins; and 3.6±0.5 respectively. In hearts exposed to iIRI, RT-PCR and immunostaining showed Ucn induction at the mRNA (255% of basic levels, p<0.05) and protein level (28±2.1% positive myocytes vs 3.1±0.6% of internal control; p<0.01) respectively. iIRI also induced a selective increase of PKC-ϵ mRNA (225% of internal control; p<0.05) and a two-fold overexpression of total PKCϵ isoform (assessed by Western blotting; p<0.05), which paralleled a 2.9 fold increase in PKCϵ phosphorylation (p<0.01). TUNEL positivity (<0.1% and 2.9±0.7% positive myocytes pre- and post-iIRI respectively; p<0.01) was only seen in Ucn-negative cells, and, of note, Ucn-positive myocytes showed concurrent mitochondrial relocation of phosphorylated PKCϵ, as documented by mitochondrial-activated PKCϵ colocalization, calculated by confocal microscopy with an image analyzer software (% overlap: 57±5 vs 11±2 in Ucn-negative cells; p<0.01). Western blotting carried out in pools of cytosolic and mitochondrial fractions confirmed a 2.5 fold increase in mitochondrial localization of phosphorylated PKC-ϵ following iIRI (p<0.05). CONCLUSIONS : In patients exposed to iIRI, Ucn expression in viable cells was selectively associated with phosphorylation and mitochondrial relocation of PKCϵ, suggesting a cardioprotective role for endogenous Ucn in the human heart.

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