scholarly journals Role of cysteine in regulating morphogenesis and mitochondrial activity in the dimorphic fungus Histoplasma capsulatum.

1981 ◽  
Vol 78 (7) ◽  
pp. 4596-4600 ◽  
Author(s):  
B. Maresca ◽  
A. M. Lambowitz ◽  
V. B. Kumar ◽  
G. A. Grant ◽  
G. S. Kobayashi ◽  
...  
Keyword(s):  
Histoplasma Capsulatum ◽  
Mitochondrial Activity ◽  
Dimorphic Fungus

scholarly journals Ndufs4 ablation decreases synaptophysin expression in hippocampus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Subrata Kumar Shil ◽  
Yoshiteru Kagawa ◽  
Banlanjo Abdulaziz Umaru ◽  
Fumika Nanto-Hara ◽  
Hirofumi Miyazaki ◽  
...  
Keyword(s):  
Nadh Dehydrogenase ◽  
Leigh Syndrome ◽  
Mitochondrial Respiratory Chain ◽  
Mitochondrial Activity ◽  
Mitochondrial Complex ◽  
Neuronal Function ◽  
Mouse Hippocampus ◽  
Extracellular Regulated Kinase ◽  
Presynaptic Protein

AbstractAltered function of mitochondrial respiratory chain in brain cells is related to many neurodegenerative diseases. NADH Dehydrogenase (Ubiquinone) Fe-S protein 4 (Ndufs4) is one of the subunits of mitochondrial complex I and its mutation in human is associated with Leigh syndrome. However, the molecular biological role of Ndufs4 in neuronal function is poorly understood. In this study, upon Ndufs4 expression confirmation in NeuN-positive neurons, and GFAP-positive astrocytes in WT mouse hippocampus, we found significant decrease of mitochondrial respiration in Ndufs4-KO mouse hippocampus. Although there was no change in the number of NeuN positive neurons in Ndufs4-KO hippocampus, the expression of synaptophysin, a presynaptic protein, was significantly decreased. To investigate the detailed mechanism, we silenced Ndufs4 in Neuro-2a cells and we observed shorter neurite lengths with decreased expression of synaptophysin. Furthermore, western blot analysis for phosphorylated extracellular regulated kinase (pERK) revealed that Ndufs4 silencing decreases the activity of ERK signalling. These results suggest that Ndufs4-modulated mitochondrial activity may be involved in neuroplasticity via regulating synaptophysin expression.

scholarly journals Peptidogalactomannan from Histoplasma capsulatum yeast cell wall: role of the chemical structure in recognition and activation by peritoneal macrophages

2021 ◽  
Author(s):  
Giulia Maria Pires dos Santos ◽  
Gustavo Ramalho Cardoso dos Santos ◽  
Mariana Ingrid Dutra da Silva Xisto ◽  
Rodrigo Rollin-Pinheiro ◽  
Andréa Regina de Souza Baptista ◽  
...  
Keyword(s):  
Cell Wall ◽  
Yeast Cell ◽  
Chemical Structure ◽  
Histoplasma Capsulatum ◽  
Peritoneal Macrophages ◽  
Yeast Cell Wall

scholarly journals What Is the Metabolic Amplification of Insulin Secretion and Is It (Still) Relevant?

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 355
Author(s):  
Ingo Rustenbeck ◽  
Torben Schulze ◽  
Mai Morsi ◽  
Mohammed Alshafei ◽  
Uwe Panten
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Adenine Nucleotides ◽  
Pancreatic Beta Cell ◽  
Secretory Response ◽  
Mitochondrial Activity ◽  
Insulin Synthesis ◽  
Sequence Of Events ◽  
Insulin Granules

The pancreatic beta-cell transduces the availability of nutrients into the secretion of insulin. While this process is extensively modified by hormones and neurotransmitters, it is the availability of nutrients, above all glucose, which sets the process of insulin synthesis and secretion in motion. The central role of the mitochondria in this process was identified decades ago, but how changes in mitochondrial activity are coupled to the exocytosis of insulin granules is still incompletely understood. The identification of ATP-sensitive K+-channels provided the link between the level of adenine nucleotides and the electrical activity of the beta cell, but the depolarization-induced Ca2+-influx into the beta cells, although necessary for stimulated secretion, is not sufficient to generate the secretion pattern as produced by glucose and other nutrient secretagogues. The metabolic amplification of insulin secretion is thus the sequence of events that enables the secretory response to a nutrient secretagogue to exceed the secretory response to a purely depolarizing stimulus and is thus of prime importance. Since the cataplerotic export of mitochondrial metabolites is involved in this signaling, an orienting overview on the topic of nutrient secretagogues beyond glucose is included. Their judicious use may help to define better the nature of the signals and their mechanism of action.

scholarly journals Cellular and mitochondrial mechanisms of atrial fibrillation

2020 ◽  
Vol 115 (6) ◽  
Author(s):  
Fleur E. Mason ◽  
Julius Ryan D. Pronto ◽  
Khaled Alhussini ◽  
Christoph Maack ◽  
Niels Voigt
Keyword(s):  
Atrial Fibrillation ◽  
Nicotinamide Adenine Dinucleotide ◽  
Molecular Mechanisms ◽  
Treatment Options ◽  
Specific Treatment ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Nicotinamide Adenine ◽  
Mitochondrial Activity ◽  
Atp Production

AbstractThe molecular mechanisms underlying atrial fibrillation (AF), the most common form of arrhythmia, are poorly understood and therefore target-specific treatment options remain an unmet clinical need. Excitation–contraction coupling in cardiac myocytes requires high amounts of adenosine triphosphate (ATP), which is replenished by oxidative phosphorylation in mitochondria. Calcium (Ca2+) is a key regulator of mitochondrial function by stimulating the Krebs cycle, which produces nicotinamide adenine dinucleotide for ATP production at the electron transport chain and nicotinamide adenine dinucleotide phosphate for the elimination of reactive oxygen species (ROS). While it is now well established that mitochondrial dysfunction plays an important role in the pathophysiology of heart failure, this has been less investigated in atrial myocytes in AF. Considering the high prevalence of AF, investigating the role of mitochondria in this disease may guide the path towards new therapeutic targets. In this review, we discuss the importance of mitochondrial Ca2+ handling in regulating ATP production and mitochondrial ROS emission and how alterations, particularly in these aspects of mitochondrial activity, may play a role in AF. In addition to describing research advances, we highlight areas in which further studies are required to elucidate the role of mitochondria in AF.

Expression of alpha- and beta-tubulin genes during dimorphic-phase transitions of Histoplasma capsulatum

1989 ◽  
Vol 9 (5) ◽  
pp. 2042-2049
Author(s):  
G S Harris ◽  
E J Keath ◽  
J Medoff
Keyword(s):  
Phase Transitions ◽  
Histoplasma Capsulatum ◽  
Blot Hybridization ◽  
Dot Blot ◽  
Dimorphic Fungus ◽  
Tubulin Gene ◽  
Beta Tubulin ◽  
Two Dimensional Gel Electrophoresis ◽  
Western Blots ◽  
Alpha Tubulin

Recent investigations have confirmed the presence of one alpha-tubulin gene (TUB1) and one beta-tubulin gene (TUB2) in the dimorphic fungus Histoplasma capsulatum. In the present study, Northern blot (RNA blot) analyses revealed multiple alpha-tubulin transcripts and a single beta-tubulin transcript in the yeast and mycelial phases of the high-virulence 217B strain and low-virulence Downs strain. S1 nuclease protection assays demonstrated one initiation start site and two major stop sites for the TUB1 transcripts, suggesting that variations in 3' processing generate the alpha-tubulin messages of 2.5 and 2.0 kilobases. Dot blot hybridization experiments indicated that tubulin gene expression is developmentally regulated during the dimorphic phase transitions. alpha- and beta-tubulin mRNAs increased six- to eightfold during the yeast-to-mycelium conversion and decreased two- to threefold during the reverse transition. These changes in tubulin mRNA content coincided with major morphological events associated with H. capsulatum development. Western blots (immunoblots) of H. capsulatum yeast-specific proteins resolved by two-dimensional gel electrophoresis demonstrated a single alpha- and a single beta-tubulin isoform. Multiple tubulin polypeptides expressed in mycelia are probably products of posttranslational modifications.

scholarly journals The interaction between Histoplasma capsulatum cell wall carbohydrates and host components: relevance in the immunomodulatory role of histoplasmosis

2009 ◽  
Vol 104 (3) ◽  
pp. 492-496 ◽  
Author(s):  
Patricia Gorocica ◽  
Maria Lucia Taylor ◽  
Noé Alvarado-Vásquez ◽  
Armando Pérez-Torres ◽  
Ricardo Lascurain ◽  
...  
Keyword(s):  
Cell Wall ◽  
Histoplasma Capsulatum ◽  
Cell Wall Carbohydrates

scholarly journals Disseminated histoplasmosis in a renal transplant recipient – a fatal case report

2011 ◽  
Vol 12 (2) ◽  
pp. 163-165
Author(s):  
Tânia Mara L.B. Araújo ◽  
Geraldo B. Silva Junior ◽  
Orivaldo A. Barbosa ◽  
Rafael S.A. Lima ◽  
Elizabeth F. Daher
Keyword(s):  
Renal Transplant ◽  
Transplant Recipient ◽  
Renal Transplant Recipient ◽  
Histoplasma Capsulatum ◽  
Fatal Case ◽  
Tracheal Aspirate ◽  
Respiratory Pattern ◽  
Vasoactive Drugs ◽  
Dimorphic Fungus ◽  
Disseminated Histoplasmosis

Histoplasmosis is an infectious disease caused by the dimorphic fungus Histoplasma capsulatum.. The disseminated form is usually found in immunocompromised patients. A 53 year-old man, renal transplant recipient, was admitted with fever, dyspnea, productive cough, adynamia and weight loss. He was septic, but hemodynamically stable. The tracheal aspirate found intracellular fungi and the peripheral blood exam was compatible with histoplasmosis. The patient presented a progressive worsening of respiratory pattern and needed mechanical ventilation, vasoactive drugs and hemodialysis. A large spectrum antimicrobial therapy was started, including amphotericin B, but the patient died. Keyword: Disseminated histoplasmosis. Kidney transplantation. Immunosuppression DOI: http://dx.doi.org/10.3329/jom.v12i2.7125 JOM 2011; 12(2): 163-165

scholarly journals Cystine reductase in the dimorphic fungus Histoplasma capsulatum.

1978 ◽  
Vol 135 (3) ◽  
pp. 987-992 ◽  
Author(s):  
B Maresca ◽  
E Jacobson ◽  
G Medoff ◽  
G Kobayashi
Keyword(s):  
Histoplasma Capsulatum ◽  
Dimorphic Fungus

scholarly journals Mitochondrial-Targeted Antioxidant MitoQ Prevents E. coli Lipopolysaccharide-Induced Accumulation of Triacylglycerol and Lipid Droplets Biogenesis in Epithelial Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Ekaterina Fock ◽  
Vera Bachteeva ◽  
Elena Lavrova ◽  
Rimma Parnova
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Lipid Droplets ◽  
Cellular Respiration ◽  
Mitochondrial Activity ◽  
Energy Regulation ◽  
Metabolic Shift ◽  
Functional Connections ◽  
The Impact

The effect of bacterial lipopolysaccharide (LPS) on eukaryotic cell could be accompanied by a significant metabolic shift that includes accumulation of triacylglycerol (TAG) in lipid droplets (LD), ubiquitous organelles associated with fatty acid storage, energy regulation and demonstrated tight spatial and functional connections with mitochondria. The impairment of mitochondrial activity under pathological stimuli has been shown to provoke TAG storage and LD biogenesis. However the potential mechanisms that link mitochondrial disturbances and TAG accumulation are not completely understood. We hypothesize that mitochondrial ROS (mROS) may play a role of a trigger leading to subsequent accumulation of intracellular TAG and LD in response to a bacterial stimulus. Using isolated epithelial cells from the frog urinary bladder, we showed that LPS decreased fatty acids oxidation, enhanced TAG deposition, and promoted LD formation. LPS treatment did not affect the mitochondrial membrane potential but increased cellular ROS production and led to impairment of mitochondrial function as revealed by decreased ATP production and a reduced maximal oxygen consumption rate (OCR) and OCR directed at ATP turnover. The mitochondrial-targeted antioxidant MitoQ at a dose of 25 nM did not prevent LPS-induced alterations in cellular respiration, but, in contrast to nonmitochondrial antioxidant α-tocopherol, reduced the effect of LPS on the generation of ROS, restored the LPS-induced decline of fatty acids oxidation, and prevented accumulation of TAG and LD biogenesis. The data obtained indicate the key signaling role of mROS in the lipid metabolic shift that occurs under the impact of a bacterial pathogen in epithelial cells.

scholarly journals The Role of Mitochondria from Mature Oocyte to Viable Blastocyst

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Scott Chappel
Keyword(s):  
Cell Division ◽  
Animal Studies ◽  
Oocyte Quality ◽  
Mature Oocyte ◽  
Reproductive Age ◽  
Mitochondrial Activity ◽  
Dna Deletions ◽  
Blastocyst Implantation ◽  
Cytoplasmic Transfer

The oocyte requires a vast supply of energy after fertilization to support critical events such as spindle formation, chromatid separation, and cell division. Until blastocyst implantation, the developing zygote is dependent on the existing pool of mitochondria. That pool size within each cell decreases with each cell division. Mitochondria obtained from oocytes of women of advanced reproductive age harbor DNA deletions and nucleotide variations that impair function. The combination of lower number and increased frequency of mutations and deletions may result in inadequate mitochondrial activity necessary for continued embryo development and cause pregnancy failure. Previous reports suggested that mitochondrial activity within oocytes may be supplemented by donor cytoplasmic transfer at the time of intracytoplasmic sperm injection (ICSI). Those reports showed success; however, safety concerns arose due to the potential of two distinct populations of mitochondrial genomes in the offspring. Mitochondrial augmentation of oocytes is now reconsidered in light of our current understanding of mitochondrial function and the publication of a number of animal studies. With a better understanding of the role of this organelle in oocytes immediately after fertilization, blastocyst and offspring, mitochondrial augmentation may be reconsidered as a method to improve oocyte quality.

Sign in / Sign up

Export Citation Format

Share Document