Publications by authors named "Amadou Camara"
Article Synopsis
- The study investigates the role of HDAC6 in regulating myocardial ischaemia/reperfusion injury (MIRI) in both type 1 and type 2 diabetic mice, highlighting its connection to inflammation and mitochondrial function.
- The research shows that both diabetes and MIRI increase HDAC6 activity and TNF-α levels, leading to cardiac issues like mitochondrial fission and reduced adenosine triphosphate production.
- Inhibiting HDAC6 through genetic knockout or the drug tubastatin A significantly decreases TNF-α and improves mitochondrial function, reducing heart damage and enhancing cardiac performance post-injury.
Article Synopsis
- Cardiovascular disease is a major health issue, and exercise training (TRN) significantly lowers the risk and protects the heart.
- Recent studies reveal that the mechanisms behind exercise's heart-protective effects involve changes in potassium channel activity, how β-adrenergic and adenosine influence heart cells, and the regulation of calcium in mitochondria.
- TRN enhances heart cell function and resilience against damage, but there's also an increased risk of atrial fibrillation with age and among those who have exercised throughout their lives.
Background: Diabetes augments activity of histone deacetylase 6 (HDAC6) and generation of tumor necrosis factor α (TNFα) and impairs the physiological function of mitochondrial complex I (mCI) which oxidizes reduced nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide to sustain the tricarboxylic acid cycle and β-oxidation. Here we examined how HDAC6 regulates TNFα production, mCI activity, mitochondrial morphology and NADH levels, and cardiac function in ischemic/reperfused diabetic hearts.
Methods: HDAC6 knockout, streptozotocin-induced type 1 diabetic, and obese type 2 diabetic db/db mice underwent myocardial ischemia/reperfusion injury or in a Langendorff-perfused system.
Article Synopsis
- Vascular regression in the kidneys leads to significant changes in blood vessel volume and density, particularly 90 days after a single dose of radiation.
- This regression is marked by substantial reductions in total vessel volume (55%), vessel density (57%), and other key metrics.
- The study suggests that vascular changes occur in a manner specific to each organ, with notable effects seen in both small and large blood vessels post-irradiation.
Article Synopsis
- Mitochondria are crucial for energy production and adapting cell functions based on environmental conditions, utilizing a stable transmembrane charge potential to manage ion uptake and maintain cell balance.
- Potassium (K) plays a significant role in regulating mitochondrial volume and bioenergetics, with its influx and efflux likely impacting hydrogen (H) cycling and respiration through specific potassium-hydrogen exchange mechanisms.
- Experimental results showed that manipulating potassium levels in guinea pig heart mitochondria affected mitochondrial volume, respiration rates, and pH, suggesting a deeper connection between K transport and mitochondrial function regulation.
Article Synopsis
- The study investigates how hypothermia (H), cardioplegia (CP), and their combination (HCP) can protect heart mitochondria during myocardial ischemia-reperfusion injury.
- Rats were divided into groups to assess cardiac function and mitochondrial changes after different treatment durations and temperatures following a period of ischemia.
- Results show that H and HCP treatments are more effective at preserving mitochondrial integrity compared to control treatments, suggesting they enhance protection against cell death during heart injury.
Mitochondrial Calcium Handling in Isolated Mitochondria from a Guinea Pig Heart.
Methods Mol Biol
July 2022
Article Synopsis
- Mitochondrial calcium (Ca) is crucial for normal heart function, as its increase boosts ATP production during heart contractions.
- A pathological rise in mitochondrial Ca can cause oxidative stress and disrupt energy production, leading to heart failure symptoms.
- The text outlines a protocol for measuring how mitochondria in guinea pig heart tissue handle calcium.
Article Synopsis
- A study using the rCHIMERA model on rats simulated repeated mild traumatic brain injury (mTBI) to explore its long-term effects on behavior and brain function.
- Behavioral tests showed significant disruptions in grooming, exploration, and memory tasks in rats after the injury, indicating cognitive impairments.
- The results indicated that these cognitive issues may be linked to impaired mitochondrial function and altered neuronal activity in the medial prefrontal cortex, suggesting a mechanism for long-term effects of mTBI.
Article Synopsis
- The study aimed to explore the effects of various pre-reperfusion treatments on pig livers following warm and cold ischemic injuries, simulating conditions relevant to liver transplants.
- Results indicated that the subnormothermic regulated hepatic reperfusion (RHR-S) treatment significantly improved liver cell viability, reduced indicators of injury, and enhanced mitochondrial function compared to other treatment methods.
- The findings suggest that RHR-S not only mitigates ischemia-reperfusion injury but also activates protective genes, indicating its potential for improving liver transplantation outcomes.
Significance: Three-dimensional (3D) vascular and metabolic imaging (VMI) of whole organs in rodents provides critical and important (patho)physiological information in studying animal models of vascular network.
Aim: Autofluorescence metabolic imaging has been used to evaluate mitochondrial metabolites such as nicotinamide adenine dinucleotide (NADH) and flavine adenine dinucleotide (FAD). Leveraging these autofluorescence images of whole organs of rodents, we have developed a 3D vascular segmentation technique to delineate the anatomy of the vasculature as well as mitochondrial metabolic distribution.
Article Synopsis
- Complex formation between hexokinase-II (HKII) and mitochondrial VDAC1 is essential for cell growth and survival, with HKII inserting into the outer membrane of mitochondria to bind VDAC1.
- The research employs a hybrid method involving molecular dynamics (MD) and Brownian dynamics (BD) simulations to analyze HKII's membrane binding and its interaction with VDAC1, leading to the creation of a stable binary complex.
- Findings reveal that the HKII/VDAC1 complex partially blocks VDAC1's permeation pathway and that phosphorylation of VDAC1 disrupts HKII binding, suggesting implications for regulating cell death in mitochondria.
Article Synopsis
- Mitochondrial dysfunction plays a significant role in various injuries and diseases, making it crucial to understand how it affects metabolism.
- A custom-designed 3D optical cryo-imager can measure the bioenergetics of organs in small animals by capturing autofluorescence from tissues at low temperatures.
- The device quantifies the redox ratio (NADH/FAD) as an indicator of the mitochondrial redox state, providing insights into mitochondrial function.
Introduction: the objective was to identify the predictive factors contributing to COVID-related deaths in Intensive Care Unit.
Methods: this was a 4-month (12 March to 12 July 2020) cross sectional study carried out in the intensive care unit of the COVID treatment center of Donka National Hospital, the only hospital with a COVID intensive care unit in Guinea.
Results: during our period of study 140 patients were hospitalized in the COVID intensive care unit and 35 patients died (25%).
Article Synopsis
- Nearly 20 years after being identified as a gene linked to Wolf-Hirschhorn Syndrome, the exact role of the LETM1 protein in the inner mitochondrial membrane remains unclear.
- LETM1 is believed to influence key cellular functions like development, respiration, metabolism, and programmed cell death (apoptosis).
- This mini-review discusses the various cellular functions affected by LETM1 and emphasizes its importance in both health and disease contexts.
Mitochondria are recognized as the main source of ATP to meet the energy demands of the cell. ATP production occurs by oxidative phosphorylation when electrons are transported through the electron transport chain (ETC) complexes and develop the proton motive force across the inner mitochondrial membrane that is used for ATP synthesis. Studies since the 1960s have been concentrated on the two models of structural organization of ETC complexes known as "solid-state" and "fluid-state" models.
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- Mitochondrial calcium (Ca) handling is regulated through a balance of Ca uptake via the mitochondrial calcium uniporter (MCU), Ca buffering, and efflux via exchangers like Na/Ca (NCLX) and Ca/H (CHE) exchangers.
- This study examined Ca efflux through CHE in rat cardiac mitochondria, finding that factors like the amount of matrix Ca and external pH significantly influence this process, with acidic pH enhancing Ca efflux and ADP reducing it.
- Results suggest that the CHE's role in cardiac mitochondria is more complex than previously thought, potentially involving interactions with matrix Ca levels and pH changes, along with a potential contribution from LETM1
Article Synopsis
- VDAC1, a key protein in cell death regulation, shows varying effects on apoptosis depending on the cell type; its role in cardiac cells amidst oxidative stress was specifically examined using H9c2 cells.
- CRISPR-Cas9 was employed to knock out VDAC1 in H9c2 cells, revealing that VDAC1 deletion led to increased cell death and oxidative stress when exposed to agents like tBHP and ROT, in contrast to wildtype cells.
- Restoring VDAC1 levels in the knockout cells reduced oxidative stress markers and cell death, indicating its critical role in managing oxidative stress-induced cell death without affecting overall mitochondrial respiration.
Article Synopsis
- This study investigates the production of reactive nitrogen species (ONOO) in isolated cardiac mitochondria under oxidative stress and the role of nitric oxide synthesis (specifically mtNOS).
- Experiments show that excess calcium and succinate increase the formation of dityrosine (a marker for ONOO) and reactive oxygen species, highlighting a connection between calcium overload and mitochondrial oxidant stress.
- Inhibition of nitric oxide synthase (NOS) significantly reduces ONOO production, with evidence of NOS presence in heart tissue and mitochondria, suggesting that mtNOS is a specific source of NO leading to ONOO formation during stress.
Article Synopsis
- Mitochondria, evolved from bacteria, are key organelles responsible for producing ATP, crucial for energy in cells and involved in regulating life and death processes.
- They are linked to various human diseases and aging through different signaling pathways, yet their specific role in dysfunction during disease is still not fully understood.
- A Special Issue featuring 24 articles uncovers recent research on mitochondria, exploring their functions in both healthy conditions and various disease models, aiming to enhance understanding of mitochondrial biology.
Article Synopsis
- Over half of cancer patients receive radiation therapy, but normal tissue side effects often limit the radiation doses, particularly concerning for thoracic cancers affecting the heart.
- There are currently no known biomarkers for radiation-induced cardiotoxicity, and complex genetic factors influencing the risk remain poorly understood.
- Research using rat models has shown that genetic variations on chromosome 3 can reduce sensitivity to radiation-induced heart damage, with differences in mitochondrial gene expression observed between sensitive and resistant rat strains following radiation treatment.
Article Synopsis
- The study investigates the impact of thiazolidinediones (TZDs), particularly rosiglitazone and pioglitazone, on heart function and injury during ischemia/reperfusion (IR) in isolated rat hearts.
- ROSI administration prior to IR did not significantly improve heart function but increased injury compared to controls.
- Findings suggest that TZDs may lead to excessive mitochondrial uncoupling through mechanisms independent of PPARγ, raising concerns for patients using these drugs and their potential risk during cardiac events.
Article Synopsis
- Anesthetic preconditioning (APC) effectively reduces cardiac injury by nearly 50% during ischemia/reperfusion (I/R), enhancing heart recovery and lowering damage markers.
- The study found that BH4 (a cofactor for nitric oxide synthase) levels decreased and BH2 levels increased during I/R, while APC treatment increased BH4 and improved the BH4:BH2 ratio.
- Treatments with sepiapterin or 2,4-Diamino-6-hydroxypyrimidine affected the NOS3 activity linked to HSP90, indicating that BH4 plays a crucial role in APC-mediated cardiac protection against I/R injury.
Article Synopsis
- Genomic amplification at the 3q26.2 locus leads to higher levels of microRNA 551b-3p (miR551b-3p) in triple-negative breast cancer (TNBC) and helps it move to the nucleus where it activates the STAT3 transcription factor.
- This activation results in the upregulation of genes associated with the "oncostatin signaling module," including OSM and IL-31RA, which are linked to aggressive cancer behavior and poor patient outcomes.
- Targeting miR551b-3p with anti-miR551b-3p treatment effectively decreases the expression of this signaling module, leading to reduced tumor growth, migration, and invasion in breast cancer cells.