A5011757516- Heme Oxygenase-1 and Carbon Monoxide
- Neonatal Health and Biochemistry
- Autophagy in Disease and Therapy
- Mitochondrial Function and Pathology
- Cell death mechanisms and regulation
- Hemoglobin structure and function
- RNA Interference and Gene Delivery
- Neuroinflammation and Neurodegeneration Mechanisms
- Viral Infectious Diseases and Gene Expression in Insects
- ATP Synthase and ATPases Research
- Cannabis and Cannabinoid Research
- Traumatic Brain Injury and Neurovascular Disturbances
- Cardiac Ischemia and Reperfusion
- Phytochemicals and Antioxidant Activities
- Transgenic Plants and Applications
- Adenosine and Purinergic Signaling
- Viral gastroenteritis research and epidemiology
- Neuroscience of respiration and sleep
- Virus-based gene therapy research
- HIV Research and Treatment
- Acute Ischemic Stroke Management
- Adipose Tissue and Metabolism
- Sulfur Compounds in Biology
- Alcohol Consumption and Health Effects
- Molecular Biology Techniques and Applications
Universidade Nova de Lisboa
2016-2025
Instituto de Biologia Experimental e Tecnológica
2012-2021
Instituto de Biologia Molecular e Celular
2021
Weatherford College
2021
Rede de Química e Tecnologia
2020
Nova Medical (United States)
2016-2019
Ordem dos Médicos
2015-2016
Federal Senate
2016
Faculdade de Ciências Médicas de Minas Gerais
2015
Instituto Politécnico de Lisboa
2015
The proapoptotic Bax protein induces cell death by acting on mitochondria. binds to the permeability transition pore complex (PTPC), a composite proteaceous channel that is involved in regulation of mitochondrial membrane permeability. Immunodepletion from PTPC or purification Bax-deficient mice yielded could not permeabilize membranes response atractyloside, ligand adenine nucleotide translocator (ANT). and ANT coimmunoprecipitated interacted yeast two-hybrid system. Ectopic expression...
Viral protein R (Vpr) encoded by HIV-1 is a facultative inducer of apoptosis. When added to intact cells or purified mitochondria, micromolar and submicromolar doses synthetic Vpr cause rapid dissipation the mitochondrial transmembrane potential (ΔΨm), as well release apoptogenic proteins such cytochrome c apoptosis inducing factor. The same structural motifs relevant for cell killing are responsible mitochondriotoxic effects Vpr. Both cytotoxic prevented Bcl-2, an inhibitor permeability...
Viral protein R (Vpr), an apoptogenic accessory encoded by HIV-1, induces mitochondrial membrane permeabilization (MMP) via a specific interaction with the permeability transition pore complex, which comprises voltage-dependent anion channel (VDAC) in outer (OM) and adenine nucleotide translocator (ANT) inner membrane. Here, we demonstrate that synthetic Vpr-derived peptide (Vpr52-96) specifically binds to intermembrane face of ANT affinity nanomolar range. Taking advantage this interaction,...
The present work demonstrates the ability of CO to prevent apoptosis in a primary culture astrocytes. For first time, antiapoptotic behavior can be clearly attributed inhibition mitochondrial membrane permeabilization (MMP), key event intrinsic apoptotic pathway. In isolated non-synaptic mitochondria, partially inhibits (i) loss potential, (ii) opening nonspecific pore through inner membrane, (iii) swelling, and (iv) cytochrome c release, which are induced by calcium, diamide, or...
Mitochondrial autophagy, also known as mitophagy, is an autophagosome-based mitochondrial degradation process that eliminates unwanted or damaged mitochondria after cell stress. Most studies dealing with mitophagy rely on the analysis by fluorescence microscopy of mitochondrial-autophagosome colocalization. However, given fundamental role in physiology and pathology organisms, there urgent need for novel quantitative methods which to study this process. Here, we describe a flow...
Modulation of cerebral cell metabolism for improving the outcome hypoxia-ischemia and reperfusion is a strategy yet to be explored. Because carbon monoxide (CO) known prevent death; herein role CO in modulation astrocytic metabolism, particular, at level mitochondria was investigated. Low concentrations partially inhibited oxidative stress-induced apoptosis astrocytes, by preventing caspase-3 activation, mitochondrial potential depolarization, plasmatic membrane permeability. exposure...
MITOCHONDRIA PRESENT TWO KEY ROLES ON CELLULAR FUNCTIONING: (i) cell metabolism, being the main cellular source of energy and (ii) modulation death, by mitochondrial membrane permeabilization. Carbon monoxide (CO) is an endogenously produced gaseoustransmitter, which presents several biological functions involved in maintaining homeostasis cytoprotection. Herein, mitochondrion approached as target carbon (CO). In this paper, two perspectives concerning CO functioning are evaluated. First,...
Carbon monoxide (CO) is an endogenous product of mammalian cells generated by heme-oxygenase, presenting anti-apoptotic properties in several tissues. The present work demonstrates the ability small amounts exogenous CO to prevent neuronal apoptosis induced excitotoxicity and oxidative stress mice primary culture cerebellar granule cells. Additionally, our data show that a heme-oxygenase critical for its activity. Despite being neuroprotective, also induces reactive oxygen species generation...