6 research outputs found
Crosstalk between the Purinergic and Immune Systems: Implications for the Glutathione Antioxidant System in Health and Disease
Glutathione (GSH) represents the major nonprotein thiol in cells and, alongside with glutathione-dependent enzymes such as glutathione reductase (GR), glutathione peroxidase (GPx), and glutathione S-transferase (GST), exerts several biological functions including the protection against free radicals and other essential metabolic reactions within the body. Disturbances in the homeostasis of this complex glutathione antioxidant system may damage cells and have been implicated with the development and progression of several human diseases. In this context, the immune and purinergic systems are also essential, since the dysregulation in both systems may also be correlated with numerous diseases. These two networks are closely related and control inflammatory responses, especially by the crosstalk of signaling molecules, receptors, and enzymes; thus, they can exacerbate or slow down the progression of diseases. Based on this background, we aimed to provide a general scenario of the purinergic and immune systems and the connection between both and the modulation of glutathione and glutathione-dependent enzyme expression and activity in the context of health and disease
Diabetes and hypertension: Pivotal involvement of purinergic signaling
Diabetes mellitus (DM) and hypertension are highly prevalent worldwide health problems and frequently associated with severe clinical complications, such as diabetic cardiomyopathy, nephropathy, retinopathy, neuropathy, stroke, and cardiac arrhythmia, among others. Despite all existing research results and reasonable speculations, knowledge about the role of purinergic system in individuals with DM and hypertension remains restricted. Purinergic signaling accounts for a complex network of receptors and extracellular enzymes responsible for the recognition and degradation of extracellular nucleotides and adenosine. The main components of this system that will be presented in this review are: P1 and P2 receptors and the enzymatic cascade composed by CD39 (NTPDase; with ATP and ADP as a substrate), CD73 (5′-nucleotidase; with AMP as a substrate), and adenosine deaminase (ADA; with adenosine as a substrate). The purinergic system has recently emerged as a central player in several physiopathological conditions, particularly those linked to inflammatory responses such as diabetes and hypertension. Therefore, the present review focuses on changes in both purinergic P1 and P2 receptor expression as well as the activities of CD39, CD73, and ADA in diabetes and hypertension conditions. It can be postulated that the manipulation of the purinergic axis at different levels can prevent or exacerbate the insurgency and evolution of diabetes and hypertension working as a compensatory mechanism
Assessment of glycohemoglobin, plasma glucose curve and C-reactive protein as complementary predictors to diagnose prediabetes: a transversal study
Aluminum-Induced Alterations in Purinergic System Parameters of BV-2 Brain Microglial Cells
Aluminum (Al) is ubiquitously present in the environment and known to be a neurotoxin for humans. The trivalent free Al anion (Al3+) can cross the blood-brain barrier (BBB), accumulate in the brain, and elicit harmful effects to the central nervous system (CNS) cells. Thus, evidence has suggested that Al increases the risk of developing neurodegenerative diseases, particularly Alzheimer’s disease (AD). Purinergic signaling has been shown to play a role in several neurological conditions as it can modulate the functioning of several cell types, such as microglial cells, the main resident immune cells of the CNS. However, Al effects on microglial cells and the role of the purinergic system remain elusive. Based on this background, this study is aimed at assessing the modulation of Al on purinergic system parameters of microglial cells. An in vitro study was performed using brain microglial cells exposed to Al chloride (AlCl3) and lipopolysaccharide (LPS) for 96 h. The uptake of Al, metabolism of nucleotides (ATP, ADP, and AMP) and nucleoside (adenosine), and the gene expression and protein density of purinoceptors were investigated. The results showed that both Al and LPS increased the breakdown of adenosine, whereas they decreased nucleotide hydrolysis. Furthermore, the findings revealed that both Al and LPS triggered an increase in gene expression and protein density of P2X7R and A2AR receptors, whereas reduced the A1R receptor expression and density. Taken together, the results showed that Al and LPS altered the setup of the purinergic system of microglial cells. Thus, this study provides new insights into the involvement of the purinergic system in the mechanisms underlying Al toxicity in microglial cells