10 documents found, page 1 of 1
Elevated Pressure Changes the Purinergic System of Microglial Cells
Rodrigues-Neves, Ana C.; Aires, Inês D.; Vindeirinho, Joana R.; Boia, Raquel; Madeira, Maria H.; Gonçalves, Francisco Q.; Cunha, Rodrigo A.Glaucoma is the second cause of blindness worldwide and is characterized by the degeneration of retinal ganglion cells (RGCs) and optic nerve atrophy. Increased microglia reactivity is an early event in glaucoma that may precede the loss of RGCs, suggesting that microglia and neuroinflammation are involved in the pathophysiology of this disease. Although global changes of the purinergic system have been reporte...
Sweet Stress: Coping With Vascular Dysfunction in Diabetic Retinopathy
Santiago, Ana R.; Boia, Raquel; Aires, Inês D.; Ambrósio, Francisco; Fernandes, RosaOxidative stress plays key roles in the pathogenesis of retinal diseases, such as diabetic retinopathy. Reactive oxygen species (ROS) are increased in the retina in diabetes and the antioxidant defense system is also compromised. Increased ROS stimulate the release of pro-inflammatory cytokines, promoting a chronic low-grade inflammation involving various signaling pathways. An excessive production of ROS can l...
Treatment with A2A receptor antagonist KW6002 and caffeine intake regulate micr...
Boia, Raquel; Elvas, Filipe; Madeira, Maria H.; Aires, Inês D.; Rodrigues-Neves, Ana C.; Tralhão, Pedro; Szabó, Eszter C; Baqi, YounisTransient retinal ischemia is a major complication of retinal degenerative diseases and contributes to visual impairment and blindness. Evidences indicate that microglia-mediated neuroinflammation has a key role in the neurodegenerative process, prompting the hypothesis that the control of microglia reactivity may afford neuroprotection to the retina against the damage induced by ischemia-reperfusion (I-R). The...
Having a Coffee Break: The Impact of Caffeine Consumption on Microglia-Mediated...
Madeira, Maria H.; Boia, Raquel; Ambrósio, António F.; Santiago, Ana R.Caffeine is the major component of coffee and the most consumed psychostimulant in the world and at nontoxic doses acts as a nonselective adenosine receptor antagonist. Epidemiological evidence suggests that caffeine consumption reduces the risk of several neurological and neurodegenerative diseases. However, despite the beneficial effects of caffeine consumption in human health and behaviour, the mechanisms by...
Activation of Neuropeptide Y Receptors Modulates Retinal Ganglion Cell Physiolo...
Martins, João; Elvas, Filipe; Brudzewsky, Dan; Martins, Tânia; Kolomiets, Bogdan; Tralhão, Pedro; Gøtzsche, Casper R.; Cavadas, CláudiaNeuropeptide Y (NPY) is expressed in mammalian retina but the location and potential modulatory effects of NPY receptor activation remain largely unknown. Retinal ganglion cell (RGC) death is a hallmark of several retinal degenerative diseases, particularly glaucoma. Using purified RGCs and ex vivo rat retinal preparations, we have measured RGC intracellular free calcium concentration ([Ca2+]i) and RGC spiking ...
Contribution of microglia-mediated neuroinflammation to retinal degenerative di...
Madeira, Maria H.; Boia, Raquel; Santos, Paulo; Ambrósio, A. Francisco; Santiago, Ana R.Retinal degenerative diseases are major causes of vision loss and blindness worldwide and are characterized by chronic and progressive neuronal loss. One common feature of retinal degenerative diseases and brain neurodegenerative diseases is chronic neuroinflammation. There is growing evidence that retinal microglia, as in the brain, become activated in the course of retinal degenerative diseases, having a pivo...
Role of microglia adenosine A(2A) receptors in retinal and brain neurodegenerat...
Santiago, Ana R.; Baptista, Filipa I.; Santos, Paulo; Cristovão, Gonçalo; Ambrósio, A. Francisco; Cunha, Rodrigo A.; Gomes, Catarina A.Neuroinflammation mediated by microglial cells in the brain has been commonly associated with neurodegenerative diseases. Whether this microglia-mediated neuroinflammation is cause or consequence of neurodegeneration is still a matter of controversy. However, it is unequivocal that chronic neuroinflammation plays a role in disease progression and halting that process represents a potential therapeutic strategy....
Diabetes changes the levels of ionotropic glutamate receptors in the rat retina
Santiago, Ana R.; Gaspar, Joana M.; Baptista, Filipa I.; Cristóvão, Armando J.; Santos, Paulo F.; Kamphuis, Willem; Ambrósio, António F.Purpose: Diabetic retinopathy (DR) is a leading cause of vision loss and blindness among adults between the age 20 to 74. Changes in ionotropic glutamate receptor subunit composition can affect retinal glutamatergic neurotransmission and, therefore, contribute to visual impairment. The purpose of this study was to investigate whether diabetes leads to changes in ionotropic glutamate receptor subunit expression ...
Diabetes changes ionotropic glutamate receptor subunit expression level in the ...
Santiago, Ana R.; Hughes, John M.; Kamphuis, Willem; Schlingemann, Reinier O.; Ambrósio, António F.Early diabetic retinopathy is characterized by changes in subtle visual functions such as contrast sensitivity and dark adaptation. The outcome of several studies suggests that glutamate is involved in retinal neurodegeneration during diabetes. We hypothesized that the protein levels of ionotropic glutamate receptor subunits are altered in the retina during diabetes. Therefore, we investigated whether human dia...
Elevated glucose changes the expression of ionotropic glutamate receptor subuni...
Santiago, Ana R.; Rosa, Susana C.; Santos, Paulo F.; Cristovão, Armando J.; Barber, Alistair J.; Ambrósio, António F.PURPOSE. Altered glutamatergic neurotransmission and calcium homeostasis may contribute to retinal neural cell dysfunction and apoptosis in diabetic retinopathy (DR). The purpose of this study was to determine the effect of high glucose on the protein content of -amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate glutamate receptor subunits, particularly the GluR2 subunit, because it controls...