Does adenosine release taurine in the A1-receptor-rich hippocampus?

Miyamoto, T.; Miyamoto, Koho-Julio

doi:10.1007/s005400050033

Cited by 11 publications

(5 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the vitreous fluid of diabetic patients, the levels of interleukin-1 beta (IL-1 β ), IL-6, and tumor necrosis factor (TNF) are increased [8–10]. In addition, an increase in the production of cytokines, such as IL-1 β and TNF, expression of adhesion molecules, leukocyte adhesion, and vascular permeability [11–13] have been observed in the retina of diabetic animals. Moreover, in the retinas of streptozotocin-induced diabetic rats, the levels of IL-1 β are also increased [14–17], and this was correlated with an increase in BRB permeability [12, 14].…”

Section: Introductionmentioning

confidence: 99%

Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation

Baptista

Aveleira

Castilho

et al. 2017

Mediators of Inflammation

View full text Add to dashboard Cite

Diabetic retinopathy is considered a neurovascular disorder, hyperglycemia being considered the main risk factor for this pathology. Diabetic retinopathy also presents features of a low-grade chronic inflammatory disease, including increased levels of cytokines in the retina, such as interleukin-1 beta (IL-1β). However, how high glucose and IL-1β affect the different retinal cell types remains to be clarified. In retinal neural cell cultures, we found that IL-1β and IL-1RI are present in microglia, macroglia, and neurons. Exposure of retinal neural cell cultures to high glucose upregulated both mRNA and protein levels of IL-1β. High glucose decreased microglial and macroglial cell proliferation, whereas IL-1β increased their proliferation. Interestingly, under high glucose condition, although the number of microglial cells decreased, they showed a less ramified morphology, suggesting a more activated state, as supported by the upregulation of the levels of ED-1, a marker of microglia activation. In conclusion, IL-1β might play a key role in diabetic retinopathy, affecting microglial and macroglial cells and ultimately contributing to neural changes observed in diabetic patients. Particularly, since IL-1β has an important role in retinal microglia activation and proliferation under diabetes, limiting IL-1β-triggered inflammatory processes may provide a new therapeutic strategy to prevent the progression of diabetic retinopathy.

show abstract

Section: Introductionmentioning

confidence: 99%

Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation

Baptista

Aveleira

Castilho

et al. 2017

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…[5][6][7] Taurine is released by adenosine in all areas of the brain in in vivo animals, 8 including areas with predominantly A1 receptors, such as the hippocampus, in a dose-dependent manner. 9 Although we have not proven that taurine is released in the spinal cord as well, there are no reasons to believe that it would not be.…”

Section: Alternate Explanation Of the Additive Protective Effects Of Regional Infusion Of Hypothermic Saline And Adenosine Solutionsmentioning

confidence: 88%

Alternate explanation of the additive protective effects of regional infusion of hypothermic saline and adenosine solutions

Miyamoto

2000

The Journal of Thoracic and Cardiovascular Surgery

View full text Add to dashboard Cite

“…Adenosine is a very short-acting substance released from the ischemia induced degradation product of ATP. During ischemia, adenosine activates the A1 receptor on the cell membrane initiating a series of intracellular events including activation of G-proteins, phospholipase C, protein kinase C, and ATP-sensitive potassium channels, and release of neurotransmitters [13,14,15]. The specific roles that adenosine, ATP sensitive potassium channels, or other agents may play in models of acute preconditioning remain unknown.…”

Section: Discussionmentioning

confidence: 99%

Spinal Cord Blood Flow after Ischemic Preconditioning in a Rat Model of Spinal Cord Ischemia

Zvara

Zboyovski

Deal

et al. 2004

The Scientific World JOURNAL

View full text Add to dashboard Cite

Spinal cord blood flow after ischemic preconditioning is poorly characterized. This study is designed to evaluate spinal cord blood flow patterns in animals after acute ischemic preconditioning. Experiment 1: After a laminectomy and placement of a laser Doppler probe over the lumbar spinal cord to measure spinal cord blood flow, 16 male Sprague-Dawley rats were randomized into two groups: ischemic preconditioning (IPC, n = 8), and control (CTRL, n = 8). Rats in the CTRL and the IPC groups were subjected to 12 min of ischemia directly followed by 60 min of reperfusion. IPC rats received 3 min of IPC and 30 min of reperfusion prior to the 12-min insult period. Experiment 2: After instrumentation, the rats were randomized into three groups: control (CTRL, n = 7), ischemic preconditioning (IPC, n = 7), and time control (TC, n = 4). Rats in the CTRL and the IPC groups were subjected to the same ischemia and reperfusion protocol as above. The TC group was anesthetized for the same time period as the CTRL and the IPC groups, but had no ischemic intervention. Microspheres were injected at baseline and at 15 and 60 min into the final reperfusion. All rats were euthanized and tissue harvested for spinal cord blood flow analysis. In Experiment 1, there was a slight, significant difference in spinal cord blood flow during the ischemic period; however, this difference soon disappeared during reperfusion. In experiment 2, there was no difference in blood flow at any experimental time. The results of these experiments demonstrate that IPC slightly enhances blood flow to the spinal cord during ischemia; however, this effect is not sustained during the reperfusion period.

show abstract

Does adenosine release taurine in the A1-receptor-rich hippocampus?

Cited by 11 publications

References 27 publications

Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation

Elevated Glucose and Interleukin-1β Differentially Affect Retinal Microglial Cell Proliferation

Alternate explanation of the additive protective effects of regional infusion of hypothermic saline and adenosine solutions

Spinal Cord Blood Flow after Ischemic Preconditioning in a Rat Model of Spinal Cord Ischemia

Contact Info

Product

Resources

About