Astrocytes, emerging stars of energy homeostasis

Camandola, Simonetta

doi:10.15698/cst2018.10.157

Cited by 15 publications

(6 citation statements)

References 104 publications

(129 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Glucose is the primary energy substrate of not only neurons but also microglia [ 10 ]. Glucose sensing by hypothalamic neurons, astrocytes, and tanycytes is an important component of CNS regulation of whole-body metabolism [ 11 , 12 ]. Previous studies have demonstrated that central administration of the pro-inflammatory cytokine interleukin-1 (IL-1) alpha or beta reduces food intake in rodents [ 13 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Regulation of the Fructose Transporter Gene Slc2a5 Expression by Glucose in Cultured Microglial Cells

Mizuno

Lew

Jhanji

2021

IJMS

View full text Add to dashboard Cite

Microglia play a role in the regulation of metabolism and pathogenesis of obesity. Microglial activity is altered in response to changes in diet and the body’s metabolic state. Solute carrier family 2 member 5 (Slc2a5) that encodes glucose transporter 5 (GLUT5) is a fructose transporter primarily expressed in microglia within the central nervous system. However, little is known about the nutritional regulation of Slc2a5 expression in microglia and its role in the regulation of metabolism. The present study aimed to address the hypothesis that nutrients affect microglial activity by altering the expression of glucose transporter genes. Murine microglial cell line SIM-A9 cells and primary microglia from mouse brain were exposed to different concentrations of glucose and levels of microglial activation markers and glucose transporter genes were measured. High concentration of glucose increased levels of the immediate-early gene product c-Fos, a marker of cell activation, Slc2a5 mRNA, and pro-inflammatory cytokine genes in microglial cells in a time-dependent manner, while fructose failed to cause these changes. Glucose-induced changes in pro-inflammatory gene expression were partially attenuated in SIM-A9 cells treated with the GLUT5 inhibitor. These findings suggest that an increase in local glucose availability leads to the activation of microglia by controlling their carbohydrate sensing mechanism through both GLUT5-dependent and –independent mechanisms.

show abstract

Section: Introductionmentioning

confidence: 99%

Regulation of the Fructose Transporter Gene Slc2a5 Expression by Glucose in Cultured Microglial Cells

Mizuno

Lew

Jhanji

2021

IJMS

View full text Add to dashboard Cite

show abstract

“…They are highly heterogeneous, exhibiting variations in their appearance and functionality across brain regions and even within substructures, such as the hippocampus (Amundson, Goderie, & Kimelberg, 1992; Lin et al, 2017; Wallraff, Odermatt, Willecke, & Steinhäuser, 2004). Astrocytes contribute to a multitude of brain processes by modulating synaptic plasticity and neuronal activity (Alfonso Araque et al, 2014; Rusakov, Bard, Stewart, & Henneberger, 2014; Ullian, Sapperstein, Christopherson, & Barres, 2001), controlling extra‐synaptic space (Flores‐Méndez, Mendez‐Flores, & Ortega, 2016) and neurotransmitter clearance (Rose et al, 2018; Sibille, Pannasch, & Rouach, 2014), regulating cerebral blood flow (Mishra, 2017), ensuring energy supply to neurons, and orchestrating the rhythms of neuronal firing patterns (Camandola, 2018; Lee et al, 2014; Sheikhbahaei et al, 2018; Stobart & Anderson, 2013).…”

Section: Introductionmentioning

confidence: 99%

Serotonin receptor 4 regulates hippocampal astrocyte morphology and function

Müller

Schade

Cherkas

et al. 2020

Glia

View full text Add to dashboard Cite

Astrocytes are an important component of the multipartite synapse and crucial for proper neuronal network function. Although small GTPases of the Rho family are powerful regulators of cellular morphology, the signaling modules of Rho‐mediated pathways in astrocytes remain enigmatic. Here we demonstrated that the serotonin receptor 4 (5‐HT4R) is expressed in hippocampal astrocytes, both in vitro and in vivo. Through fluorescence microscopy, we established that 5‐HT4R activation triggered RhoA activity via Gα13‐mediated signaling, which boosted filamentous actin assembly, leading to morphological changes in hippocampal astrocytes. We investigated the effects of these 5‐HT4R‐mediated changes in mixed cultures and in acute slices, in which 5‐HT4R was expressed exclusively in astrocytes. In both systems, 5‐HT4R‐RhoA signaling changed glutamatergic synaptic transmission: It increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in mixed cultures and reduced the paired‐pulse‐ratio (PPR) of field excitatory postsynaptic potentials (fEPSPs) in acute slices. Overall, our present findings demonstrate that astrocytic 5‐HT4R‐Gα13‐RhoA signaling is a previously unrecognized molecular pathway involved in the functional regulation of excitatory synaptic circuits.

show abstract

“… 20 Astrocytes are closely associated with the pathogenesis of neurodegenerative diseases, mood disorders and energy balance. 21 , 22 , 23 Inflammation‐associated GFAP astrocytes interact with neuronal activation. 8 , 9 We also found that neuronal activation and proinflammatory cytokines were reduced following the inhibition of activated astrocytes in the PVN and then VA occurrence was reduced at 24 h after AMI.…”

Section: Discussionmentioning

confidence: 99%

“…Astrocytes are non‐neuronal cells and historically considered as structural supporting cells for neurons, but recently more and more evidence indicated that astrocyte plays an essential role in maintaining proper neuronal health and function 20 . Astrocytes are closely associated with the pathogenesis of neurodegenerative diseases, mood disorders and energy balance 21–23 . Inflammation‐associated GFAP astrocytes interact with neuronal activation 8,9 .…”

Section: Discussionmentioning

confidence: 99%

Cardiac sympathetic afferent ablation to prevent ventricular arrhythmia complicating acute myocardial infarction by inhibiting activated astrocytes

Chen

Chu

Gao

et al. 2022

J Cellular Molecular Medi

View full text Add to dashboard Cite

Enhanced cardiac sympathetic afferent reflex (CSAR) contributes to ventricular arrhythmia (VA) after acute myocardial infarction (AMI). However, central regulation mechanisms remain unknown. The aim of this study was to investigate whether local cardiac sympathetic afferent ablation (LCSAA) could reduce VA by inhibiting activated astrocytes in the hypothalamus paraventricular (PVN) in an AMI rat model. The rats were randomly divided into AMI, AMI + BD (baroreceptor denervation), AMI + LCSAA and AMI + BD+ LCSAA groups. Before the generation of AMI, BD and (or) LCSAA were performed. At 24 h after AMI, the incidence and duration of VA in AMI + LCSAA group and AMI + BD + LCSAA group were significantly reduced than AMI group ( P < 0.05 ). Furthermore, LCSAA significantly reduced GFAP (a marker for activated astrocytes) positive cells and their projections as well as the level of TNF‐α and IL‐6 in the PVN of AMI + LCSAA group and AMI + BD+ LCSAA group, along with the decrease of neuronal activation in PVN and sympathetic nerve activity ( P < 0.05 ). but BD had no obvious difference between AMI + LCSAA and AMI + BD + LCSAA group ( P > 0.05 ). Therefore, LCSAA could decrease sympathoexcitation and VA occurrence in AMI rats by inhibiting astrocyte and neuronal activation in the PVN. Our study demonstrates that activated astrocytes may play an important role on CSAR in AMI.

show abstract

Astrocytes, emerging stars of energy homeostasis

Cited by 15 publications

References 104 publications

Regulation of the Fructose Transporter Gene Slc2a5 Expression by Glucose in Cultured Microglial Cells

Regulation of the Fructose Transporter Gene Slc2a5 Expression by Glucose in Cultured Microglial Cells

Serotonin receptor 4 regulates hippocampal astrocyte morphology and function

Cardiac sympathetic afferent ablation to prevent ventricular arrhythmia complicating acute myocardial infarction by inhibiting activated astrocytes

Contact Info

Product

Resources

About