Interaction between astrocytic colony stimulating factor and its receptor on microglia mediates central sensitization and behavioral hypersensitivity in chronic post ischemic pain model

Tang, Yuying; Liu, Lian; Xu, Dan; Zhang, Wensheng; Zhang, Yi; Zhou, Jieshu; Huang, Wei

doi:10.1016/j.bbi.2017.10.023

Cited by 57 publications

(54 citation statements)

References 65 publications

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“…CSF1R knockout mice are devoid of microglia 59 . Moreover, it has been reported that repeated treatment with CSF1R inhibitors, such as PLX3397, cause a dramatic reduction in the number of microglia within the adult brain [48][49][50] .…”

Section: Discussionmentioning

confidence: 99%

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Essential role of microglial transforming growth factor-β1 in antidepressant actions of (R)-ketamine and the novel antidepressant TGF-β1

et al. 2020

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In rodent models of depression, (R)-ketamine has greater potency and longer-lasting antidepressant effects than (S)ketamine; however, the precise molecular mechanisms underlying the antidepressant actions of (R)-ketamine remain unknown. Using RNA-sequencing analysis, we identified novel molecular targets that contribute to the different antidepressant effects of the two enantiomers. Either (R)-ketamine (10 mg/kg) or (S)-ketamine (10 mg/kg) was administered to susceptible mice after chronic social defeat stress (CSDS). RNA-sequencing analysis of prefrontal cortex (PFC) and subsequent GSEA (gene set enrichment analysis) revealed that transforming growth factor (TGF)-β signaling might contribute to the different antidepressant effects of the two enantiomers. (R)-ketamine, but not (S)-ketamine, ameliorated the reduced expressions of Tgfb1 and its receptors (Tgfbr1 and Tgfbr2) in the PFC and hippocampus of CSDS susceptible mice. Either pharmacological inhibitors (i.e., RepSox and SB431542) or neutralizing antibody of TGF-β1 blocked the antidepressant effects of (R)-ketamine in CSDS susceptible mice. Moreover, depletion of microglia by the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX3397 blocked the antidepressant effects of (R)-ketamine in CSDS susceptible mice. Similar to (R)-ketamine, the recombinant TGF-β1 elicited rapid and long-lasting antidepressant effects in animal models of depression. Our data implicate a novel microglial TGF-β1-dependent mechanism underlying the antidepressant effects of (R)-ketamine in rodents with depression-like phenotype. Moreover, TGF-β1 and its receptor agonists would likely constitute a novel rapid-acting and sustained antidepressant in humans.

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Section: Discussionmentioning

confidence: 99%

“…PLX3397 was reported to eliminate microglia in the brain [48][49][50] . For preliminary experiment, PLX3397 (10 μM or 100 μM, 2 μl, i.c.v.)…”

Section: Depletion Of Microglia By Plx3397mentioning

confidence: 99%

Essential role of microglial transforming growth factor-β1 in antidepressant actions of (R)-ketamine and the novel antidepressant TGF-β1

et al. 2020

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“…G-CSF can also protect ischemic neurons through G-CSF receptors on nerve cell membranes (Hamzei Taj et al, 2018). In addition, G-CSF can effectively cross the blood-brain barrier and stimulate the expression of G-CSF in the central nervous system (Tang et al, 2018). After binding to its receptor, it activates the JAK3 and STAT3 pathways to increase STAT3 levels in neurons in the peripheral zone of the ischemic foci, and STAT3 then indirectly exerts an anti-apoptotic effect by activating Bcl-2.…”

Section: Granulocyte Colony Stimulating Factor (G-csf)mentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

329

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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“…On the other hand, the main inhibitory GABAergic input to the vlPAG, relevant to the micturition, projects from dlPAG [44]. Glutamatergic cells of the vlPAG also control other important functions, including freezing [53] and nociception [54], which are controlled by two separate cell groups in the vlPAG [53]. Whether these cell groups are different from those vlPAG glutamatergic cells controlling voiding, or have some overlap, remains to be elucidated.…”

Section: The Role Of Distinct Cell Groups In Pag Functionmentioning

confidence: 99%

“…We applied two different ways of visualizing cFos. For the brain sections, we used the indirect immunohistochemical (3,3'-Diaminobenzidine (DAB)) staining method employing amplification by means of streptavidin and nickel-diaminobenzidine chromogen enhancement according to previous protocols [54] whereas for spinal cord sections we chose fluorescent visualization. Because brain sections are known for possessing auto-fluorescence after formaldehyde fixation [55][56][57] and we expected low cFos epitope expression, we opted for the indirect immunohistochemical visualization in the brain.…”

Section: Cfos Immunohistochemistrymentioning

confidence: 99%

Unveiling the sensory connections between the bladder and the brain that involve the periaqueductal gray matter

Zare¹

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Interaction between astrocytic colony stimulating factor and its receptor on microglia mediates central sensitization and behavioral hypersensitivity in chronic post ischemic pain model

Cited by 57 publications

References 65 publications

Essential role of microglial transforming growth factor-β1 in antidepressant actions of (R)-ketamine and the novel antidepressant TGF-β1

Essential role of microglial transforming growth factor-β1 in antidepressant actions of (R)-ketamine and the novel antidepressant TGF-β1

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Unveiling the sensory connections between the bladder and the brain that involve the periaqueductal gray matter

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