CX3C chemokine receptor 1 deficiency modulates microglia morphology but does not affect lesion size and short-term deficits after experimental stroke

Maten, Gerlinde van der; Henck, Vivien; Wieloch, Tadeusz; Ruscher, Karsten

doi:10.1186/s12868-016-0325-0

Cited by 16 publications

(13 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Regarding CX3CR1, its deficiency provides a neuroprotective effect against ischemia-induced brain injury in mice following focal cerebral ischemia (18,22,37). However, a recent study has shown that CX3CR1 deficiency does not affect lesion size after transient focal cerebral ischemia in mice (38).…”

Section: Discussionmentioning

confidence: 99%

Expression changes of CX3CL1 and CX3CR1 proteins in the hippocampal CA1 field of the gerbil following transient global cerebral ischemia

et al. 2019

View full text Add to dashboard Cite

Chemokine C-X3-C motif ligand 1 (CX3CL1) and its sole receptor, CX3CR1, are known to be involved in neuronal damage/death following brain ischemia. In the present study, time-dependent expression changes of CX3CL1 and CX3CR1 proteins were investigated in the hippocampal CA1 field following 5 min of transient global cerebral ischemia (tgCI) in gerbils. To induce tgCI in gerbils, bilateral common carotid arteries were occluded for 5 min using aneurysm clips. Expression changes of CX3CL1 and CX3CR1 proteins were assessed at 1, 2 and 5 days after tgCI using western blotting and immunohistochemistry. CX3CL1 immunoreactivity was strong in the CA1 pyramidal cells of animals in the sham operation group. Weak CX3CL1 immunoreactivity was detected at 6 h after tgCI, recovered at 1 day after tgCI and disappeared from 5 days after tgCI. CX3CR1 immunoreactivity was very weak in CA1 pyramidal cells of the sham animals. CX3CR1 immunoreactivity in CA1 pyramidal cells was significantly increased at 1 days after tgCI and gradually decreased thereafter. On the other hand, CX3CR1 immunoreactivity was significantly increased in microglia from 5 days after tgCI. These results showed that CX3CL1 and CX3CR1 protein expression levels in pyramidal cells and microglia in the hippocampal CA1 field following tgCI were changed, indicating that tgCI-induced expression changes of CX3CL1 and CX3CR1 proteins might be closely associated with tgCI-induced delayed neuronal death and microglial activation.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression changes of CX3CL1 and CX3CR1 proteins in the hippocampal CA1 field of the gerbil following transient global cerebral ischemia

et al. 2019

View full text Add to dashboard Cite

show abstract

“…stroke (60,61). Although the CC3CL1/CX3CR1 pathway has been shown to contribute to ischemic injury in mice (62)(63)(64), whether this is due to changes in neuronal-microglial interactions remains to be established.…”

Section: Complementmentioning

confidence: 99%

Immune responses to stroke: mechanisms, modulation, and therapeutic potential

Iadecola

Buckwalter

Anrather

2020

Journal of Clinical Investigation

496

376

View full text Add to dashboard Cite

tors on innate immune cells, enabling recognition of a wide variety of molecular complexes that are perceived as foreign and potentially damaging (dangerassociated molecular patterns [DAMPs]). Innate immune cells include neutrophils, monocytes, macrophages, and DCs, as well as selected groups of lymphocytes, e.g., NK cells, γδ T cells, and others (33). The ensuing response is directed at eliminating the potential threat through a massive and indiscriminate humoral and cellular inflammatory response. In contrast to innate immunity, adaptive immunity requires several days to develop and retains memory of antigen exposure (32). Adaptive immunity is based on highaffinity receptors, including T cell receptors and immunoglobulins.Innate and adaptive immunity are closely interrelated (32). Innate immune cells, DCs in particular, initiate adaptive immune responses via antigen presentation to lymphocytes, the typical adaptive immune cell. In turn, lymphocytes undergo clonal expansion in lymphoid organs and return to the circulation to engage the antigen throughout the body. The resulting humoral and cellular responses seek to neutralize the offending antigen with a remarkable degree of selectivity and specificity. As detailed below, cerebral ischemia engages both innate and adaptive immunity (Figures 1 and 2), which play a critical role in both the acute and chronic phases of the damage. Cerebral ischemia and innate immunity: the brain viewCirculating innate immune cells are quickly engaged at the onset of arterial occlusion, ultimately resulting in invasion of the ischemic brain by blood-borne immune cells and activation of brain-resident cells, which can be either beneficial or detrimental (Figure 1).

show abstract

“…24 h might be due to effects on multiple processes i.e. brain edema without consequences for the final ischemic lesion and function [ 44 ]. Also, differences in results might be due to different experimental stroke models.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-124-loaded nanoparticles increase survival and neuronal differentiation of neural stem cells in vitro but do not contribute to stroke outcome in vivo

et al. 2018

Self Cite

View full text Add to dashboard Cite

There is a high quest for novel therapeutic strategies to enhance recovery after stroke. MicroRNA-124 (miR-124) has been described as neuroprotective and anti-inflammatory molecule. Moreover, miR-124 is a well described enhancer of adult neurogenesis that could offer potentially beneficial effects. Herein, we used miR-124-loaded nanoparticles (miR-124 NPs) to evaluate their therapeutic potential in an in vitro and in vivo model of stroke. For that, neuroprotective and neurogenic responses were assessed in an in vitro model of stroke. Here, we found that miR-124 NPs decreased cell death and improved neuronal differentiation of subventricular zone (SVZ) neural stem cell cultures after oxygen and glucose deprivation. In contrast, intravenous injection of miR-124 NPs immediately after permanent focal ischemia induced by photothrombosis (PT) did not provide a better neurological outcome. In addition, treatment did not affect the number of 5-bromo-2'-deoxyuridine (BrdU)- and doublecortin/BrdU- positive cells in the SVZ at the study endpoint of 14 days after PT. Likewise, the ischemic insult did not affect the numbers of neuronal progenitors in the SVZ. However, in PT mice miR-124 NPs were able to specifically augment interleukin-6 levels at day 2 post-stroke. Furthermore, we also showed that NPs reached the brain parenchyma and were internalized by brain resident cells. Although, promising in vitro data could not be verified in vivo as miR-124 NPs treatment did not improve functional outcome nor presented beneficial actions on neurogenesis or post-stroke inflammation, we showed that our NP formulation can be a safe alternative for drug delivery into the brain.

show abstract

CX3C chemokine receptor 1 deficiency modulates microglia morphology but does not affect lesion size and short-term deficits after experimental stroke

Cited by 16 publications

References 32 publications

Expression changes of CX3CL1 and CX3CR1 proteins in the hippocampal CA1 field of the gerbil following transient global cerebral ischemia

Expression changes of CX3CL1 and CX3CR1 proteins in the hippocampal CA1 field of the gerbil following transient global cerebral ischemia

Immune responses to stroke: mechanisms, modulation, and therapeutic potential

MicroRNA-124-loaded nanoparticles increase survival and neuronal differentiation of neural stem cells in vitro but do not contribute to stroke outcome in vivo

Contact Info

Product

Resources

About