MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1

Liu, Yulan; Deng, Shanshan; Song, Zhibing; Zhang, Qian; Guo, Yuchen; Yu, Yongsheng; Wang, Yuliang; Li, Tiejun; Megahed, Fayed Attia Koutb; Addissouky, Tamer A.; Mao, Junqin; Zhang, Yuefan

doi:10.3389/fphar.2021.725268

Cited by 21 publications

(20 citation statements)

References 40 publications

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“…Compared with the vehicle group, selective sEH inhibitor‐treated rats showed a reduction in M1 monocyte/macrophage activation and proinflammatory mRNA expression in the infarct cortex of rats ( 41 ). Similar results were found in another study, while the authors delivered MLIF (monocyte locomotion inhibitory factor, a pentapeptide known to play anti‐inflammatory effects) to rodents with IS, and found increased M2 transformation from M1 phenotype, which was related with better behavioral performance and smaller infarcted area ( 42 ).…”

Section: The Activation and Differentiation Of The Mps ...supporting

confidence: 81%

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Friends or foes: The mononuclear phagocyte system in ischemic stroke

Ziqing

Liu

et al. 2023

Brain Pathology

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Ischemic stroke (IS) is a major cause of disability and death in adults, and the immune response plays an indispensable role in its pathological process. After the onset of IS, an inflammatory storm, with the infiltration and mobilization of the mononuclear phagocyte system (MPS), is triggered in the brain. Microglia are rapidly activated in situ, followed by waves of circulating monocytes into the ischemic area. Activated microglia and monocytes/macrophages are mainly distributed in the peri‐infarct area. These cells have similar morphology and functions, such as secreting cytokines and phagocytosis. Previously, the presence of the MPS was considered a marker of an exacerbated inflammatory response that contributes to brain damage. However, recent studies have suggested a rather complicated role of the MPS in IS. Here, we reviewed articles focusing on various functions of the MPS among different phases of IS, including recruitment, polarization, phagocytosis, angiogenesis, and interaction with other types of cells. Moreover, due to the characteristics of the MPS, we also noted clinical research addressing alterations in the MPS as potential biomarkers for IS patients for the purposes of predicting prognosis and developing novel therapeutic strategies.

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Section: The Activation and Differentiation Of The Mps ...supporting

confidence: 81%

“…Additionally, the blockade of adrenergic activity significantly reversed these cytokine levels and improved neurological results (73). Rajan Liu et al (42) inflammatory changes in the CNS of patients. Hints could only be illustrated from studies of peripheral immune changes in IS patients.…”

Section: Inflammation Regulationmentioning

confidence: 99%

Friends or foes: The mononuclear phagocyte system in ischemic stroke

Ziqing

Liu

et al. 2023

Brain Pathology

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“…Values are mean ± SD, # P < 0.05 compared with Sirt3 f/f group, + P < 0.05 compared with ICH + IF + Vehicle group microglia is to engulf RBCs and remove cellular debris [31]. Under certain conditions, microglia can also express arginase1 (Arg1), insulin-like growth factor (IGF-1), Ym1 and anti-inflammatory cytokines, such as IL-10 and IL-4, which facilitate recovery of CNS injury including ischemic stroke [32]. Considering the high plasticity of microglia according to different pathologic events or microenvironments [33], deeper insight into the regulatory mechanisms of microglial phenotype variations may help maintain the homeostasis of microglia activation.…”

Section: Discussionmentioning

confidence: 99%

Intermittent fasting reduces neuroinflammation in intracerebral hemorrhage through the Sirt3/Nrf2/HO-1 pathway

Dai

Wei

Zhang

et al. 2022

J Neuroinflammation

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Background Inflammation contributes to the poor prognosis of intracerebral hemorrhage (ICH). Intermittent fasting (IF) has been shown to be protective against inflammation in multiple pathogenic processes. In the present study, we aimed to investigated the beneficial effects of IF in attenuating neuroinflammation and neurological deficits in a mouse model of ICH and to investigate the underlying mechanism. Methods ICH was modeled by intrastriatal injection of autologous blood and IF was modeled by every-other-day feeding in male control mice (C57BL/6), mice with and microglia specific knockout Sirt3f/f;Cx3cr1-Cre (Sirt3 cKO), and Sirt3f/f (wild-type) mice. Brain tissues and arterial blood were harvested at 1, 3, 7 and 28 days after ICH for immunohistochemistry analysis of Iba-1, DARPP-32 and HO-1, morphological analysis by HE staining and inflammatory factor release tests by ELISA. Neurological functions were approached by corner test and cylinder test. Fluorescent double-labeled staining of Iba-1 with CD16, Arg1 or Sirt3 was used to provide direct image of co-expression of these molecules in microglia. TUNEL, cleaved caspase-3 and Nissl staining was performed to evaluate cellular injuries. Results IF alleviated neurological deficits in both acute and chronic phases after ICH. Morphologically, IF enhanced hematoma clearance, reduced brain edema in acute phase and attenuated striatum atrophy in chronic phase. In addition, IF decreased the numbers of TUNEL+ cells and increased Nissl+ neuron number at day 1, 3 and 7 after ICH. IF suppressed CD16+Iba-1+ microglia activation at day 3 after ICH and reduced inflammatory releases, such as IL-1β and TNF-α. The above effects of IF were attenuated by microglia Sirt3 deletion partly because of an inhibition of Nrf2/HO-1 signaling pathway. Interestingly, IF increased Iba-1+ microglia number at day 7 which mainly expressed Arg1 while decreased the proinflammatory factor levels. In mice with microglia-specific Sirt3 deletion, the effects of IF on Iba-1+ microglia activation and anti-inflammatory factor expressions were attenuated when compared with wild-type Sirt3f/f mice. Conclusions IF protects against ICH by suppressing the inflammatory responses via the Sirt3/Nrf2/HO-1 pathway.

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“…Recent studies have shown that EEF1A1 and Cag A synergistically regulate IL-6 expression by impacting the activation of p-STATS727 in the cell nucleus [12]. Yulan Liu et al [13] found that EEF1A1 may have a signi cant role in moderating microglia polarization. These reports indicate that EEF1A1 may be essential in regulating in ammatory processes.…”

Section: Introductionmentioning

confidence: 99%

EEF1A1 knock-down regulates the expression and alternative splicing of genes associated with Parkinson`s disease in U251 cells

Lei,

aisha,

zhang

et al. 2023

Preprint

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Eukaryotic Elongation Factor 1A1 (EEF1A1) is an RNA-binding protein that is associated with PARK2 activity in cells, predicting a possible important role in Parkinson`s disease (PD). However, it is not clear whether EEF1A1 will play a role in PD through transcriptional or post-transcriptional regulation. In this study, the GSE68719 data set was downloaded from the GEO database, and the RNA-seq data of BA9 brain tissue autopsy were obtained from 29 PD patients and 44 neurologically normal control subjects. The analysis found that EEF1A1 was significantly over-expressed in PD brain tissue. Then, to inhibit EEF1A1 from being expressed in U251 cells, siRNA was transfected into those cells, and the RNA-seq high-throughput sequencing was used to determine the Differentially Expressed Genes (DEGs) and differentially alternative splicing events (ASEs) resulting from the EEF1A1 knockdown. Further, GO and KEGG enrichment analysis revealed that EEF1A1 knockdown significantly up-regulated the expression of genes CXCL10, NGF, PTX3, IL6, ST6GALNAC3, NUPR1, TNFRSF21, CXCL2, and up-regulated alternative splicing of genes ACOT7, DDX10, SHMT2, MYEF2, NDUFAF5. These genes were enriched to pathways related to PD pathogenesis, such as apoptosis, inflammatory response, and mitochondrial dysfunction, suggesting that EEF1A1 may be involved in the development of PD by regulating differential expression and alternative splicing of genes. This study preliminarily investigated the potential role and mechanism of EEF1A1 in the pathogenesis of PD, providing a theoretical basis for subsequent research.

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MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1

Cited by 21 publications

References 40 publications

Friends or foes: The mononuclear phagocyte system in ischemic stroke

Friends or foes: The mononuclear phagocyte system in ischemic stroke

Intermittent fasting reduces neuroinflammation in intracerebral hemorrhage through the Sirt3/Nrf2/HO-1 pathway

EEF1A1 knock-down regulates the expression and alternative splicing of genes associated with Parkinson`s disease in U251 cells

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