Modulating poststroke inflammatory mechanisms: Novel aspects of mesenchymal stem cells, extracellular vesicles and microglia

Xin, Wenqiang; Wei, Wei; Pan, Yongli; Cui, Bao-Long; Yang, Xinyu; Bähr, Mathias; Doeppner, Thorsten R.

doi:10.4252/wjsc.v13.i8.1030

Cited by 15 publications

(29 citation statements)

References 152 publications

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“…Normally, the microglia are in the rest state to keep homeostasis in the fields around microglia cells. 123 Upon an inflammatory condition, the activation of microglia is the first step of response to inflammation, and then other immune cells like neutrophils, T cells, natural killer cells, and so on were activated in the brain. [123][124][125] Stimuli results in the activation of microglia, which represents the first step of an inflammatory response, followed by four distinct phenotypes, such as ramified, intermediate, amoeboid, and round phenotypes.…”

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

“…123 Upon an inflammatory condition, the activation of microglia is the first step of response to inflammation, and then other immune cells like neutrophils, T cells, natural killer cells, and so on were activated in the brain. [123][124][125] Stimuli results in the activation of microglia, which represents the first step of an inflammatory response, followed by four distinct phenotypes, such as ramified, intermediate, amoeboid, and round phenotypes. 123,126 Based on the morphological progression and its substance secretion, microglia are characterized as M1-type and M2-type.…”

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

“…[123][124][125] Stimuli results in the activation of microglia, which represents the first step of an inflammatory response, followed by four distinct phenotypes, such as ramified, intermediate, amoeboid, and round phenotypes. 123,126 Based on the morphological progression and its substance secretion, microglia are characterized as M1-type and M2-type. 123 M1-type, the proinflammatory phenotype, produces various pro-inflammatory factors such as IL-1β, IL-6, interferon-α, motif chemokine ligand, cyclooxygenase-2, and inducible nitric oxide synthase.…”

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

“…123,126 Based on the morphological progression and its substance secretion, microglia are characterized as M1-type and M2-type. 123 M1-type, the proinflammatory phenotype, produces various pro-inflammatory factors such as IL-1β, IL-6, interferon-α, motif chemokine ligand, cyclooxygenase-2, and inducible nitric oxide synthase. 123,[127][128][129][130] M2, anti-inflammatory phenotype, microglia involve the states of both alternative activation and acquired deactivation, which are accompanied by IL-4/IL-13 and IL-10/transforming growth factor (TGF)-β, respectively.…”

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

“…123 M1-type, the proinflammatory phenotype, produces various pro-inflammatory factors such as IL-1β, IL-6, interferon-α, motif chemokine ligand, cyclooxygenase-2, and inducible nitric oxide synthase. 123,[127][128][129][130] M2, anti-inflammatory phenotype, microglia involve the states of both alternative activation and acquired deactivation, which are accompanied by IL-4/IL-13 and IL-10/transforming growth factor (TGF)-β, respectively. 123,131,132 Ni et al 62 exposed Neat1 knockdown BV-2 cells to oxygen-glucose deprivation/reoxygenation (OGD/R) and then detected the various levels of markers of M1 (CD16, CD32, and CD86) and M2 (BDNF, PDGF, and Arg-1) microglia, demonstrating that Neat1 knockdown suppresses M1microglial polarization but does not promote M2 microglial polarization.…”

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

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Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

Pan

Wang

Zhao

et al. 2022

JIR

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Nuclear paraspeckle assembly transcript 1 (Neat1) located at chromosome 11 is a long non-coding RNA that is widely expressed in mammalian cell types, and which is overexpressed in several inflammation-related disorders. Inflammation implies a plethora of mutual interactions between both soluble factors and cells due to various stimuli including tissue injury. Although there is no doubt that inflammation is critically involved in multiple biological and pathological processes alike, the precise mechanisms being involved are still open for debate. In this context, the role of Neat1 as a regulator of inflammation, microglial activation, and lipid accumulation under various inflammatory conditions remains elusive. Herein, we review the regulation of Neat1 and how it modulates the expression of its target genes. Thereafter, we will review the impact of Neat1 on inflammation by activating or inhibiting various signaling pathways, such as microRNAs, AKT, TLR4, TRAF6, and NF-κB.

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Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

Section: Neat1 Can Regulate the Activation Of Microgliamentioning

confidence: 99%

See 3 more Smart Citations

Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

Pan

Wang

Zhao

et al. 2022

JIR

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The dual role of microglia in ischemic stroke and its modulation via extracellular vesicles and stem cells

Haupt,

Gerner,

Doeppner

2024

Neuroprotection

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Stem cell‐based therapies and extracellular vesicle (EV) treatment have demonstrated significant potential for neuroprotection against ischemic stroke. Although the neuroprotective mechanisms are not yet fully understood, targeting microglia is central to promoting neuroprotection. Microglia are the resident immune cells of the central nervous system. These cells are crucial in the pathogenesis of ischemic stroke. They respond rapidly to the site of injury by releasing pro‐inflammatory cytokines, phagocytizing dead cells and debris, and recruiting peripheral immune cells to the ischemic area. Although these responses are essential for clearing damage and initiating tissue repair, excessive or prolonged microglial activation can exacerbate brain injury, leading to secondary neuroinflammation and neurodegeneration. Moreover, microglia exhibit a dynamic range of activation states with the so‐called M1 pro‐inflammatory and M2 anti‐inflammatory phenotypes, representing the two ends of the spectrum. The delivery of both EVs and stem cells modulates microglial activation, suppressing pro‐inflammatory genes, influencing the expression of transcription factors, and altering receptor expression, ultimately contributing to neuroprotection. These findings underscore the importance of understanding the complex and dynamic role of microglia in the development of effective neuroprotective strategies to reduce the effects of ischemic stroke. In this review, we examine the current state of knowledge regarding the role of microglia in ischemic stroke, including their molecular and cellular mechanisms, activation states, and interactions with other cells. We also discuss the multifaceted contributions of microglia to stem cell‐ and EV‐based neuroprotection during an ischemic stroke to provide a comprehensive understanding of microglial functions and their potential implications in stroke therapies.

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Nanowired Delivery of Cerebrolysin with Mesenchymal Stem Cells Attenuates Heat Stress-Induced Exacerbation of Neuropathology Following Brain Blast Injury

Mureșanu¹,

Sharma²,

Tian³

et al. 2023

Advances in Neurobiology

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Modulating poststroke inflammatory mechanisms: Novel aspects of mesenchymal stem cells, extracellular vesicles and microglia

Cited by 15 publications

References 152 publications

Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

The dual role of microglia in ischemic stroke and its modulation via extracellular vesicles and stem cells

Nanowired Delivery of Cerebrolysin with Mesenchymal Stem Cells Attenuates Heat Stress-Induced Exacerbation of Neuropathology Following Brain Blast Injury

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