Progress in Research on TLR4-Mediated Inflammatory Response Mechanisms in Brain Injury after Subarachnoid Hemorrhage DOI Creative Commons
Lintao Wang,

Guangping Geng,

Tao Zhu

et al.

Cells, Journal Year: 2022, Volume and Issue: 11(23), P. 3781 - 3781

Published: Nov. 26, 2022

Subarachnoid hemorrhage (SAH) is one of the common clinical neurological emergencies. Its incidence accounts for about 5-9% cerebral stroke patients. Even surviving patients often suffer from severe adverse prognoses such as hemiplegia, aphasia, cognitive dysfunction and even death. Inflammatory response plays an important role during early nerve injury in SAH. Toll-like receptors (TLRs), pattern recognition receptors, are components body's innate immune system, they usually activated by damage-associated molecular molecules. Studies have shown that with TLR 4 essential member TLRs family, inflammatory transduction pathway mediated it a vital brain after After SAH occurrence, large amounts blood enter subarachnoid space. This can produce massive molecules bind to TLR4, which activates causes injury, thus resulting serious prognoses. In this paper, process research on TLR4-mediated mechanism was reviewed provide new thought treatment.

Language: Английский

Immune‐mediated disruption of the blood–brain barrier after intracerebral hemorrhage: Insights and potential therapeutic targets DOI Creative Commons

Peijun Jia,

Qinfeng Peng,

Xiaochong Fan

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(7)

Published: July 1, 2024

Intracerebral hemorrhage (ICH) is a condition that arises due to the rupture of cerebral blood vessels, leading flow into brain tissue. One pathological alterations occurs during an acute ICH impairment blood-brain barrier (BBB), which leads severe perihematomal edema and immune response.

Language: Английский

Citations

11

Hypoxic‐preconditioned mesenchymal stem cell‐derived small extracellular vesicles promote the recovery of spinal cord injury by affecting the phenotype of astrocytes through the miR‐21/JAK2/STAT3 pathway DOI Creative Commons
Zhelun Yang,

Zeyan Liang,

Jian Rao

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2023, Volume and Issue: 30(3)

Published: Aug. 29, 2023

Secondary injury after spinal cord (SCI) is a major obstacle to their neurological recovery. Among them, changes in astrocyte phenotype regulate secondary dominated by neuroinflammation. Hypoxia-preconditioned mesenchymal stem cells (MSCs)-derived extracellular vesicle (H-EV) plays multifaceted role interacting with cellular components and signaling pathways. They possess anti-inflammatory properties, oxidative stress, modulate apoptotic pathways, promoting cell survival reducing neuronal loss. Given the unique aspects of injury, H-EV shows promise as therapeutic approach mitigate its devastating consequences. Our study aimed determine whether could promote SCI repair altering astrocytes.

Language: Английский

Citations

22

Glial cells: an important switch for the vascular function of the central nervous system DOI Creative Commons

Ling Gao,

Xuezhen Pan,

John H. Zhang

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2023, Volume and Issue: 17

Published: May 3, 2023

In this review, we first describe the current understanding of glial-mediated vascular function affecting role blood-brain barrier (BBB) in central nervous system (CNS) disorders. BBB, mainly composed glial and endothelial cells (ECs), is protective structure that orchestrates transport substances, including ions, molecules, from brain vessels into or out CNS. Then, display multiple communication between based on angiogenesis, wrapping, blood perfusion brain. Glial can support microvascular ECs to form a network connecting neurons. Astrocytes, microglia, oligodendrocytes are common types surrounding vessel. Glial-vessel interaction required for permeability integrity BBB. cerebral transmit signals regulate activity growth factor (VEGF) Wnt-dependent angiogenesis mechanism. addition, these monitor flow via Ca

Language: Английский

Citations

15

Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview DOI Creative Commons
Henry W. Sanicola, Caleb Stewart,

Patrick Luther

et al.

Pathophysiology, Journal Year: 2023, Volume and Issue: 30(3), P. 420 - 442

Published: Sept. 14, 2023

Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke resulting from the rupture an arterial vessel within brain. Unlike other types, SAH affects both young adults (mid-40s) and geriatric population. Patients with often experience significant neurological deficits, leading to substantial societal burden in terms lost potential years life. This review provides comprehensive overview SAH, examining its development across different stages (early, intermediate, late) highlighting pathophysiological pathohistological processes specific each phase. The clinical management also explored, focusing on tailored treatments interventions address unique pathological changes that occur during stage. Additionally, paper reviews current treatment modalities pharmacological based evolving guidelines provided by American Heart Association (AHA). Recent advances our understanding will facilitate clinicians’ improved reduce incidence delayed cerebral ischemia patients.

Language: Английский

Citations

15

The role of crosstalk between cerebral immune cells and peripheral immune cells in the damage and protection of blood–brain barrier after intracerebral hemorrhage DOI Creative Commons
Yihui Wang,

Wen-Cao Liu,

Jianing Zhang

et al.

Brain Hemorrhages, Journal Year: 2024, Volume and Issue: 5(3), P. 117 - 130

Published: Feb. 15, 2024

Blood-brain barrier (BBB) damage is a major pathological change after intracerebral hemorrhage (ICH) and both the cause result of brain edema inflammatory response post-ICH. Cerebral immune cells (CICs), including microglia, pericytes, astrocytes play crucial role in protection BBB ICH. Recent evidence suggests that peripheral (PICs) also an important protection, edema, neurological function impairment. Therefore, regulating interactions between glial expected to alleviate ICH-induced damage. In this review, we first introduce CICs, endothelial (ECs), oligodendrocytes (OLs), PICs ICH, focusing on their polarization response. Next, specifically discuss crosstalk CICs PICs, such as brain-spleen axis brain-gut Finally, suggest cells, and, meningeal lymphatic system may be potential targets for alleviating some molecular strategies ICH by modulating ECs, PICs.

Language: Английский

Citations

5

Ion transporter cascade, reactive astrogliosis and cerebrovascular diseases DOI Creative Commons

Md Shamim Rahman,

Rabia Islam, Mohammad Iqbal H. Bhuiyan

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: April 9, 2024

Cerebrovascular diseases and their sequalae, such as ischemic stroke, chronic cerebral hypoperfusion, vascular dementia are significant contributors to adult disability cognitive impairment in the modern world. Astrocytes an integral part of neurovascular unit CNS play a pivotal role homeostasis, including ionic p H balance, neurotransmission, blood flow, metabolism. respond insults, inflammation, through unique molecular, morphological, functional changes, collectively known reactive astrogliosis. The function astrocytes has been subject debate. Initially, were thought primarily supportive maintaining structure nervous system. However, recent studies suggest that may have both beneficial detrimental effects. For example, can cause oligodendrocyte death demyelination. In this review, we will summarize (1) roles ion transporter cascade astrogliosis, (2) related dementias, (3) potential therapeutic approaches for dementing disorders targeting astrocytes. Understanding relationship between cascade, cerebrovascular reveal mechanisms targets development therapies brain associated with

Language: Английский

Citations

5

The role of astrocyte in neuroinflammation in traumatic brain injury DOI Creative Commons
Liang He, Ruqiang Zhang,

Maiqiao Yang

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2023, Volume and Issue: 1870(3), P. 166992 - 166992

Published: Dec. 19, 2023

Language: Английский

Citations

13

mRNA and lncRNA co-expression network in mice of acute intracerebral hemorrhage DOI Creative Commons
Zhe Yu, En Hu, Yiqing Cai

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2023, Volume and Issue: 16

Published: April 28, 2023

Background Intracerebral hemorrhage (ICH) is a severe subtype of stroke lacking effective pharmacological targets. Long noncoding RNA (lncRNA) has been confirmed to participate in the pathophysiological progress various neurological disorders. However, how lncRNA affects ICH outcomes acute phase not completely clear. In this study, we aimed reveal relationship lncRNA-miRNA-mRNA following ICH. Method We conducted autologous blood injection model and extracted total RNAs on day 7. Microarray scanning was used obtain mRNA profiles, which were validated by RT-qPCR. GO/KEGG analysis differentially expressed mRNAs performed using Metascape platform. calculated Pearson correlation coefficients (PCCs) lncRNA-mRNA for co-expression network construction. A competitive endogenous (Ce-RNA) established based DIANALncBase miRDB database. Finally, Ce-RNA visualized analyzed Cytoscape. Results total, 570 313 lncRNAs identified (FC ≥ 2 value p <0.05). The function mainly enriched immune response, inflammation, apoptosis, ferroptosis, other typical pathways. contained 57 nodes (21 36 mRNAs) 38 pairs. ce-RNA generated with 303 (29 lncRNAs, 163 mRNAs, 111 miRNAs) 906 edges. Three hub clusters selected indicate most significant interactions. Conclusion Our study suggests that top molecules may be biomarker Furthermore, pairs correlations provide new clues treatment.

Language: Английский

Citations

11

Ruxolitinib improves the inflammatory microenvironment, restores glutamate homeostasis, and promotes functional recovery after spinal cord injury DOI Creative Commons
Jiang Cao,

Xiao Yu,

Jingcheng Liu

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 19(11), P. 2499 - 2512

Published: Jan. 31, 2024

JOURNAL/nrgr/04.03/01300535-202411000-00030/figure1/v/2024-04-10T160327Z/r/image-tiff The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration functional recovery after spinal cord injury. Ruxolitinib, a JAK-STAT inhibitor, exhibits effectiveness in autoimmune diseases, arthritis, managing cytokine storms. Although studies have shown the neuroprotective potential of ruxolitinib neurological trauma, exact mechanism by which it enhances injury, particularly its effect on astrocytes, remains unclear. To address this gap, we established mouse model T10 contusion found that effectively improved hindlimb motor function reduced area Transcriptome sequencing analysis showed alleviated inflammation immune response restored EAAT2 expression, glutamate levels, excitatory toxicity. Furthermore, inhibited phosphorylation JAK2 STAT3 injured decreased level nuclear factor kappa-B expression factors interleukin-1β, interleukin-6, tumor necrosis factor-α. Additionally, glutamate-induced excitotoxicity increased uptake inhibiting activation STAT3, thereby reducing neurotoxicity, calcium influx, oxidative stress, cell apoptosis, increasing complexity dendritic branching. Collectively, these results indicate restores homeostasis rescuing reduces alleviates responses promoting

Language: Английский

Citations

4

Extracellular vesicle encapsulated Homer1a as novel nanotherapeutics against intracerebral hemorrhage in a mouse model DOI Creative Commons
Xiaowei Fei, Li Wang,

Yanan Dou

et al.

Journal of Neuroinflammation, Journal Year: 2024, Volume and Issue: 21(1)

Published: April 6, 2024

Abstract Homer1a and A2 astrocytes are involved in the regulation of inflammation induced by intracerebral hemorrhage (ICH). However, there is no anticipated treatment strategy based on anti-inflammatory effect astrocytes. Here, we successfully vitro, then report an efficient method to prepare + EVs derived from which making it more stable, safe, targetable injured neurons. promotes conversion A1 ICH mice. inhibits activation nuclear translocation NF-κB, thereby regulating transcription IL-17A RAGE/NF-κB/IL-17 signaling pathway binding ability IL-17A: IL17-AR RAGE: DIAPH1. In addition, ameliorates pathology, behavior, survival rate GFAP Cre Homer1 fl/− ± Nestin RAGE fl/fl Our study provides a novel insight potential for clinical translation ICH.

Language: Английский

Citations

4