Beyond the neuron: Role of non-neuronal cells in stress disorders

Neuron, Год журнала: 2022, Номер 110(7), С. 1116 - 1138

Опубликована: Фев. 18, 2022

Язык: Английский

---

Role of lipocalin 2 in stroke

Neurobiology of Disease, Год журнала: 2023, Номер 179, С. 106044 - 106044

Опубликована: Фев. 17, 2023

Stroke is the second leading cause of death worldwide; however, treatment choices available to neurologists are limited in clinical practice. Lipocalin 2 (LCN2) a secreted protein, belonging lipocalin superfamily, with multiple biological functions mediating innate immune response, inflammatory iron-homeostasis, cell migration and differentiation, energy metabolism, other processes body. LCN2 expressed at low levels brain under normal physiological conditions, but its expression significantly up-regulated acute stimulations chronic pathologies. An up-regulation has been found blood/cerebrospinal fluid patients ischemic/hemorrhagic stroke, could serve as potential biomarker for prediction severity stroke. activates reactive astrocytes microglia, promotes neutrophil infiltration, amplifies post-stroke inflammation, blood-brain barrier disruption, white matter injury, neuronal death. Moreover, involved injury induced by thrombin erythrocyte lysates, well microvascular thrombosis after hemorrhage. In this paper, we review role pathological ischemic stroke; intracerebral hemorrhage; subarachnoid stroke-related diseases, such vascular dementia depression, their underlying mechanisms. We hope that will help elucidate value therapeutic target

Язык: Английский

---

Microglial IL‐1RA ameliorates brain injury after ischemic stroke by inhibiting astrocytic CXCL1‐mediated neutrophil recruitment and microvessel occlusion

Glia, Год журнала: 2023, Номер 71(7), С. 1607 - 1625

Опубликована: Март 17, 2023

Acute ischemic stroke (AIS), one of the leading causes mortality worldwide, is characterized by a rapid inflammatory cascade resulting in exacerbation brain injury. Microglia are first immune responders. However, role postischemic microglial activity injury remains far from being fully understood. Here, using transgenic mouse line CX3 CR1creER :R26iDTR to genetically ablate microglia, we showed that deletion exaggerated Associated with this worse outcome, there were increased neutrophil recruitment, microvessel blockade and blood flow stagnation acute phase, accompanied transcriptional upregulation chemokine (C-X-C motif) ligand 1 (CXCL1). Our study interleukin-1 receptor antagonist (IL-1RA) suppressed astrocytic CXCL1 expression induced oxygen glucose deprivation inhibited migration. Furthermore, neutralizing antibody therapy against or administration recombinant IL-1RA protein reduced infarct volume improved motor coordination performance mice after stroke. suggests microglia protect secreting inhibit expression, which reduces recruitment neutrophil-derived occlusion.

Язык: Английский

---

Reactive Astrocytes and Emerging Roles in Central Nervous System (CNS) Disorders

Cold Spring Harbor Perspectives in Biology, Год журнала: 2024, Номер 16(7), С. a041356 - a041356

Опубликована: Фев. 5, 2024

In addition to their many functions in the healthy central nervous system (CNS), astrocytes respond CNS damage and disease through a process called "reactivity." Recent evidence reveals that astrocyte reactivity is heterogeneous spectrum of potential changes occur context-specific manner. These are determined by diverse signaling events vary not only with nature severity different insults but also location CNS, genetic predispositions, age, potentially "molecular memory" previous events. Astrocyte can be associated both essential beneficial as well harmful effects. The available information rapidly expanding much has been learned about molecular diversity reactivity. Emerging functional associations point toward roles for determining outcome disorders.

Язык: Английский

---

M2 Microglia-derived Exosomes Promote Spinal Cord Injury Recovery in Mice by Alleviating A1 Astrocyte Activation

Molecular Neurobiology, Год журнала: 2024, Номер 61(9), С. 7009 - 7025

Опубликована: Фев. 17, 2024

Язык: Английский

---