Publications by authors named "Mei-Juan Shi"

Article Synopsis
  • Increasing evidence suggests that neuroinflammation plays a role in the progression of Parkinson's disease (PD), with long noncoding RNAs (lncRNAs) significantly impacting inflammatory processes in various diseases.
  • The study focused on lncRNA KCNQ1OT1, finding that its knockdown reduced microglial NLRP3 inflammasome activation and decreased dopaminergic neuronal loss in PD model mice.
  • KCNQ1OT1 functions by binding with miR-186 to promote inflammasome activation and inhibit its silencing, revealing a new regulatory network that could inform future treatments for Parkinson's disease.
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Blood-brain barrier (BBB) breakdown and inflammation occurring at the BBB have a key, mainly a deleterious role in the pathophysiology of ischemic stroke. Neddylation is a ubiquitylation-like pathway that is critical in various cellular functions by conjugating neuronal precursor cell-expressed developmentally down-regulated protein 8 (NEDD8) to target proteins. However, the roles of neddylation pathway in ischemic stroke remain elusive.

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Intracerebral hemorrhage associated with thrombolytic therapy with tissue plasminogen activator (tPA) in acute ischemic stroke continues to present a major clinical problem. Here, we report that infusion of tPA resulted in a significant increase in markers of neutrophil extracellular traps (NETs) in the ischemic cortex and plasma of mice subjected to photothrombotic middle cerebral artery occlusion. Peptidylarginine deiminase 4 (PAD4), a critical enzyme for NET formation, is also significantly upregulated in the ischemic brains of tPA-treated mice.

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Article Synopsis
  • - Neutrophils gather in the brain after a stroke, particularly between 3-5 days post-event, and their release of neutrophil extracellular traps (NETs) hinders brain repair by damaging the blood-brain barrier (BBB) and impeding new blood vessel formation.
  • - The enzyme PAD4, essential for NET formation, is elevated in the affected brain regions, and its excess leads to more NETs, worsened BBB integrity, and decreased neovascularization.
  • - Strategies to break down NETs or inhibit their formation, such as using DNase 1 or targeting PAD4, result in improved vascular repair, less BBB damage, and better recovery after a stroke.
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Biological modifications of the silk fibroin (silk) material have broad applications in textiles, biomedical materials and other industrial materials. It is economical to incorporate nanoparticles to the biosynthesis of silk fibroin by adding them to silkworm larval diets. This strategy may result in the rapid stable production of modified silk.

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As a relay center between the cerebral cortex and various subcortical brain areas, the thalamus is repeatedly associated with the dysfunction of brain-gut interaction in patients with irritable bowel syndrome (IBS). However, the regional morphological alterations of the thalamus in IBS are not well defined. We acquired structural magnetic resonance data from 34 patients with IBS and 34 demographically similar healthy subjects.

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Blood-brain barrier (BBB) defects and cerebrovascular dysfunction contribute to amyloid-β (Aβ) brain accumulation and drive Alzheimer disease (AD) pathology. By regulating vascular functions and inflammation in the microvasculature, a disintegrin and metalloprotease with thrombospondin type I motif, member 13 (ADAMTS13) plays a significant protective effect in atherosclerosis and stroke. However, whether ADAMTS13 influences AD pathogenesis remains unclear.

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Growth differentiation factor 11 (GDF11), a member of transforming growth factor-β (TGF-β) superfamily, was shown to rejuvenate cardiac and skeletal muscle function and to improve cerebral vasculature and neurogenesis in old mice. However, recent experimental data reported that raising GDF11 levels inhibited skeletal muscle regeneration and had no effect on cardiac hypertrophy. Our aim was to investigate the effects of GDF11 on brain repair during the recovery phase after stroke.

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