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Analysis of Microglial Phagocytosis in Ischemic Stroke

Microglia are the main phagocytes in the central nervous system and are responsible for removing myelin debris and pruning synapses. Whether microglia-mediated phagocytosis plays a beneficial or detrimental role in stroke is still unclear and requires further investigation. Microglia phagocytose tissue debris in experimental models of ischemic stroke, which contributes to tissue repair and neuronal network reconstruction. However over-activated microglia phagocytose live or stressed neuronal cells, leading to neurological deficits and brain atrophy. Following an ischemic challenge, microglial phagocytosis is caused by the exposure to "eat me" signals or the loss of "don't eat me" signals. The stroke research and clinical community needs to seek new research directions, and microglial phagocytosis is a promising frontier.

Fig. 1. Microglia phagocytose tissue debris in experimental models of ischemic stroke.Fig. 1. The engulfment properties of microglia and its potential pathological outcome after ischemic stroke. (Jia et al., 2022)

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At Ace Therapeutics, we focus on analyzing the role of microglial phagocytosis in ischemic stroke. Our cutting-edge methods and expertise help clients investigate the potential microglial phagocytosis as a therapeutic target for stroke.

Identifying and Validating Targets Associated with Microglial phagocytosis for Stroke

We help clients identify potential therapeutic targets that improve neurological function after stroke by analyzing multiple molecular mechanisms and cellular pathways associated with microglial phagocytosis. We offer single-cell RNA sequencing technology to analyze the heterogeneity of microglia populations in the brain of transient middle cerebral artery occlusion (tMCAO) animals. By analyzing the transcriptome of individual microglia, we help clients determine the number of distinct cell populations in samples, calculate differential gene expression between clusters, and identify biological pathways enriched in each cluster.

  • TREM-2/DAP12/ERK/PKC pathway
  • TLR mediated phagocytosis by MyD88-dependent IRAK4/p38/scavenger receptors pathway or MyD88-independent actin-Cdc42/Rac signaling pathway
  • TAM receptor
  • P2Y6R/PLC/InsP3 pathway
  • The phosphatidylserine receptor PS
  • CD47-SIRPα signaling
  • C1q/C3 system

Mechanism Analysis of Microglial Phagocytosis in Experimental Models of Stroke

We offer multiple techniques (e.g. optical, genetic, chemical genetic, and behavioral approaches) to measure microglial phagocytosis in animal and in vitro models of ischemic stroke. We aim to help clients analyze the mechanisms of microglia-mediated phagocytosis in ischemic injury and discover new therapeutic targets for stroke.

Stroke Drug Development Servies Targeting Microglial phagocytosis

Our experts are actively help clients develop potential microglia-based interventions for stroke. Specific protocols can be customized to meet client needs.

  • Microglia-targeted pharmacotherapy for stroke
  • Microglia-targeted stem cell therapies for stroke
  • Microglia-targeted Dietary therapy for stroke

Ace Therapeutics provides reliable services to analyze the molecular mechanisms of microglial phagocytosis and develop stroke drugs that selectively modulate microglial phagocytosis. If you are interested in our services, please do not hesitate to contact us!

Reference
  1. Jia, J., et al. (2022). The role of microglial phagocytosis in ischemic stroke. Frontiers in immunology, 12, 790201.
All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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