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Related Experiment Video

Updated: Sep 14, 2025

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Lars2 Deficiency-Induced Mitochondrial Dysfunction Drives the Emergence of a Pro-Inflammatory Stroke-Specific

Qing Zou¹, Jianxin Zhou¹, Ying Li¹

¹School of Life Sciences, Shanghai University, Shanghai, China.

Aging and Disease

|July 18, 2025

Summary

Stroke triggers a distinct microglial subset (Mc) with low leucyl-tRNA synthetase 2 (Lars2) expression and pro-inflammatory features. Lars2 deficiency impairs mitochondrial repair, driving neuroinflammation post-stroke.

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Published on: December 28, 2014

Area of Science:

Neuroscience
Immunology
Cell Biology

Background:

Microglial immune status is altered post-stroke, extending beyond M1/M2 classifications.
Stroke induces changes in mitochondrial autophagy and assembly processes in microglia.

Purpose of the Study:

To identify novel microglial subsets and molecular mechanisms involved in post-stroke neuroinflammation.
To investigate the role of leucyl-tRNA synthetase 2 (Lars2) in microglial function and response to stroke.

Main Methods:

Single-cell RNA sequencing of mouse striatal microglia after hemorrhagic and ischemic stroke.
Gene Ontology functional enrichment analysis and cell-cell communication analysis.
In vitro experiments involving Lars2 overexpression and conditioned media treatments.

Main Results:

A distinct microglial subset (Mc) with low Lars2 expression was identified post-stroke.
Lars2 deficiency correlated with impaired mitochondrial function and increased pro-inflammatory cytokine release.
The pleiotrophin-syndecan-4 (PTN-SDC4) pathway was identified as a key mediator in neuron-Mc communication.

Conclusions:

Mc represents a stroke-induced pro-inflammatory microglial population characterized by low Lars2 expression.
Lars2 acts as a mitochondrial checkpoint, linking microglial reprogramming to neuroinflammation after stroke.
Targeting Lars2 or the PTN-SDC4 pathway may offer therapeutic strategies for stroke recovery.