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Updated: Mar 14, 2026
Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
Published on: February 12, 2016
Cell Surface CD36 Protein in Monocyte/Macrophage Contributes to Phagocytosis during the Resolution Phase of Ischemic
Moon-Sook Woo1, Jiwon Yang1, Cesar Beltran1
1From the Burke-Cornell Medical Research Institute, White Plains, New York 10605 and the Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, New York 10065.
Abstract:
Infiltrating monocyte-derived macrophages (M-MΦ) influence stroke-induced brain injury. Although the inflammatory nature of M-MΦ in acute stroke has been well documented, their role during the resolution phase of stroke is less clear. With emerging evidence for the involvement of scavenger receptors in innate immunity, this study addresses an M-MΦ CD36 role in mediating phagocytosis during the recovery phase of stroke. Stroke increases CD36 and TSP-1/2 mRNA levels in the ipsilateral hemisphere at acute (3-day (d)) and recovery (7d) periods. Quantification of total, intracellular, and cell surface CD36 protein levels showed relatively unchanged expression at 3d post-ischemia. At 7d, there was a significant increase in cell surface CD36 (p < 0.05) with a concurrent reduction of intracellular CD36 (p < 0.05) in the ipsilateral hemisphere. Both cell surface and intracellular CD36 were found in whole brain lysates, whereas cell surface CD36 was predominantly detected in isolated brain mononuclear cells, blood monocytes, and peritoneal macrophages, suggesting that cell surface CD36 expressed in the post-ischemic brain originates from the periphery. The stroke-induced CD36 mRNA level correlated with increased expression of lysosomal acid lipase, an M2 macrophage marker. Functionally, higher CD36 expression in M-MΦ is correlated with higher phagocytic indices in post-ischemic brain immune cells. Moreover, pharmacological inhibition of CD36 attenuated phagocytosis in peritoneal macrophages and brain M-MΦ These findings demonstrate that cell surface CD36 on M-MΦ mediates phagocytosis during the recovery phase in post-stroke brains and suggests that CD36 plays a reparative role during the resolution of inflammation in ischemic stroke.
Insights
Monocyte-derived macrophages (M-MΦ) use CD36 to clear debris after stroke. This scavenger receptor on M-MΦ promotes phagocytosis, aiding brain repair during stroke recovery.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Monocyte-derived macrophages (M-MΦ) are key players in brain injury after stroke.
- While their acute inflammatory role is known, their function during stroke recovery is less understood.
- Scavenger receptors are increasingly recognized for their role in innate immunity.
Purpose of the Study:
- To investigate the role of the scavenger receptor CD36 in M-MΦ phagocytosis during the recovery phase of stroke.
- To determine if CD36 expression and function change post-stroke.
- To explore the origin and reparative potential of CD36-expressing M-MΦ in the ischemic brain.
Main Methods:
- Assessed CD36 and TSP-1/2 mRNA levels in mouse stroke models at acute (3-day) and recovery (7-day) stages.
- Quantified CD36 protein expression (total, intracellular, cell surface) in brain hemispheres and isolated immune cells.
- Correlated CD36 expression with lysosomal acid lipase (M2 marker) and phagocytic activity.
- Utilized pharmacological inhibition of CD36 to assess its functional impact on phagocytosis.
Main Results:
- Stroke elevated CD36 mRNA in the brain at 3 and 7 days post-injury.
- Cell surface CD36 significantly increased, while intracellular CD36 decreased at 7 days post-stroke.
- Increased cell surface CD36 on brain M-MΦ correlated with enhanced phagocytic capacity.
- Peripherally derived CD36 was detected on brain M-MΦ, blood monocytes, and peritoneal macrophages.
- CD36 inhibition reduced phagocytosis in both brain M-MΦ and peritoneal macrophages.
Conclusions:
- Cell surface CD36 on M-MΦ mediates phagocytosis during the stroke recovery phase.
- CD36 expression on M-MΦ suggests a reparative role in resolving inflammation after ischemic stroke.
- The findings highlight CD36 as a potential therapeutic target for stroke recovery.
