Microglial Responses after Ischemic Stroke and Intracerebral Hemorrhage

Table 1

Mediators of microglial activation after cerebral ischemia and intracerebral hemorrhage.

Mediator	Measurements used	Results	Citation
Ischemic stroke
Galectin 3	Galectin 3^−/− mice subjected to 60-minute MCAO followed by reperfusion for either 24 or 72 hours	Galectin 3 reduces cell death and infarct volume	[23]
Notch	Primary cell cultures and in  vivo models of microglial activation (LPS) and MCAO in antisense Notch mice	Notch leads to increased neuroinflammation	[44]
SPARC	Focal photothrombotic model of ischemic stroke in SPARC^−/− mice	SPARC^−/− microglia have increased processes length and branching and increased microgliosis	[45]
HMGB1	shRNA and HMGB1 inhibitor used to knock down HMGB1 in ischemic stroke model and primary microglial cultures	HMGB1 promotes neuroinflammation	[46–48]
CX3CL1	Behavioral outcomes, edema, peripheral cell infiltration, cytokine production in CX3CR1 knockout mice in 30- and 60-minute MCAO	CX3CL1-CX3CR1 signaling leads to worse functional outcome and higher neuroinflammation	[49–54]
Intracerebral hemorrhage
Thrombin	Thrombin injection in rats and in culture caused neuronal apoptosis and increased cytokine production	Activates microglia and promotes cytokine production	[55–60]
Heme	Blood or hemin injection	Activates microglia and leads to neuroinflammation	[61–63]

SPARC: secreted protein acidic rich in cysteine; HMGB1: high mobility group box 1.