Table 5.

Rat retinal miRs showing higher connectivity in the large gene networks associated with early and late post-IR injury periods along with their reported activities in other systems and relevant citations

miRNA	Time point	Regulation/function	Refs
Rno-miR-495	Early (24 h)	inhibition of miR-495 increased neovascularization and recovery of blood flow after cardiac ischemia in mice	[60]
Rno-miR-214		miR-214 protected the mouse heart from ischemic injury by controlling Ca2+ overload and cell death	[61]
Rno-miR-298		miR-298 was up-regulated in brain and blood after ischemic stroke	[62]
Rno-miR-206		miR-206 was significantly deregulated during the conditions of unfolded protein response in H9c2 rat cardiomyoblasts	[79]
Rno-miR-221		miR-221 was suggested as a biomarker for cerebrovascular disease. Stroke patients and atherosclerosis subjects showed significantly lower miR-221 serum levels than healthy controls	[80]
Rno-miR-873	Late (7d)	miR-873 was up-regulated after onset of focal cerebral ischemia in mice	[63]
Rno-miR-223		miR-223 targeted glutamate receptors in mice brain. Overexpression of miR-223 decreased the levels of GluR2 and NR2B, inhibited NMDA-induced calcium influx in hippocampal neurons, and protected the brain from neuronal cell death following transient global ischemia and excitotoxic injury	[64]
Rno-miR-185		miR-185 has been associated with inflammatory responses during brain ischemic stroke in mice and may provide underlying target for prevention and treatment of stroke	[65]
Rno-miR-329		Inhibition of miR-329 increased neovascularization and blood flow recovery after ischemia in mice subjected to double femoral artery ligation	[60]
Rno-miR-138		hypoxia-induced miR-138 is an essential mediator of endothelial cell dysfunction via targeting S100A1 Ca2+ sensor	[81]