Table 2.

Possible miR targets for vascular tissue engineering dedicated to patients.

miR	Target	Targeted cells	Modulation	Modulation strategy/factor	Outcome	Ref
17–92	Jak1	EC	Downregulation	Antagomir	Increased angiogenesis	[153]
217	SIRT1	EC	Downregulation	Antagomir	Reduced senescence and increased angiogenesis	[73]
34	Vinculi, Notch1, semaphorin 4B	EC	Downregulation	LNA	Increased angiogenesis	[76]
143/145	Klf-2	EC, VSMC	Upregulation	Laminar shear stress	Inhibit VSMC dedifferentiation	[109]
19a	Cyclin D1	EC	Upregulation	Laminar shear stress	Induce endothelial senescence	[154]
155	MYLK	EC	Upregulation	Laminar shear stress	Inhibit EC proliferation and migration	[155]
92a	Klf-2/4	EC	Upregulation	Low shear stress	Induce endothelial inflammation	[156]
663	Klf-4	EC	Upregulation	Oscillatory shear stress	Induce endothelial inflammation	[157]
126-5p	Dlk-1	EC	Downregulation	Disturbed flow and low shear stress	Inhibit EC proliferation	[158]
10a	MAP3K7	EC	Downregulation	Disturbed flow and low shear stress	Induce EC inflammation, hyperpermeability	[159]
205/712	TIMP3	VSMC	Upregulation	Disturbed flow	Induce VSMC migration	[160]
126	SPRED-1, PIK3R2	EC	Upregulation	Blood flow	Pro-angiogenic	[161]
17-5p	TIMP1	HUVEC	Upregulation	VEGF	Pro-angiogenic	[162]
18a	Tsp1	HUVEC	Upregulation	VEGF	Pro-angiogenic	[162]
31	UD	HUVEC	Upregulation	VEGF	Pro-angiogenic	[162]
155	ATR1	EC	Upregulation	VEGF	Pro-angiogenic	[162]
210	Ephrin A3	EC	Upregulation	Hypoxia	Pro-angiogenic	[65]
424	CUL2	EC	Upregulation	Hypoxia	Pro-angiogenic	[85]
200c	Zeb1	EC	Upregulation	ROS	Induce EC death and senescence	[86]
217	SirT1	EC	Downregulation	Antagomir	Reduce senescence in ageing EC	[73]
34	SirT1	EC	Downregulation	Antagomir	Reduce senescence in ageing EC	[88]
503	CCNE1, cdc25A	EC	Downregulation	Adenovirus-mediated miR-503 decoy delivery	Enhance post LI vascular repair	[90]
101	EZH2	HUVEC	Downregulation	Antagomir	Increased EC tube formation and migration	[91]
132	RasGTPase activating protein, methyl-CpG-binding protein 2	Pericytes	Downregulation	Antagomir	Decreased pericyte capacity to improve contractility, reparative angiogenesis	[78]
143/145	Elk-1, Klf-4	VSMC	Downregulation	Antagomir	Induction of synthetic phenotype	[106]
221/222	p27 (Kip1), p57 (Kip2)	VSMC	Downregulation	2′-O-methyl modified antagomir	Induction of contractile phenotype	[110]
21	Pten, Bcl2	VSMC	Upregulation	TGF-b and BMP signalling	Induction of contractile phenotype	[114]
21	PDCD4, Sprouty-2, PPAR	VSMC	Upregulation	Hypoxia	Induction of synthetic phenotype	[114]
24	Trb3	VSMC	Upregulation	PDGF β	Induction of synthetic phenotype	[112]
34a	SIRT1	VSMC	Upregulation	miR-34a mimic	Induction of cell cycle arrest	[116]
29a	VDAC1/2	VSMC, fibroblasts	Downregulation	miR-29a inhibitor	Induce elastin production	[115]
99b, 181a, 181b	Prox1	hESC	Upregulation	Lentiviral	Enhance efficiency of EC lineage commitment, improved post ischemic blood flow recovery	[11]
200c, 150	Zeb1	hESC	Upregulation	Precursor miR-200c, 150	Induce differentiation to EC	[122]
145	KLF-4/5	hESC	Upregulation	Precursor miR-145	Induce differentiation to VSMC	[126]
1	KLF-4	mESC	Upregulation	miR-1 mimic	Induce differentiation to VSMC	[128]
10a	histone deacetylase 4	mESC	Downregulation	Inhibitor	Reduction in VSMC differentiation	[130]
15a/16	VEGF-A, AKT-3	EPC	Downregulation	Antagomir	Improved survival and migratory capacity	[83]
150	CXCR4	MNC	Downregulation	Lentiviral	Increased MNC migration from bone marrow to peripheral blood	[133]

ECs: endothelial cells, VSMCs: vascular smooth muscle cells, HUVECs: human umbilical vein endothelial cells, hESCs: human embryonic stem cells, mESCs: mouse embryonic stem cells, EPCs: endothelial progenitor cells, MNC: mononuclear cell, UD: undefined.