Table 4.

List of miRNAs whose expression has been down-regulated in the psoriasis.

miRNA	Numbers of clinical samples	Source	Targets/Regulators	Signaling Pathways	Function and comments	Reference
miR-125b	25 psoriasis patients and 27 normal individuals were recruited.	Keratinocytes	FGFR2	Cell proliferation and differentiation	Overexpression of miR-125b in primary human keratinocytes repressed proliferation and induced the expression of several known differentiation markers.	[25]
	A total of 32 psoriasis subjects and 10 healthy volunteers were enrolled in the present study.	Serum, HaCaT and 293T cells	BRD4	Jagged-1/Notch signaling pathway	miR-125b tightly binds to BRD4 and confines the translation process of the Jagged-1 ligand. By suppressing the activation of the Notch signaling pathway, miR-125b inhibits the proliferation of psoriasis cells.	[26]
let-7b	4 patients with psoriasis and 4 healthy subjects were enrolled.	Keratinocytes	IL-6	ERK1/2 signaling pathway	Let-7b directly targets IL-6, an indispensable cytokine regulating cell differentiation, which is induced in the affected epidermis of psoriasis patients.	[27]
miR-145-5p	10 patients with psoriasis and 10 healthy subjects were recruited in this study.	Keratinocytes	MLK3, STAT3 and NF-ҡB	AKT/GSK, MAPK, mTOR and NF-κB signaling pathways	Overexpression of miR-145-5p in normal human epidermal keratinocytes inhibited cell proliferation and production of chemokines. Silencing miR-145-5p enhanced NHEK proliferation and augmented chemokine secretion.	[28]
miR-187	Psoriatic skin samples and adjacent uninvolved psoriatic skin samples were obtained.	Keratinocytes	CD276	CD276‐STAT3 signaling pathways	Overexpression of miR‐187 reduced keratinocytes hyperproliferation.	[29]
miR-194	15 patients with psoriasis and 10 healthy subjects were enrolled in the present study	Keratinocytes	GRHL2		Overexpression of miR-194 repressed the proliferation and stimulated the differentiation of primary human keratinocytes, whereas miR-194 suppression stimulated the proliferation and repressed their differentiation.	[30]
miR-4516	Biopsies from lesional (n = 15) and non-lesional (n = 3) area were obtained from psoriasis patients. Foreskin samples served as healthy controls.	Keratinocytes	FN1, ITGA9, STAT3, Bcl xl and Cyclin D1		miR-4516 silencing in psoriatic skin might contribute in enhanced migration, resistance to apoptosis and differentiation as seen in psoriasis lesional keratinocytes.	[31]
miR-876-5p	Psoriasis and normal skin tissues were collected from 10 psoriasis patients.	Keratinocytes/plasma	Ang-1	PI3K/AKT and ERK signaling pathway	Invasion and adhesion, serving as important behavioral traits of epidermal keratinocytes cells, were suppressed by excessive miR-876-5p in psoriasis cells	[32]
miR-181b-5p	35 cases of psoriatic lesional skin tissues and 25 cases of healthy skin tissues were collected.	Human epidermal keratinocytes (HEKs)	Akt3	Akt/mTOR Signaling	Upregulation of miR-181b-5p inhibited HEKs proliferation at least partly by targeting Akt3.	[33]
miR‐181b	28 patients diagnosed with psoriasis and 20 healthy controls who underwent plastic surgery were recruited.	Human epidermal keratinocytes (HEKs)	TLR4	TLR4 pathway	miR‐181b negatively regulates the proliferation of HEKs in psoriasis and might provide new insights for seeking novel targets of treatment and prognosis of psoriasis.	[11]
miR-486-3p	Psoriatic lesions and the adjacent non-lesional skin were collected from 25 patients. Normal skin harvested from 25 healthy Participants.	Epidermis	K17	TGFβ/SMAD/miR-486-3p Signaling	Downregulated miR-486-3p, allowed over-expression of K17, driving keratinocyte proliferation, and thus contributes to the development of psoriasis.	[34]
miR-126	147 psoriasis patients and 120 healthy volunteers were enrolled in this clinical study.	Plasma			miR-126 plays a positive role in the inhibition of inflammation, and its low concentration may allow a greater influx of inflammatory cells to enter the skin, further aggravating inflammation in psoriasis patients.	[35]
miR-143	In total, 194 psoriasis patients and 175 healthy controls were recruited.	Skin tissues/PBMCs	Bcl-2		miR-143 expression in PBMCs is negatively correlates with disease severity in psoriasis and thus a low-expression of miR-143 in PBMCs would indicate poor prognosis for this disease.	[36]
miR-424	Skin specimens were obtained from 6 psoriasis patients and 6 healthy controls. Serum samples were taken from 15 patients with psoriasis and sex- and age- matched healthy volunteers.	Skin tissue/serum	MEK1	miR-424 ⁄MEK1⁄ cyclin E1 pathway	Inhibiting miR-424 in normal human keratinocytes led to upregulation of MEK1 or cyclin E1 protein, and resulted in increased cell proliferation.	[37]
miR-138	40 patients with psoriasis and 35 healthy subjects were included in this study.	CD4(+) T cells	RUNX3		Overexpression of miR-138 inhibits RUNX3 expression and decreased the ratio of Th1/Th2 in CD4(+) T cells.	[38]