MicroRNAs as biological regulators in skin disorders

Singhvi, Gautam; Manchanda, Prachi; Rapalli, Vamshi Krishna; Dubey, Sunil Kumar; Gupta, Gaurav; Dua, Kamal

doi:10.1016/j.biopha.2018.09.090

Cited by 65 publications

(44 citation statements)

References 102 publications

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“…MicroRNAs belong to small, noncoding RNAs that represent crucial regulators of cell differentiation, proliferation, apoptosis and immune response [25,28]. Thus far, according to miRBase, 1917 microRNAs encoding sequences have been determined in the human genome.…”

Section: Micrornamentioning

confidence: 99%

“…2). Synthesis of miRNA starts within nucleus where RNA polymerase II transcribes genes encoding miRNA to form primary microRNA (pri-microRNA)-a steam loop structure that is composed of several hundred to few thousands nucleotides [13,28]. The primary transcript is cleaved by microprocessor complex (RNase III enzyme Drosha and DGCR8) into premature miRNA (pre-microRNA) that consists of 60-70 nucleotides [5,8].…”

Section: Micrornamentioning

confidence: 99%

“…The primary transcript is cleaved by microprocessor complex (RNase III enzyme Drosha and DGCR8) into premature miRNA (pre-microRNA) that consists of 60-70 nucleotides [5,8]. Pre-microRNA is then translocated into the cytoplasm by exportin-5 (XPO5) and further processed by endonuclease Dicer into mature double-stranded microRNA (22 nucleotides long) [3,28]. One strand (passenger stands/complementary stand) is destructed by Argonaute proteins, the other strand (guide strand/mature strand) associates with RISC (RNA-induced silencing complex).…”

Section: Micrornamentioning

confidence: 99%

“…One strand (passenger stands/complementary stand) is destructed by Argonaute proteins, the other strand (guide strand/mature strand) associates with RISC (RNA-induced silencing complex). The mature miRNA interact with 3′untranslated region (UTR) of target mRNA by one of two mechanisms of gene regulation-mRNA degradation or repression of mRNA translation, depending on the degree of complementarity of microRNA and mRNA [13,28]. Compelling complementarity lead to mRNA degradation, whereas confined complementarity guide repression of mRNA translation [3,28].…”

Section: Micrornamentioning

confidence: 99%

See 3 more Smart Citations

MicroRNA in localized scleroderma: a review of literature

2019

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Section: Micrornamentioning

confidence: 99%

Section: Micrornamentioning

confidence: 99%

Section: Micrornamentioning

confidence: 99%

Section: Micrornamentioning

confidence: 99%

See 2 more Smart Citations

MicroRNA in localized scleroderma: a review of literature

2019

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“…MicroRNAs (miRNAs) are small noncoding RNAs functioning as biological regulators in some skin diseases . In previous study, we found that miR‐100‐5p was downregulated in both familial HS and keratinocyte‐specific Ncstn ‐knockout ( Ncstn ΔKC ) mice .…”

mentioning

confidence: 99%

AKT‐dependent hyperproliferation of keratinocytes in familial hidradenitis suppurativa with a NCSTN mutation: a potential role of defective miR‐100‐5p

et al. 2019

Br J Dermatol

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miR‐203a‐3p promotes loureirin A‐induced hair follicle stem cells differentiation by targeting Smad1

Luo

Dou

Xie

et al. 2020

The Anatomical Record

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MicroRNAs (miRNAs) participate in the repair of skin trauma. Our previous study indicated that loureirin A promoted hair follicle stem cells (HFSCs) to repair skin epidermis. However, the mechanism of miRNA‐mediated regulation of loureirin A‐induced HFSC differentiation remained to be explored. In the present study, HFSCs from rat vibrissa were identified by immunofluorescence in vitro. Microarray and quantitative real time polymerase chain reaction analyses demonstrated that miR‐203a‐3p was upregulated in differentiated HFSCs induced by loureirin A. The expression of cytoskeletal keratin (CK) 5 and involucrin was promoted by miR‐203a‐3p mimics while repressed by a miR‐203a‐3p inhibitor. Smad1 was identified as a key target of miR‐203a‐3p using target prediction tools. Luciferase reporter gene test confirmed a special target association between miR‐203a‐3p and Smad1. Short interfering Smad1 was transfected into HFSCs, and the expression levels of CK5 and involucrin were upregulated. Thus, it can be inferred that miR‐203a‐3p negatively regulated the expression of Smad1 and promoted the differentiation of loureirin A‐induced HFSCs. Bone morphogenetic protein (BMP) signal inhibition and Wnt activation coregulate skin injury repair. BMP/Smad1 signaling is involved in maintaining the characteristics of HFSCs and inhibiting their differentiation. Our results showed that miR‐203a‐3p reduces Smad1 to release BMP inhibition. Taken together, miR‐203a‐3p/Smad1 is a potential therapeutic molecular target in skin wound healing, and may play an active role in wound repair and regenerative medicine.

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MicroRNAs as biological regulators in skin disorders

Cited by 65 publications

References 102 publications

MicroRNA in localized scleroderma: a review of literature

MicroRNA in localized scleroderma: a review of literature

AKT‐dependent hyperproliferation of keratinocytes in familial hidradenitis suppurativa with a NCSTN mutation: a potential role of defective miR‐100‐5p

miR‐203a‐3p promotes loureirin A‐induced hair follicle stem cells differentiation by targeting Smad1

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