Molecular signalings in keloid disease and current therapeutic approaches from natural based compounds

Unahabhokha, Thitita; Sucontphunt, Apirada; Nimmannit, Ubonthip; Chanvorachote, Pithi; Yongsanguanchai, Nuttida; Pongrakhananon, Varisa

doi:10.3109/13880209.2014.918157

Cited by 53 publications

(50 citation statements)

References 50 publications

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“…In recent years, the relationship between insulin-like growth factor (IGF)-1 and the scar has received increasing attention [15]. Studies displayed that the expression of IGF-1 in the wound area was upregulated after the injury of cornea, skin and other tissues [16], and exogenous IGF-1 could improve the healing of skin and wounds [17].…”

Section: Introductionmentioning

confidence: 99%

Baicalein inhibits proliferation and collagen synthesis of mice fibroblast cell line NIH/3T3 by regulation of miR-9/insulin-like growth factor-1 axis

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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The aberrant scar is a challenging problem. Baicalein has effects in attenuating hypertrophic scar formation. Herein, the roles of baicalein in NIH-3T3 were obtained. Cells were treated by baicalein. CCK-8 method and western blot were used to detect cell viability and proliferation-related factors. Furthermore, collagen 1, collagen 3 and a-SMA expression were detected by qRT-PCR and western blot. Besides, total soluble collagen was detected by Sircol assay. In addition, the levels of NF-jB and Wnt/b-catenin signal pathways related factors were determined by western blot. The relationship between miR-9 and insulin-like growth factor (IGF)-1 were tested by luciferase reporter assay, qRT-PCR and western blot. We found baicalein cell restrained proliferation and collagen production. Besides, baicalein increased expression of miR-9 and further experiments validated that transfection with miR-9 inhibitor reversed the results led by baicalein. Moreover, baicalein decreased the phosphorylation of pathway-related proteins while transfection with miR-9 inhibitor revised this result. Otherwise, IGF-1 was authenticated as a target of miR-9 and si-IGF-1 reversed the miR-9 inhibitor-induced change in cell proliferation and collagen production. In conclusion, baicalein restrained cell proliferation and collagen production by regulating miR-9/IGF-1 axis through NF-jB and Wnt/b-catenin signal pathways. HIGHLIGHTS:1. Baicalein restrains NIH/3T3 cell proliferation and collagen production. 2. Baicalein restrains NF-jB and Wnt/b-catenin signal pathways. 3. IGF-1 is a target of miR-9. 4. Baicalein exerts its functions by regulating miR-9/IGF-1 axis. ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 99%

Baicalein inhibits proliferation and collagen synthesis of mice fibroblast cell line NIH/3T3 by regulation of miR-9/insulin-like growth factor-1 axis

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Chen et al (8) found 250 upregulated and 152 downregulated genes in keloid compared with normal skin. Moreover, several signaling pathways and transcriptional factors are found associated (9,10). However, the precise linkage gene and pathological process are still controversial.…”

Section: Introductionmentioning

confidence: 99%

LncRNA expression profiles and validation in keloid and normal skin tissue

Liang

Long

et al. 2015

International Journal of Oncology

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Keloid is a type of pathological skin scar. Pathogenesis of keloid is complex and is not fully understood. lncRNA can regulate gene expression on different levels. It also participates in cell cycle regulation and cell proliferation. The present study investigated the potential biological function of lncRNA in keloid. We identified differential expression of lncRNAs and mRNAs between 3 pairs of keloid and normal skin tissue by microarray. Differentially expressed lncRNAs were validated by quantitative reverse transcriptase-PCR (qRT-PCR). Gene ontology (GO) and pathway analysis presented the characteristics of associated protein-coding genes. Additionally, a co-expression network of lncRNA and mRNA was constructed to find potential underlying regulation targets. There were 1,731 lncRNAs constantly upregulated and 782 downregulated, 1,079 mRNAs upregulated and 3,282 downregulated in keloid respectively (fold change ≥ 2.0, p<0.05). We chose, respectively, 3 upregulated and 1 downregulated lncRNA for qRT-PCR and results were consistent with microarray. Moreover, 11 pathways were related with upregulated transcripts and 44 with downregulated in keloid. The co-expression network revealed that one lncRNA was connected with numerous mRNAs, and vice versa. Furthermore, bioinformation analysis suggested that lncRNA CACNA1G-AS1 may be crucial to keloid formation. In conclusion, groups of lncRNAs were aberrantly expressed in keloid compared with normal skin tissue, which indicated that differentially expressed lncRNAs may play a key role in keloid formation. The present study provides new insights into keloid pathology and potential targets for treatment of keloid.

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“…R epresenting the extreme end of the cutaneous scarring spectrum, keloid disease is a fibroproliferative tumour characterised by excess extracellular matrix (ECM) deposition, increased inflammatory cytokine expression and aggressive local invasion (1). Although keloid is often referred to as benign, in that it does not metastasize, it behaves in a tumorigenic fashion by actively invading adjacent normal skin and spreading beyond the boundaries of the original wound (2,3). To date, although significant progress has been made, the mechanisms underlying the migration required for keloid invasion have not been fully elucidated.…”

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confidence: 99%

A Role for Neuregulin-1 in Promoting Keloid Fibroblast Migration via ErbB2-mediated Signaling

Jumper¹,

Hodgkinson²,

Paus³

2017

Acta Derm Venerol

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Keloid disease is a fibroproliferative tumour characterised by aggressive local invasion, evident from a clinically and histologically active migrating margin. During combined laser capture microdissection and microarray analysis-based in situ gene expression profiling, we identified upregulation of the polypeptide growth factor neuregulin-1 (NRG1) and ErbB2 oncogene in keloid margin dermis, leading to the hypothesis that NRG1 contributed to keloid margin migration through ErbB2-mediated signalling. The aim of this study was to probe this hypothesis through functional in vitro studies. Exogenous NRG1 addition to keloid and normal skin fibroblasts altered cytokine expression profiles, significantly increased in vitro migration and keloid fibroblast Src and protein tyrosine kinase 2 (PTK2/FAK) gene expression. ErbB2 siRNA knockdown attenuated both keloid fibroblast migration and Src/PTK2 expression, which were not recovered following NRG1 administration, suggesting the NRG1/ErbB2/Src/PTK2 signaling pathway may be a novel regulator of keloid fibroblast migration, and representing a potential new therapeutic target.

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Molecular signalings in keloid disease and current therapeutic approaches from natural based compounds

Abstract: The present review may be helpful to future studies that further examine the molecular mechanism of keloid etiology as well as investigate the anti-keloid property in natural compounds.

Cited by 53 publications

References 50 publications

Baicalein inhibits proliferation and collagen synthesis of mice fibroblast cell line NIH/3T3 by regulation of miR-9/insulin-like growth factor-1 axis

Baicalein inhibits proliferation and collagen synthesis of mice fibroblast cell line NIH/3T3 by regulation of miR-9/insulin-like growth factor-1 axis

LncRNA expression profiles and validation in keloid and normal skin tissue

A Role for Neuregulin-1 in Promoting Keloid Fibroblast Migration via ErbB2-mediated Signaling

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