Titrated extract of Centella asiatica provides a UVB protective effect by altering microRNA expression profiles in human dermal fibroblasts

An, In‐Sook; An, Sungkwan; Kang, ⋅Sang-Mo; Choe, Taeboo; Lee, Sung Nae; Jang, Hyun Hee; Bae, Seunghee

doi:10.3892/ijmm.2012.1117

Cited by 29 publications

(24 citation statements)

References 42 publications

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“…Moreover, An et al studying the protective activity of a titrated extract of Centella asiatica against photoaging showed that the extract may serve as a potential natural chemoprotective agent against UVB-mediated damage through inducing changes in the expression of specific miRNAs in dermal fibroblasts. Using functional bioinformatic tools, it was determined that miRNAs that showed alteration in expression after treatment with the extract were functionally related with inhibition of apoptosis, positive regulation of cell proliferation and activation of MAP Kinases [35]. …”

Section: Micrornas and Uv-exposed Skinmentioning

confidence: 99%

MicroRNAs in Skin Response to UV Radiation

Syed

Khan²,

Shabbir³

et al. 2013

CDT

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Solar ultraviolet (UV) radiation, an ubiquitous environmental carcinogen, is classified depending on the wave-length, into three regions; short-wave UVC (200–280 nm), mid-wave UVB (280–320 nm), and long-wave UVA (320–400 nm). The human skin, constantly exposed to UV radiation, particularly the UVB and UVA components, is vulnerable to its various deleterious effects such as erythema, photoaging, immunosuppression and cancer. To counteract these and for the maintenance of genomic integrity, cells have developed several protective mechanisms including DNA repair, cell-cycle arrest and apoptosis. The network of damage sensors, signal transducers, mediators, and various effector proteins is regulated through changes in gene expression. MicroRNAs (miRNAs), a group of small non-coding RNAs, act as post-transcriptional regulators through binding to complementary sequences in the 3′-untranslated region of their target genes, resulting in either translational repression or target degradation. Recent studies show that miRNAs add an additional layer of complexity to the intricately controlled cellular responses to UV radiation. This review summarizes our current knowledge of the role of miRNAs in the regulation of the human skin response upon exposure to UV radiation.

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Section: Micrornas and Uv-exposed Skinmentioning

confidence: 99%

MicroRNAs in Skin Response to UV Radiation

Syed

Khan²,

Shabbir³

et al. 2013

CDT

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“…MiRNAs are endogenously expressed small RNA molecules that mediate posttranscriptional gene silencing and have the capacity to simultaneously regulate tens to hundreds of target genes [9]. As a result, they are potential targets for anti-aging, and more specifically anti-photoaging, therapy [10, 11]. For example, a recent unbiased miRNA screen discovered that miR-34c-5p human primary dermal fibroblasts from UVB-induced premature senescence via regulations of some senescence-related molecules [12].…”

Section: Introductionmentioning

confidence: 99%

MiR-23a-depressed autophagy is a participant in PUVA- and UVB-induced premature senescence

Zhang

Zhou

et al. 2016

Oncotarget

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Autophagy is a cellular catabolic mechanism that is activated in response to stress conditions, including ultraviolet (UV) irradiation, starvation, and misfolded protein accumulation. Abnormalities in autophagy are associated with several pathologies, including aging and cancer. Furthermore, recent studies have demonstrated that microRNAs (miRNAs) are potent modulators of the autophagy pathway. As a result, the current study aims to elucidate the role of the autophagy-related miRNA miR-23ain the process of photoaging. Experiments demonstrated that the antagomir-mediated inactivation of miR-23a resulted in the stimulation of PUVA- and UVB-depressed autophagy flux and protected human fibroblasts from premature senescence. Furthermore, AMBRA1 was identified as a miR-23a target. AMBRA1 cellular levels increased following the introduction of miR-23a antagomirs. And a bioinformatics analysis revealed that the AMBRA1 3′ UTR contains functional miR-23a responsive sequences. Finally, it was also demonstrated that both AMBRA1 overexpression and Rapamycin treatment were both able to rescue fibroblasts from PUVA and UVB irradiation-induced autophagy inhibition, but that these effects could also be mitigated by miR-23a overexpression. Therefore, this study concludes that miR-23a-regulated autophagy is a novel and important regulator of ultraviolet-induced premature senescence and AMBRA1 is a rate-limiting miRNA target in this pathway.

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“…The fusion gene of HPRT-SS-luciferase was analyzed by cDNA sequencing. We confi rmed that TECA and EGCG-treatment decreased UV-induced cell accumulation in the sub-G1 phase (apoptosis phase), indicating that these reagents block UV-induced cell death in human dermal fi broblasts (14,15). Changes in the number of mutations aft er treatment of DREAM-F cells with each reagent and UV irradiation are currently under investigation.…”

Section: Other Potential Applications Of the Dream Systemmentioning

confidence: 79%

“…Our group recently found that TECA exerts a UV-protective eff ect in human dermal fi broblasts by downregulating UV-induced cellular and DNA damage (14). Furthermore, it was demonstrated that EGCG has a UV-protective eff ect in human dermal fi broblasts (15).…”

Section: Establishing a System To Identify Novel Reagents Regulating mentioning

confidence: 99%

Development of a high-throughput screening system for identification of novel reagents regulating DNA damage in human dermal fibroblasts

Bae

2015

Acta Pharmaceutica

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Development of a high-throughput screening system for identifi cation of novel reagents regulating DNA damage in human dermal fi broblasts Ultraviolet (UV) radiation is a major inducer of skin aging and accumulated exposure to UV radiation increases DNA damage in skin cells, including dermal fi broblasts. In the present study, we developed a novel DNA repair regulating material discovery (DREAM) system for the high-throughput screening and identifi cation of putative materials regulating DNA repair in skin cells. First, we established a modifi ed lentivirus expressing the luciferase and hypoxanthine phosphoribosyl transferase (HPRT) genes. Then, human dermal fi broblast WS-1 cells were infected with the modifi ed lentivirus and selected with puromycin to establish cells that stably expressed luciferase and HPRT (DREAM-F cells).The fi rst step in the DREAM protocol was a 96-well-based screening procedure, involving the analysis of cell viability and luciferase activity aft er pretreatment of DREAM-F cells with reagents of interest and post-treatment with UVB radiation, and vice versa. In the second step, we validated certain eff ective reagents identifi ed in the fi rst step by analyzing the cell cycle, evaluating cell death, and performing HPRT-DNA sequencing in DREAM-F cells treated with these reagents and UVB. This DREAM system is scalable and forms a time-saving high-throughput screening system for identifying novel anti-photoaging reagents regulating DNA damage in dermal fi broblasts.Keywords: human dermal fi broblasts, DNA damage, high --throughput screening, agingThe skin is the largest organ and forms the outermost layer of the human body. Therefore, the skin is more easily exposed to toxic environmental agents, particularly ultraviolet (UV) radiation, than are other tissues, except for the eyes. Human skin consists of the epidermis, dermis and hypodermis. The most abundant cells in the dermis layer are human dermal fi broblasts (HDFs), which contribute to skin fi rmness and elasticity by upregulating

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Titrated extract of Centella asiatica provides a UVB protective effect by altering microRNA expression profiles in human dermal fibroblasts

Cited by 29 publications

References 42 publications

MicroRNAs in Skin Response to UV Radiation

MicroRNAs in Skin Response to UV Radiation

MiR-23a-depressed autophagy is a participant in PUVA- and UVB-induced premature senescence

Development of a high-throughput screening system for identification of novel reagents regulating DNA damage in human dermal fibroblasts

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