Ssc-miR-221-3p regulates melanin production in Xiang pigs melanocytes by targeting the TYRP1 gene
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ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE218870 | GEO | 2022/11/30
REPOSITORIES: GEO
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Project description:BackgroundMicroRNAs (miRNAs) are small endogenous non-coding RNAs that regulate gene expression by down-regulating it. Several studies have suggested that miRNAs plays a crucial role in mammalian skin color production. The TYRP1 gene, a member of the tyrosine family, is an important candidate gene that affects melanogenesis. This study aimed to identify genes and miRNAs that affect melanin production in Xiang pigs by transcriptome sequencing, and to validate their targeted regulatory relationships.Results17 miRNAs and 1,230 genes were significantly differentially expressed (P < 0.05) in the black and white skin tissues of Jianbai Xiang pigs. miRNA-221-3p was identified as a candidate miRNA for melanin formation and its target gene, TYRP1, was selected. The TYRP1 gene is a member of the TYR gene family, which evolved from the TYR gene through chromosome segmental duplication. The function of the gene was highly conserved throughout the evolutionary process. overexpression of TYRP1 gene significantly increased the expression of TYR, TYRP1, and DCT genes P < 0.01, which led to an increase in the relative content of melanin. Silencing of TYRP1 through the use of TYRP1-siRNA significantly reduced the expression of TYR, TYRP1, and DCT genes in Jianbai Xiang pig melanocytes P < 0.01, which in turn decreased the relative melanin content. The targeted binding relationship between ssc-miR-221-3p and TYRP1 gene was validated. After transfection of porcine melanocytes with ssc-miR-221-3p mimic, the expression of ssc-miR-221-3p was significantly up-regulated (P < 0.01). Furthermore, the mRNA and protein levels of TYR, TYRP1, and DCT genes were significantly down-regulated (P < 0.01), and melanin content in cells was significantly reduced (P < 0.01).ConclusionThe TYRP1 gene affects melanogenesis in melanocytes of Jianbai Xiang pigs, and ssc-miR-221-3p targets the TYRP1 gene to regulate melanogenesis in melanocytes of Jianbai Xiang pigs.
| S-EPMC10314631 | biostudies-literature
Project description:Nrf2-Keap1 signaling pathway protects cells against photo-oxidative stress. Yet in recent works, its role in melanogenesis together with cell protection functions against oxidative stress has been gaining interest. However, its effect on melanogenesis still has contradictory results from different studies. The aims of our study were to investigate the effect of Keap1 silencing in melanocyte on melanogenesis and its associated mechanism. Primary human epidermal melanocytes and melan-a cell line were used for this experiment. RNA sequencing was done to identify genes involved in melanocyte biology using Keap1 knockdown through siRNA techniques. And melanogenesis and the expression of melanogenesis-associated molecules were evaluated in Keap1 silenced melanocyte to examine the effects of Keap1 on melanogenesis, melanocyte growth, and related pathways. RNA-sequencing data revealed that Keap1 knockdown in primary human epidermal melanocytes (PHEMs) induced cell survival-related gene expression. Additionally, siRNA-mediated inhibition of Keap1 led to upregulation of MITF and melanogenesis-associated molecules along with Nrf2 activation in PHEMs. HO-1, a major gene that is upregulated in RNA-sequencing using Keap1-silenced PHEMs, protected melanocytes against H2O2-induced cell death and upregulated MITF and β-catenin expression. Further, increased expression of melanogenesis-associated molecules after Keap1 silencing was validated to occur through HO-1-associated β-catenin activation in a Keap1 and HO-1 double knockdown experiment. This work suggests that Keap1 silencing in melanocytes induced melanogenesis and the expression of melanogenesis-associated molecules through HO-1-associated β-catenin activation. Keap1 downregulation in melanocytes is important for cell proliferation and survival.
2018-01-20 | GSE93895 | GEO
Project description:Purpose: Determine the mechanism of particulate matter-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with particulate matter (5 μg/cm2) and incubated for 24 h. Total RNA (1 ug) from melanocytes were extracted and subjected to library synthesis. Results: Particulate matter-treated melanocytes exhibited upregulation of ER stress, unfolded protein response, and melanogenesis-related molecules. Conclusion: Particulate matter-induced melanocyte signaling was well evaluated using RNA sequencing.
2021-08-19 | GSE165333 | GEO
Project description:In this study, we sought to determine how IL-17 and TNF influence normal human melanocytes, either alone, or with both cytokines together. We reveal a dichotomous effect of IL-17 and TNF, which not only elicit essential mitogenic cytokines but also suppress melanogenesis by down-regulating genes of melanogenesis pathway
2013-06-15 | GSE40413 | GEO
Project description:In this study, we sought to determine how IL-17 and TNF influence normal human melanocytes, either alone, or with both cytokines together. We reveal a dichotomous effect of IL-17 and TNF, which not only elicit essential mitogenic cytokines but also suppress melanogenesis by down-regulating genes of melanogenesis pathway Comparison of one batch of primary human melanocyte line cultured in serum free media, treated with TNF and/or IL-17, for either 24 or 48 hours.
2013-06-15 | E-GEOD-40413 | biostudies-arrayexpress
Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.
2010-09-05 | E-GEOD-19411 | biostudies-arrayexpress
Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages.
2010-09-05 | GSE19411 | GEO
Project description:Extracellular vesicle(EV) secretion and capture is an important method of communication between cells. Melanocytes and their surrounding keratinocytes form epidermal melanin units in the thin, outermost layer of the skin to protect the skin from ultraviolet radiation damage. It is important to understand the mechanisms by which changes in melanocyte EV signal transduction influence pigmentation. Mouse melanocytes (melan-α cell) overexpressing MITF and CD63-GFP were used to to investigate the effect on vesicle formation by WB and SEM. Coculturing of melanocyte with keratinocyte(PAM212) was used to explore the polarization of vesicles and transfer between cells by immunofluorescence, flow cytometry. EVs from melanocytes were extracted and used to investigate changes in the miRNA profile of EVs, and the effect of exosomal miR-28 on keratinocyte growth and transcriptomics was analyzed by flow cytometry, TEM, particle size analysis, WB, the iCELLigence system and RNA-seq analysis.Our results indicate that melanocytes in the skin affected vesicle synthesis under the condition of enhanced melanin synthesis function: the expression of CD81, VPS37, VPS36B and Rab27b (melanosome and vesicle transport protein during ESCRT machinery) increased. Keratinocytes can cause the polarization of vesicles in melanocytes and capture EVs from melanocytes via plasmalemma fusion. Analysis of the miRNA profile derived from melanocyte EVs showed that the expression levels of miR-125, miR-130, miR-211, miR-127, miR-692 and miR-709 were increased, while the expression levels of miR-28, miR-744, let-7g and miR-6240 were decreased. The content of miR-28 in EVs may be reduced to induce keratinocytes to prevent carcinogenesis, resist infection and prevent premature apoptosis.
2022-03-23 | GSE199035 | GEO
Project description:Cold atmospheric plasma is assembled out of various components such as UV-radiation, electrons, ions and an electromagnetic field at low temperature. In recent years cold atmospheric plasma gains interest as a medical tool used for improved healing of chronic wounds. In order to examine the impact of cold atmospheric plasma on the melanogenesis in human skin, the gene expression signature of differently treated lightly pigmented primary human melanocytes was analysed. Melanocytes were either treated in vitro indirectly by cold atmospheric plasma or irradiated by UV-radiation. After 2 h incubation the microarray analysis was performed.
2020-09-15 | GSE157824 | GEO
Project description:This microarray experiment was performed for identifying the signaling pathways that could be differentially regulated in response to changes in the pigmentation levels in human melanocytes. Melanocytes were either treated with pigmentation inducing agent or depigmenting compound targeting tyrosinase (key enzyme involved in the melanogenesis). The samples were then processed for analyzing the differentially regulated signaling pathway by performing microarray on agilent platform. The pathway enrichment analysis was executed on DAVID software. The plot has been generated using the average enrichment score for the pathways under similar category of function. Interestingly, along with the expected melanogenic and cAMP pathways, we observed differential regulation of Ca2+ signaling during pigmentation. We then performed several experiments for evaluating the contribution of cytoplasmic and endoplasmic reticulum (ER) Ca2+ homeostasis to pigmentation. After extensive studies in in vitro and in vivo pigmentation models, we demonstrate a critical role for ER Ca2+ sensor, STIM1 protein in the process of pigmentation. Taken together, we performed the microarray experiment for identifying potential pathways wherein Ca2+ homeostasis came out as one of the several hits. We then specifically studied cytoplasmic and endoplasmic reticulum (ER) Ca2+ homeostasis and identified a novel regulator of pigmentation based on several lines of evidences including in vivo model system
2018-01-03 | GSE107450 | GEO