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miRBase |
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![]() 2 publications mentioning hsa-mir-3196Open access articles that are associated with the species Homo sapiens and mention the gene name mir-3196. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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Other miRNAs from this paper: hsa-mir-203a, hsa-mir-203b
To further test the impact of these exosome -associated miRNAs on the process of pigmentation, Black and Caucasian ultraviolet B-irradiated keratinocytes were treated with anti-miR-203 or anti-miR-3196, respectively, to specifically downregulate their expressions and subsequent loading into exosomes (Supplementary Fig. 4c,d).
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Interestingly, only one miRNA, hsa-miR-3196 for which a precise target has not been reported in the literature, was differentially expressed between irradiated and non-irradiated Caucasian NHK exosomes (Fig. 4a).
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Pre-miR-3196 transfection increased the intracellular melanin content of Caucasian normal human melanocyte (21.5±6.3% as compared with the control; Supplementary Fig. 5c; P<0.05, t-test) and the gene expression of MITF-M (395±98.7%; P<0.01, t-test) and of Rab27a (225±6.3%; P<0.01, t-test) without greatly modifying TYR expression (Supplementary Fig. 5a).
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Exosomes from Caucasian ultraviolet B-irradiated keratinocytes transfected with anti-miR-3196 lose the ability to upregulate melanin production in melanocytes (Fig. 4e).
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Different from exosomes released by Black keratinocytes and on ultraviolet exposure, exosomes from Caucasian keratinocytes show an upregulation of miR-3196.
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Similarly, these results reinforce a role of miR-203 in the upregulation of TYR in primary melanocytes in addition to melanoma cells as reported 32 and reveal for the first time a role for miR-3196 in melanogenesis.
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Pre-miR-203 transfection increased the intracellular melanin content (57.5±17%; Fig. 5d; P<0.01, t-test) and, in contrast to mir-3196, enhanced the expression of TYR (41±6.8%; P<0.01, t-test) and Rab27a (17±4.3%; P<0.01, t-test; Supplementary Fig. 5b).
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In sum, our results highlight that keratinocyte exosomes modulate their miRNA content to fine-tune melanocyte pigmentation via different signalling pathways (that is, miR-3196 and MITF -dependent or miR-203 and MITF-independent).
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Keratinocytes were transfected with anti-miR-203, anti-miR-3196 or anti-miR-NC (as control) and conditioned media were recovered after 48 h to isolate exosomes.
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Melanocytes were transfected with pre-miR-203, pre-miR-3196 or pre-miR-NC (as control) using Oligofectamine (Invitrogen).
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Other miRNAs from this paper: hsa-mir-199a-1, hsa-mir-139, hsa-mir-183, hsa-mir-199a-2, hsa-mir-125b-1, hsa-mir-125b-2, hsa-mir-150, hsa-mir-328, hsa-mir-483, hsa-mir-494, hsa-mir-572, hsa-mir-574, hsa-mir-638, hsa-mir-762, hsa-mir-885, hsa-mir-940, hsa-mir-1225, hsa-mir-1238, hsa-mir-1202, hsa-mir-1207, hsa-mir-1275, hsa-mir-1915, hsa-mir-1973, hsa-mir-3162, hsa-mir-4299, hsa-mir-4284, hsa-mir-3679, hsa-mir-3940, hsa-mir-4485, hsa-mir-4516, hsa-mir-4530, hsa-mir-4649, hsa-mir-4728, hsa-mir-4739, hsa-mir-371b, hsa-mir-4787, hsa-mir-5787, hsa-mir-6069, hsa-mir-6090
Nineteen of the downregulated miRNAs in chronic patients were found to be associated with carcinogenesis in various organs and tissues, such as miR-1207 [40], miR-3162-5p [41, 42], miR-3196 [43, 44], miR-371b-5p [45], miR-574-5p [46, 47], miR-1225-5p [48], miR-4485 [49], miR-572 [50], miR-4299 [51], miR-3679-5p [52], miR-3940-5p [53], miR-638 [54, 55], miR-1202 [56], miR-5787 [57], miR-1973 [58], miR-4532 [59], miR-1275 [60], miR-4728-5p [61], and miR-1915-3p [62].
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