Induction of retinal‐dependent calcium influx in human melanocytes by <scp>UVA</scp> or <scp>UVB</scp> radiation contributes to the stimulation of melanosome transfer

Hu, Qing‐Mei; Yi, Wenjuan; Su, Meng‐Yun; Jiang, Shan; Xu, Shang‐Zhong; Lei, Tiechi

doi:10.1111/cpr.12372

Cited by 29 publications

(24 citation statements)

References 31 publications

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“…The present study showed that p53 regulates MMP9 expression at the transcriptional level via a novel miR-211-mediated mechanism. Previous studies have revealed that the exons within the TRPM1 gene encode a ca 2+ -permeable cation channel protein (melastatin) that is involved in regulating calcium homeostasis (21) and triggering melanosome transfer (22). However, the 6th intron of the TRPM1 gene also encodes miR-211, which acts as a critical modifier of melanin synthesis by targeting transforming growth factor-β receptor 2 (23) and of cell migration by targeting MMP9 (24).…”

Section: Discussionmentioning

confidence: 99%

Role of the p53‑TRPM1/miR‑211‑MMP9 axis in UVB‑induced human melanocyte migration and its potential in repigmentation

Miao

Jiang

et al. 2020

Int J Mol Med

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clinical studies have proven that ultraviolet B (UVB) based phototherapy can induce perifollicular and marginal repigmentation patterns in the skin of vitiligo patients. It is, however, difficult to conceive how melanocytes can easily exit from their tightly interconnected epidermal microenvironment to re-enter a different location in the skin to establish a new network with neighboring keratinocytes. While it is known that matrix metalloprotease 9 (MMP9) is involved in the degradation of the extracellular matrix in physiological or pathological processes, little is known about whether MMP9 affects melanocyte migration in vitiligo repigmentation. To investigate the effects of the p53-transient receptor potential cation channel subfamily M member 1 (TRPM1)/microRNA (miR/miRNA)-211-MMP9 axis to regulate melanocyte migration following exposure to UVB, the expression profile of MMP9 in cultured human melanocytes transfected with or without the miR-211-mimic and p53-GFP lentiviral vector, respectively were determined. Quantitative polymerase chain reaction and western blotting were used to examine p53, TRPM1 and MMP9 mRNA and protein levels in UVB-exposed and unexposed cells. The capacity of melanocytes to migrate on collagen IV substrate was estimated using a Transwell migration assay. Interestingly, the upregulation of p53 and MMP9 at the mRNA and protein levels was evident in melanocytes treated with single or repeat exposures to UVB, whereas levels of TRPM1 and miR-211 were significantly suppressed in UVB-exposed melanocytes compared with the UVB-unexposed control cells. These results indicate that the p53-TRPM1/miR-211-MMP9 axis is significantly activated in melanocytes exposed to UVB. Notably, the ability of melanocyte migration was altered by the overexpression of p53 using a lentiviral vector and by the upregulation of miR-211 using an miRNA mimic. That altered migration could be neutralized by co-treatment with GM6001 (a broad-spectrum MMP inhibitor). Overall, these results show that the MMP9-mediated migration of melanocytes is regulated by a novel mechanism driven by the p53-TRPM1/miR-211-MMP9 axis. Activation of the p53-TRPM1/miR-211-MMP9 axis potentially represents an attractive therapeutic target to improve repigmentation outcomes in vitiligo patients.

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Section: Discussionmentioning

confidence: 99%

Role of the p53‑TRPM1/miR‑211‑MMP9 axis in UVB‑induced human melanocyte migration and its potential in repigmentation

Miao

Jiang

et al. 2020

Int J Mol Med

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“…sc-37007) were supplied by Santa Cruz Biotechnology (Santa Cruz, CA, USA). The transfection method was as described previously 24 .…”

Section: Methodsmentioning

confidence: 99%

miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

Yang

2020

oncol res

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In the present study, we investigated the role of miR-122 in hepatocarcinoma progression and explored the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or Transwell assay to compare cell migration or invasion ability. We then conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. We used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. miR-122 was reduced in hepatocarcinoma tissues compared to the paracarcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and overexpressed miR-122 inhibited proliferation, migration, and invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 functioned to promote cell proliferation, migration, and invasion. We could achieve the inhibition of hepatocarcinoma using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.

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“…Melanosome transfer in 2D cocultures can be assessed by flow cytometry analysis of keratinocytes labeled for melanosome-associated markers (e.g., TYR, TYRP1 [Hu et al, 2017;Lin et al, 2008]) or by conventional EM to detect pigment in keratinocytes . Several studies have exploited 3D culture systems, including the seeding of epidermal cells on either side of a porous filter or generating 3Dreconstructed epidermis for analyses by immunohistochemistry and/or EM .…”

Section: Live Cell Imagingmentioning

confidence: 99%

Research Techniques Made Simple: Cell Biology Methods for the Analysis of Pigmentation

Benito-Martínez

Zhu

Jani

et al. 2020

Journal of Investigative Dermatology

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Pigmentation of the skin and hair represents the result of melanin biosynthesis within melanosomes of epidermal melanocytes, followed by the transfer of mature melanin granules to adjacent keratinocytes within the basal layer of the epidermis. Natural variation in these processes produces the diversity of skin and hair color among human populations, and defects in these processes lead to diseases such as oculocutaneous albinism. While genetic regulators of pigmentation have been well studied in human and animal models, we are still learning much about the cell biological features that regulate melanogenesis, melanosome maturation, and melanosome motility in melanocytes, and have barely scratched the surface in our understanding of melanin transfer from melanocytes to keratinocytes. Herein, we describe cultured cell model systems and common assays that have been used by investigators to dissect these features and that will hopefully lead to additional advances in the future.

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Induction of retinal‐dependent calcium influx in human melanocytes by UVA or UVB radiation contributes to the stimulation of melanosome transfer

Abstract: The distinct time-phases of Ca influx in MCs induced by UVA or UVB contribute to the consecutive stimulation of melanosome transfer, thereby providing a potent photoprotection against harmful UV radiation.

Cited by 29 publications

References 31 publications

Role of the p53‑TRPM1/miR‑211‑MMP9 axis in UVB‑induced human melanocyte migration and its potential in repigmentation

Role of the p53‑TRPM1/miR‑211‑MMP9 axis in UVB‑induced human melanocyte migration and its potential in repigmentation

miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

Research Techniques Made Simple: Cell Biology Methods for the Analysis of Pigmentation

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