Evidence map›Paper›PMID 26340945›Full record

ArticleBiology open2015

Cooperation of endothelin-1 signaling with melanosomes plays a role in developing and/or maintaining human skin hyperpigmentation.

Daiki Murase, Akira Hachiya, Mamiko Kikuchi-Onoe, Rachel Fullenkamp, Atsushi Ohuchi, Takashi Kitahara, Shigeru Moriwaki, Tadashi Hase, Yoshinori Takema

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Daiki MuraseBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan Biological Science Americas Laboratory, Kao Corporation, Cincinnati, OH 45214, USA.
Akira HachiyaBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan hachiya.akira@kao.co.jp.
Mamiko Kikuchi-OnoeBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan.
Rachel FullenkampBiological Science Americas Laboratory, Kao Corporation, Cincinnati, OH 45214, USA.
Atsushi OhuchiBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan.
Takashi KitaharaBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan.
Shigeru MoriwakiBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan.
Tadashi HaseBiological Science Laboratories, Kao Corporation, Haga, Tochigi 321-3497, Japan.
Yoshinori TakemaResearch and Development Global, Kao Corporation, Sumida-ku, Tokyo 131-8501, Japan.
Kao Corporation (Japan) · JPKao Corporation (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skin hyperpigmentation is characterized by increased melanin synthesis and deposition that can cause significant psychosocial and psychological distress. Although several cytokine-receptor signaling cascades contribute to the formation of ultraviolet B-induced cutaneous hyperpigmentation, their possible involvement in other types of skin hyperpigmentation has never been clearly addressed. Since our continuous studies using skin specimens from more than 30 subjects with ethnic skin diversity emphasized a consistent augmentation in the expression of endothelin-1 (ET-1) and its receptor (Endothelin B receptor, ET-B) in hyperpigmented lesions, including senile lentigos (SLs), the precise function of ET-1 signaling was investigated in the present study. In line with previous studies, ET-1 significantly induced melanogenesis followed by increases in melanosome transport in melanocytes and in its transfer to keratinocytes while inhibition of ET-B function substantially depressed melanogenic ability in tissue-cultured SLs. Additionally, in agreement with a previous report that the formation of autophagosomes rather than melanosomes is stimulated according to starvation or defective melanosome production, ET-1 was found to remarkably augment the expression of components necessary for early melanosome formation, indicating its counteraction against autophagy-targeting melanosome degradation in melanocytes. Despite the lack of substantial impact of ET-1 on keratinocyte melanogenic functions, the expression of ET-1 was enhanced following melanosome uptake by keratinocytes. Taken together, our data suggest that ET-1 plays a substantial role in the development and/or maintenance of skin hyperpigmentation in reciprocal cooperation with increased melanosome incorporation.

Indexed as

Endothelin-1HyperpigmentationMelaninMelanosomeSenile lentigo

Identifiers

PMID26340945
PMCPMC4610214
OpenAlexW2109285107

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.