Evidence map›Paper›PMID 33915532›Full record

ArticleSkin pharmacology and physiology2021

[Pathogenic and Compensatory Mechanisms in Epidermis of Sphingomyelin Synthase 2-Deficient Mice].

Shota Sakai, Asami Makino, Akihito Nishi, Takeshi Ichikawa, Tadashi Yamashita, Makoto Taniguchi, Yoshihiro Tokudome, Yoshio Hirabayashi, Masashi Akiyama, Debra Crumrine and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Skin pharmacology and physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in endocrinology · 2023
    Review
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

14 authors at 8 institutions in 2 countries.

Shota SakaiLaboratory of Biomembrane and Biofunctional Chemistry, Faculty of Advanced Life Science, Hokkaido University, Sapporo, Japan.
Asami MakinoLipid Biology Laboratory, Advanced Science Institute, RIKEN Laboratory of Biochemistry, Asaka, Japan.
Akihito NishiLaboratory of Biochemistry, Azabu University School of Veterinary Medicine, Sagamihara, Japan.
Takeshi IchikawaDepartment of Life Science, Medical Research Institute, Kanazawa Medical University, Kahoku, Japan.
Tadashi YamashitaLaboratory of Biochemistry, Azabu University School of Veterinary Medicine, Sagamihara, Japan.
Makoto TaniguchiDepartment of Life Science, Medical Research Institute, Kanazawa Medical University, Kahoku, Japan.
Yoshihiro TokudomeLaboratory of Dermatological Physiology, Faculty of Pharmaceutical Sciences, Josai University, Sakado, Japan.
Yoshio HirabayashiDepartment of Dermatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masashi AkiyamaLaboratory of Dermatological Physiology, Faculty of Pharmaceutical Sciences, Josai University, Sakado, Japan.
Debra CrumrineDepartment of Dermatology, School of Medicine, University of California, San Francisco, California, USA.
Yoshikazu UchidaDepartment of Dermatology, School of Medicine, University of California, San Francisco, California, USA.
Peter M EliasDepartment of Dermatology, School of Medicine, University of California, San Francisco, California, USA.
Tetsuya TsuchidaDepartment of Dermatology, Faculty of Medicine, Saitama Medical University, Moroyama, Japan.
Sumiko HamanakaDepartment of Dermatology, Faculty of Medicine, Saitama Medical University, Moroyama, Japan.
University of California, San Francisco · USAzabu University · JPJosai University · JPKanazawa Medical University · JPSaitama Medical University · JPHokkaido University · JPNagoya University · JPRIKEN Advanced Science Institute · JP

Funding

Pathogenesis and Therapy of Ichthyosis in Disorders of Lipid MetabolismR01AR061106 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MAURO, THEODORA M · 2012 to 2022
$3.3M
S1P-Mediated Stimulation of Antimicrobial DefenseR01AR062025 · NIAMS · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI HOLLERAN, WALTER M · 2012 to 2016
$1.6M
Epidermal Mechanisms Opposing Ceramide-Induced ApoptosisR01AR051077 · NIAMS · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI UCHIDA, YOSHIKAZU · 2005 to 2009
$1.5M
NIAMS NIH HHS R01 AR051077NIAMS NIH HHS R01 AR061106NIAMS NIH HHS R01 AR062025
6 · The paper itself

Abstract

Sphingomyelin (SM) is a constituent of cellular membranes, while ceramides (Cer) produced from SM on plasma membranes serve as a lipid mediator that regulates cell proliferation, differentiation, and apoptosis. In the skin, SM also is a precursor of Cer, an important constituent of epidermal permeability barrier. We investigated the role of epidermal SM synthase (SMS)2, an isoform of SMS, which modulates SM and Cer levels on plasma membranes. Although SMS2-knockout (SMS2-KO) mice were not neonatal lethal, an ichthyotic phenotype with epidermal hyperplasia and hyperkeratosis was evident at birth, which persisted until 2 weeks of age. These mice showed abnormal lamellar body morphology and secretion, and abnormal extracellular lamellar membranes in the stratum corneum. These abnormalities were no longer evident by 4 weeks of age in SMS2-KO mice. Our study suggests that (1) exposure to a dry terrestrial environment initiates compensatory responses, thereby normalizing epidermal ichthyotic abnormalities and (2) that a nonlethal gene abnormality can cause an ichthyotic skin phenotype.

Indexed as

Lamellar BodiesTransferases (Other Substituted Phosphate Groups)AnimalsEpidermisMiceMice, Knockoutphosphatidylcholine-ceramide phosphocholine transferaseSgms2 protein, mouseTransferases (Other Substituted Phosphate Groups)DifferentiationKeratinocyteProliferationSkin barrier functionSphingomyelinSphingomyelin synthase

Identifiers

PMID33915532
PMCPMC8410625
OpenAlexW3157211970

What OpenQuestion holds

Textmetadata
LicenceTDM
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.