Evidence map›Paper›PMID 29121094›Full record

ArticlePloS one2017

Pleckstrin homology-like domain family A, member 3 (PHLDA3) deficiency improves islets engraftment through the suppression of hypoxic damage.

Naoaki Sakata, Yohko Yamaguchi, Yu Chen, Masayuki Shimoda, Gumpei Yoshimatsu, Michiaki Unno, Shoichiro Sumi, Rieko Ohki

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. PHLDA3 promotes lung adenocarcinoma cell proliferation and invasion via activation of the Wnt signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  5. Article
  6. Review
  7. p53-PHLDA3-Akt Network: The Key Regulators of Neuroendocrine Tumorigenesis.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
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

8 authors.

Naoaki SakataDepartment of Surgery, Tohoku University, Aoba-ku, Sendai, Miyagi, Japan.ORCID http://orcid.org/0000-0002-3495-4270
Yohko YamaguchiDivisions of Rare Cancer Research, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan.
Yu ChenDivisions of Rare Cancer Research, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan.
Masayuki ShimodaDepartment of Pancreatic Islet Cell Transplantation, Research Institute, National Center for Global Health and Medicine, Toyama, Shinjuku-ku, Tokyo, Japan.
Gumpei YoshimatsuDepartment of Surgery, Tohoku University, Aoba-ku, Sendai, Miyagi, Japan.
Michiaki UnnoDepartment of Surgery, Tohoku University, Aoba-ku, Sendai, Miyagi, Japan.
Shoichiro SumiDepartment of Organ and Tissue Reconstruction, Institute for Frontier Life and Medical Sciences, Kyoto University, Shogoin, Sakyo-ku, Kyoto, Japan.
Rieko OhkiDivisions of Rare Cancer Research, National Cancer Center Research Institute, Tsukiji, Chuo-ku, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Islet transplantation is a useful cell replacement therapy that can restore the glycometabolic function of severe diabetic patients. It is known that many transplanted islets failed to engraft, and thus, new approaches for overcoming graft loss that may improve the outcome of future clinical islet transplantations are necessary. Pleckstrin homology-like domain family A, member 3 (PHLDA3) is a known suppressor of neuroendocrine tumorigenicity, yet deficiency of this gene increases islet proliferation, prevents islet apoptosis, and improves their insulin-releasing function without causing tumors. In this study, we examined the potential use of PHLDA3-deficient islets in transplantation. We observed that: 1) transplanting PHLDA3-deficient islets into diabetic mice significantly improved their glycometabolic condition, 2) the improved engraftment of PHLDA3-deficient islets resulted from increased cell survival during early transplantation, and 3) Akt activity was elevated in PHLDA3-deficient islets, especially under hypoxic conditions. Thus, we determined that PHLDA3-deficient islets are more resistant against stresses induced by islet isolation and transplantation. We conclude that use of islets with suppressed PHLDA3 expression could be a novel and promising treatment for improving engraftment and consequent glycemic control in islet transplantation.

Indexed as

AnimalsCell HypoxiaCells, CulturedCell SurvivalDiabetes Mellitus, ExperimentalInsulinInsulin SecretionIslets of LangerhansIslets of Langerhans TransplantationMiceNuclear ProteinsProto-Oncogene Proteins c-aktInsulinNuclear ProteinsProto-Oncogene Proteins c-aktTSSC3 protein

Identifiers

PMID29121094
PMCPMC5679611

What Socratic holds

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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 Socratic graph.