ArticleExperimental and therapeutic medicine2018
Overexpression of indoleamine 2, 3-dioxygenase contributes to the repair of human airway epithelial cells inhibited by dexamethasone via affecting the MAPK/ERK signaling pathway.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.
What it found
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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.
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.
Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Promotion of skin wound healing using hypoimmunogenic epidermal cell sheets.Regenerative therapy · 2023Article
- A natural heme deficiency exists in biology that allows nitric oxide to control heme protein functions by regulating cellular heme distribution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- Overexpression of miR‑375 reverses the effects of dexamethasone on the viability, migration, invasion and apoptosis of human airway epithelial cells by targeting DUSP6.International journal of molecular medicine · 2022Article
- Comparative metabolomics analysis of bronchial epithelium during barrier establishment after allergen exposure.Clinical and translational allergy · 2021Article
- Dexamethasone fails to improve bleomycin-induced acute lung injury in mice.Physiological reports · 2019Article
Corrections and comments
- Retraction · 2024-02-19Author Unresponsive · Concerns/Issues about Data · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Plagiarism of Data · · See also: https://pubpeer.com/publications/FD11DCA33EE9149BB79881637B1EC5
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Indoleamine 2, 3-dioxygenase (IDO) catalyzes the degradation of trytophan, which serves a key role in immune suppression via regulating the production of several metabolites. The present study aimed to explore the effects and mechanisms of IDO in the repair of human airway epithelium suppressed by dexamethasone (DEX). Cell viability, proliferation and migration were evaluated using a Cell Counting Kit-8 (CCK-8), 5(6)-carboxyfluorescein diacetate succinimidyl ester (CFSE) labeling, and wound-healing assay, respectively. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot analysis and ELISA were performed to assess the levels of IDO, the mitogen-activated protein kinase (MAPK)/extracellular regulated kinase (ERK) pathway-related factors and epidermal growth factor (EGF) expression, respectively. The results revealed that overexpression of IDO enhanced the cell viability, and promoted the proliferation and migration of 16HBE cells which repair was inhibited by DEX. Furthermore, it was indicated that overexpression of IDO affected the MAPK/ERK pathway. In conclusion, overexpression of IDO promoted the human airway epithelium repair inhibited by DEX through affecting MAPK/ERK pathway. The present study implied that IDO may be a potential genetic therapeutic agent and supported the utilization of IDO in asthma.
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Registered trials
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.