ArticleExperimental and therapeutic medicine2019
Pim-3 alleviates lipopolysaccharide-stimulated AR42J pancreatic acinar cell injury via improving the inflammatory microenvironment.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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, 6 citations in OpenAlex.
- PIM3 Kinase: A Promising Novel Target in Solid Cancers.Cancers · 2024Review
- Protective Effects of Baicalein on Lipopolysaccharide-Induced AR42J PACs through Attenuation of Both Inflammation and Pyroptosis via Downregulation of miR-224-5p/PARP1.Mediators of inflammation · 2024Article
- Pim-2 kinase inhibits inflammation by suppressing the mTORC1 pathway in atherosclerosis.Aging · 2021Article
- Small Proline-Rich Protein 2B Facilitates Gastric Adenocarcinoma Proliferation via MDM2-p53/p21 Signaling Pathway.OncoTargets and therapy · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a common acute abdominal disease characterized by pancreatic aseptic inflammation, with ~20% of patients progressing to severe AP (SAP) with a high mortality rate. The aim of this study was to explore the protective effects of Pim-3 proto-oncogene, serine/threonine kinase (Pim-3) on rat pancreatic acinar AR4-2J cells damaged by lipopolysaccharide (LPS). The recombinant plasmid p-enhanced green fluorescent protein (pEGFP)-N2/Pim-3 was transiently transfected into AR42J cells and the AR42J cells were then treated with 2 µg/ml LPS. Subsequently, the proliferation of AR42J cells was detected using MTT assay. The cell cycle progression and apoptosis rate of the AR42J cells were examined using flow cytometry. AR42J cell migration was assessed using wound healing assays. Additionally, RT-semi quantitative PCR and western blot analyses were used to detect the mRNA and protein expression levels, respectively, of Pim-3, interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1 and Occludin in AR42J cells. The results revealed that proliferation of AR42J cells was significantly enhanced and cell apoptosis was markedly reduced in the pEGFP-N2/Pim-3 + LPS group. The proportion of AR42J cells in G1 phase in the pEGFP-N2/Pim-3 + LPS group was decreased, whereas the proportion of cells in the G2 and S phases was increased. The wound healing assays demonstrated that AR42J cell migration was significantly increased in the pEGFP-N2/Pim-3 + LPS group. Finally, the expression levels of IL-6, IL-1β, TNF-α and ICAM-1 were significantly decreased in the pEGFP-N2/Pim-3 + LPS group, whereas the expression of Occludin was significantly increased. The present study demonstrated that raised expression levels of Pim-3 can protect AR42J cells from LPS-induced injury by modifying the inflammatory microenvironment, suggesting that Pim-3 may be a potential target for AP or SAP therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.