ArticleHeliyon2019
Knockdown of TRAF3IP2 suppresses the expression of VEGFA and the proliferation of keratinocytes and vascular endothelial cells.
Article in Heliyon, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Targeted siRNA Therapy for Psoriasis: Translating Preclinical Potential into Clinical Treatments.ImmunoTargets and therapy · 2024Review
- Vascular Endothelial Growth Factor A VEGFA Inhibition: An Effective Treatment Strategy for Psoriasis.International journal of molecular sciences · 2023Review
- TRAF3IP2 drives mesenchymal stem cell senescence via regulation of NAMPT-mediated NAD biosynthesis.Heliyon · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the expression level of TRAF3IP2 in psoriasis lesion, and to explore the functional roles of TRAF3IP2 on proliferation, apoptosis, cytokine expression and secretion of both keratinocytes and vascular endothelial cells
methodsThe expression of TRAF3IP2 in skin samples of patients with psoriasis was analyzed by immunohistochemistry and qRT-PCR. To identify the effect of TRAF3IP2 knockdown on HaCaT and HUVEC cells, a plasmid vector expressing siRNA targeting TRAF3IP2 mRNA was designed and transfected into cells with Lipofectamine 2000. The levels of cytokines were identified using the ELISA Kits and qRT-PCR. Furthermore, cell proliferation, cell cycle and apoptosis were examined by using MTT, PI and Annexin V-FITC/7AAD assays, respectively. Furthermore, the expression of apoptosis-related proteins (Cleaved-Caspase 3, Caspase 3 and Bax) were detected by western blotting.
resultsTRAF3IP2 was significantly upregulated in psoriasis lesion. TRAF3IP2 knockdown reduced the expression of vascular endothelial growth factor A (VEGFA) and the release of IL-6, and IL-8, but had no effect on IL-23 in both HaCaT and HUVEC cells. In addition, knockdown of TRAF3IP2 significantly inhibited cell proliferation through blocking the cell cycle in the G2/M phase. Moreover, knockdown of TRAF3IP2 increased the expression of Caspase 3, Cleaved-Caspase 3 and Bax, which was supported by the increased apoptosis of both HaCaT and HUVEC cells.
conclusionTaken together, these results indicated that TRAF3IP2 might play a contributive role in the pathogenesis of psoriasis and may serve as a new target for the treatment of psoriasis. VEGF related pathways may be involved in the mechanism beneath.
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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 Socratic graph.