ArticleJournal of molecular histology2025
Nell-1 inhibits lipopolysaccharide-activated macrophages into M1 phenotype through the modulation of NF-κB pathway.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Nell-1 inhibits osteoclast differentiation and bone resorption in apical periodontitis.Journal of molecular histology · 2026Article
- NELL-1: role and mechanisms in disease pathogenesis and development.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nel-like molecule-1 (Nell-1), as a novel osteo-inductive molecule with great potential for clinical applications, has various functions including promoting chondrogenesis, suppressing osteoclastic activity, promoting osteogenesis, suppressing inflammation and promoting vascularization. Its anti-inflammatory potential has been widely studied. However, its anti-inflammatory potential in macrophage and possible underlying molecular mechanisms are poorly understood. Therefore, the present study aims to evaluate the anti-inflammatory potential and the regulation to macrophage polarization of Nell-1 in human myeloid cell line (THP-1) derived macrophages. M1-related markers and M2-related markers were studied in THP-1 derived macrophages. The suppressive potential of Nell-1 on lipopolysaccharide (LPS)-induced translocation of nuclear factor-kappa B (NF-κB) in THP-1 macrophage was studied. Results showed that Nell-1 significantly reduced M1 macrophage-related surface marker cluster of differentiation 86 (CD86) and inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) and reversed the LPS-induced M1 polarization of macrophages by upregulating the M2-specific markers of vascular endothelial growth factor (VEGF), arginase-1(Arg-1), and cluster of differentiation 206 (CD206) in vitro. In addition, the possible mechanism of the anti-inflammatory effects of Nell-1 is via regulating NF-κB pathway. Hence, Nell-1 is a potential suppressor of inflammation and is involved in the regulation of macrophage polarization. Nell-1 may be a potential candidate for treating inflammatory diseases and promoting tissue regeneration.
Indexed as
Identifiers
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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.