ArticleJournal of orthopaedic surgery and research2024
SP1 transcriptionally activates HTR2B to aggravate traumatic spinal cord injury by shifting microglial M1/M2 polarization.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- LEP Knockdown Improves Functional Recovery After Spinal Cord Injury and Potentially Regulates Microglial Polarization via JAK-STAT Signaling Pathway.Neuromolecular medicine · 2026Article
- Clec7a-targeted Res@GelMA hydrogels regulate macrophage polarization to reduce neuroinflammation and promote spinal cord repair.Journal of orthopaedic surgery and research · 2026Article
- Photobiomodulation mitigates chondrocyte catabolism in osteoarthritis by modulating macrophage M1 polarization through the IL-6/JAK/STAT pathway.Journal of orthopaedic surgery and research · 2025Article
- [Underlying Mechanism of the circ_0011462/miRNA-1200/SP1 Axis in Regulating Inflammatory Response, Apoptosis, and Neural Regeneration in a Spinal Cord Injury Model].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Cucurbitacin E inhibits M1 macrophage polarization and attenuates rheumatoid arthritis: a multi-omics analysis and experimental validation.Journal of orthopaedic surgery and research · 2025Article
- The mediation of circulating inflammatory proteins in the causal pathway from immune cells to osteoarthritis.Journal of orthopaedic surgery and research · 2025Article
- Ferroptosis-mediated osteoclast-osteoblast crosstalk: signaling pathways governing bone remodeling in osteoporosis.Journal of orthopaedic surgery and research · 2025Review
- Integrated bioinformatics and network pharmacology to identify and validate macrophage polarization related hub genes in the treatment of osteoarthritis with Astragalus membranaceus.Journal of orthopaedic surgery and research · 2025Article
- M2 macrophages activate the IL-10/JAK2/STAT3 pathway to induce pathological microangiogenesis in the nucleus pulposus exacerbating intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2025Article
- Development of a macrophage polarization-modulating therapeutic agent for osteoarthritis treatment.Journal of orthopaedic surgery and research · 2025Review
- P75NTR blockading inhibits Trem2+ M1 phenotype microglia activation and myelin damage following mild traumatic brain injury.Frontiers in neuroscience · 2025Article
- Macrophage-derived exosomes induce M2 microglial polarization to alleviate bone cancer pain.American journal of cancer research · 2025Article
- LC-MS-based quantitation of proteomic changes induced by Norcantharidin in MTB-Treated macrophages.Proteome science · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSpinal cord injury (SCI) can result in structural and functional damage to the spinal cord, which may lead to loss of limb movement and sensation, loss of bowel and bladder control, and other complications. Previous studies have revealed the critical influence of trans-acting transcription factor 1 (SP1) in neurological pathologies, however, its role and mechanism in SCI have not been fully studied.
methodsThe study was performed using mouse microglia BV2 stimulated using lipopolysaccharide (LPS) and male adult mice subjected to spinal hitting. Western blotting was performed to detect protein expression of SP1, 5-hydroxytryptamine (serotonin) receptor 2B (HTR2B), BCL2-associated x protein (Bax), B-cell lymphoma-2 (Bcl-2), inducible nitric oxide synthase (iNOS), clusters of differentiation 86 (CD86), Arginase 1 (Arg-1) and clusters of differentiation 206 (CD206). Cell viability and apoptosis were analyzed by MTT assay and TUNEL assay. mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-4 (IL-4) and tumor necrosis factor-β (TNF-β) were quantified by quantitative real-time polymerase chain reaction. The association of SP1 and HTR2B was identified by chromatin immunoprecipitation assay and dual-luciferase reporter assay. HE staining assay was performed to analyze the pathological conditions of spinal cord tissues.
resultsLPS treatment induced cell apoptosis and inhibited microglia polarization from M1 to M2 phenotype, accompanied by an increase of Bax protein expression and a decrease of Bcl-2 protein expression, however, these effects were relieved after SP1 silencing. Mechanism assays revealed that SP1 transcriptionally activated HTR2B in BV2 cells, and HTR2B knockdown rescued LPS-induced effects on BV2 cell apoptosis and microglial M1/M2 polarization. Moreover, SP1 absence inhibited BV2 cell apoptosis and promoted microglia polarization from M1 to M2 phenotype by decreasing HTR2B expression. SCI mouse model assay further showed that SP1 downregulation could attenuate spinal hitting-induced promoting effects on cell apoptosis of spinal cord tissues and microglial M1 polarization.
conclusionSP1 transcriptionally activated HTR2B to aggravate traumatic SCI by shifting microglial M1/M2 polarization.
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