ArticleBioengineered2017
Schwann cells genetically modified to express S100A4 increases GAP43 expression in spiral ganglion neurons in vitro.
Article in Bioengineered, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Tissue engineering strategies for spiral ganglion neuron protection and regeneration.Journal of nanobiotechnology · 2024Review
- Submicron-Grooved Films Modulate the Directional Alignment and Biological Function of Schwann Cells.Journal of functional biomaterials · 2023Article
- Transcriptional response to mild therapeutic hypothermia in noise-induced cochlear injury.Frontiers in neuroscience · 2023Article
- Shikonin Attenuates Cochlear Spiral Ganglion Neuron Degeneration by Activating Nrf2-ARE Signaling Pathway.Frontiers in molecular neuroscience · 2022Article
- Article
- Review
- S100A4 suppresses cancer stem cell proliferation via interaction with the IKK/NF-κB signaling pathway.BMC cancer · 2018Article
Corrections and comments
- Erratum issuedCorrigendum.2017
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schwann cells (SCs) have been reported as a possible source of neurotrophic support for spiral ganglion neurons (SGNs). This study was aimed to investigate whether S100A4 was contributed in the functional effects of SCs on SGNs. SCs were transfected with S100A4 vector or small interfering RNA (siRNA) against S100A4, and the transfection efficiency was verified by quantitative PCR (qPCR) and Western blot. The migration of transfected SCs was determined by Transwell assay, and the expression levels of vascular endothelial growth factor precursor (VEGF) and matrix metallopeptidase 9 (MMP-9) were measured by Western blot. Co-culture of either S100A4 overexpressed or suppressed SCs with SGNs, and the growth associated protein 43 (GAP43) expression in SGNs was detected by immunofluorescence (IF), qPCR and Western blot. The migration of SCs was significantly enhanced by S100A4 overexpression (P < 0.001), while was suppressed by S100A4 knockdown (P < 0.01). Further, the expressions of VEGF and MMP-9 were notably up-regulated by S100A4 overexpression, while were down-regulated by S100A4 knockdown. Moreover, co-culture with the S100A4 overexpressed SCs significantly increased the expression of GAP43 in SGNs (P < 0.01). As expected, co-culture with S100A4 knockdown SCs decreased GAP43 level (P < 0.05). S100A4 enhanced the migratory ability of SCs. SCs genetically modified to overexpress the S100A4 could up-regulate the GAP43 expression in SGNs.
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Registered trials
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