ArticleJournal of molecular histology2024
LncRNA GAS5 modulates Schwann cell function and enhances facial nerve injury repair via the miR-138-5p/CXCL12 axis.
Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
Abstract
Facial nerve is an integral part of peripheral nerve. Schwann cells are important microglia involved in the repair and regulation of facial nerve injury. LncRNA growth arrest‑specific transcript 5 (GAS5) is involved in the behavioral regulation of Schwann cell and the regeneration of peripheral nervous system. However, there is little research about the effect of GAS5 on the repair of facial nerve injury (FNI) by regulating Schwann cells. This study aimed to investigate the role of GAS5 in Schwann cell function and FNI repair, focusing on the miR-138-5p/CXCL12 axis. Hematoxylin and eosin staining, Luxol fast blue staining, transmission electron microscope, and immunofluorescence (IF) experiments were used to verify the effect of GAS5 on FNI rats. Reverse transcription real-time polymerase chain reaction was performed to detect GAS5, miR-138-5p, and C-X-C motif chemokine ligand 12 (CXCL12) mRNA expression. IF staining was used to detect the inflorescence of S100 calcium binding protein B (S100β), SRY-box transcription factor 10 (SOX10), and tubulin beta 3 class III (β-Tubulin III). Glial fibrillary acidic protein (GFAP), nerve growth factor receptor (NGFR), S100β, brain derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF), and CXCL12 proteins were detected using western blot. The 5-bromo-2'-deoxyuridine staining, Transwell, and flow cytometry assays were conducted to detect Schwann cell function. Dual-luciferase, RNA immunoprecipitation, and RNA pulldown assay were used to identify the interaction among GAS5, miR-138-5p, and CXCL12. Results found that GAS5 was downregulated in facial nerve tissues of FNI rats. Overexpressed GAS5 decreased facial grading, inhibited demyelination, and promoted proliferation, migration, and suppressed apoptosis of Schwann cells. Mechanistically, GAS5 was a sponge of miR-138-5p and positively regulated CXCL12 expression. GAS5 inhibition repressed CXCL12 expression and decreased cell proliferation and migration, increased apoptosis rate of Schwann cells by sponging miR-138-5p. In conclusion, overexpression of GAS5 accelerates facial nerve repair in FNI rats by regulating miR-138-5p/CXCL12 axis.
Indexed as
Identifiers
39068616What 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.