ArticleInternational journal of clinical and experimental pathology2018
CXCL12 induces migration of Schwann cells via p38 MAPK and autocrine of CXCL12 by the CXCR4 receptor.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
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- Transcriptomic and proteomic analysis of tumor suppressive effects of GZ17-6.02 against mycosis fungoides.Scientific reports · 2024Article
- Article
- Stromal Cell-Derived Factor-1a Autocrine/Paracrine Signaling Contributes to Spatiotemporal Gradients in the Brain.Cellular and molecular bioengineering · 2021Article
- The negative charge of the 343 site is essential for maintaining physiological functions of CXCR4.BMC molecular and cell biology · 2021Article
- A Zika virus primary isolate induces neuroinflammation, compromises the blood-brain barrier and upregulates CXCL12 in adult macaques.Brain pathology (Zurich, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schwann cells (SCs) play a crucially supportive role in repair of injured peripheral nerve system (PNS). CXCL12 plays a significant role in migration of stem cells and embryonic developmental cells and CXCL12 is strongly chemotactic for a variety of cells. Our study was designed to determine the role of CXCL12 in Schwann cell proliferation and migration. Our study demonstrated that CXCL12 had no effect on Schwann cell proliferation while significantly promoting Schwann cell migration. CXCL12-induced Schwann cell migration was significantly attenuated by inhibition of its receptor CXCR4 and p38 MAPK through co-treatment with AMD3100 and SB203580, separately. Besides, Western blot, QRT-PCR, and ELISA indicated that treatment with CXCL12 enhanced expression of CXCL12 by Schwann cells. In conclusion, CXCL12-enhanced SCs migration is mediated by secreting CXCL12 and p38 MAPK via receptor CXCR4, suggesting that CXCL12 has potential application value for PNS regeneration and could serve as a new therapeutic strategy in peripheral nerve diseases.
Indexed as
Identifiers
31938440PMC6958085W3006942662What 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.