Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Aug 31;7:10107. doi: 10.1038/s41598-017-10251-y

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Role of RVM CXCR2 in BMSC-produced antihyperalgesia. (a,b) Attenuation of BMSC-induced antihyperalgesia by a CXCR2 antagonists SB225002 and NVP CXCR2 20 (NVP) injected into the RVM at 1w (a) and 8w (b) post-BMSC injection. *^-***p < 0.05-0.001, p < 0.01; vs. Veh. (c) Cxcr2 shRNA Lentivirus was microinjected into the RVM at 3d after TL and BMSCs were infused i.v. at 10d post-siRNA. Pretreatment with RNAi of Cxcr2 attenuated BMSC-produced antihyperalgesia. (d) Cxcr2 shRNA Lentivirus was microinjected into the RVM at 8w after BMSC infusion when antihyperalgesia is present. RNAi of Cxcr2 led to a reduction of EF₅₀, or rekindle of hyperalgesia. ***p < 0.001, vs. Ctrl shRNA. (e) Western blot illustrating knock-down of CXCR2 in RVM after RNAi. Samples taken at 2w post-shRNA injection. **p < 0.01, n = 4. Cropped gel images are shown. See Supplementary Figure 9 for full-length blots. (f) RVM MOR mRNA levels were decreased in rats treated with Cxcr2 shRNA, compared to Ctrl shRNA-treated rats. Sample taken at 2w post-shRNA injection. *p < 0.05, n = 4. (g) Mice received chronic constriction injury of the infraorbital nerve (CCI-ION) to induce hyperalgesia. The antihyperalgesic effect of BMSC was absent in the CXCR2 knockout mice. *p < 0.05, **p < 0.01, ***p < 0.001, vs. CXCR2-wt. (a–d,g) Error bars are 95% confidence intervals, n = 6–8/group; (e,f) Error bars are S.E.M., n = 5/group. (h) Summary diagram of immune interactions of BMSCs in producing pain relief. Note reciprocal interactions between BMSCs and host immune cells and autocrine signaling of BMSCs (curved arrows). Immune cells may also directly release opioid peptide and contribute to pain relief through peripheral nervous system (PNS). The role of peripheral opioid in the BMSC-produced pain relief was not studied. Statistics: (a–d,g) Two-way ANOVA followed by post-hoc comparisons with Bonferroni corrections. (e,f) Unpaired, Two-tailed Student’s t-test.