Intrathecal bone marrow stromal cells inhibit neuropathic pain via TGF-β secretion
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(A) Selective targeting of i.t.-injected BMSCs (CM-Dil labeled) to ipsilateral L4–L6 DRGs 3 days after i.t. injection (day 7 after CCI). Scale bar: 100 μm. Note that there was only limited migration of BMSCs to contralateral DRGs. (B) ELISA analysis showing CXCL12 expression in contralateral and ipsilateral L4–L6 DRGs on days 4 and 14 after CCI. *P < 0.05; n = 4 mice/group. (C) Chemotaxis (Transwell invasion) assay showing the migration of BMSCs in response to CXCL12 (0–100 ng/ml) and the inhibitory effect of the CXCR4 antagonist AMD3100 (5 mg/ml, 30 min). *P < 0.05, compared with the control group (no treatment); #P < 0.05; n = 4 wells from separate cultures. (D) Reduction of Cxcr4 mRNA levels in BMSCs treated with Cxcr4 siRNA (1 μg/ml for 18 h). *P < 0.05; n = 3 separate cultures. (E) Antiallodynic effect of i.t. BMSCs (2.5 × 105 cells) was compromised by pretreatment of BMSCs with Cxcr4 siRNA, but not with nontargeting control siRNA. Arrow indicates BMSC injection on day 14 after CCI. *P < 0.05, compared with the vehicle group; #P < 0.05; n = 5 mice/group. (F) Migration of CM-Dil–labeled BMSCs to ipsilateral L5 DRGs 7 days after i.t. injection (day 21 after CCI). Note that this migration was blocked by Cxcr4 siRNA. Scale bar: 50 μm. (G) Number of CM-Dil–labeled BMSCs in ipsilateral L4–L6 DRGs after the treatment shown in F. *P < 0.05; n = 5 mice/group. Statistical significance was determined by 1-way ANOVA, followed by Bonferroni’s post-hoc test (B and C), 2-way, repeated-measures ANOVA, followed by Bonferroni’s post-hoc test (E), or Student’s t test (D and G). All data are expressed as the mean ± SEM.
Published Version (Please cite this version)10.1172/JCI80883
Publication InfoChen, G; Park, C-K; Xie, R-G; & Ji, R (2015). Intrathecal bone marrow stromal cells inhibit neuropathic pain via TGF-β secretion. Journal of Clinical Investigation. 10.1172/JCI80883. Retrieved from https://hdl.handle.net/10161/10285.
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Assistant Professor in Anesthesiology
Distinguished Distinguished Professor of Anesthesiology, in the School of Medicine
Chronic pain is a major health problem in the US, affecting 100 million Americans. The long-term goal of the lab is to identify molecular and cellular mechanisms that underlie the genesis of chronic pain and, furthermore, to develop novel pain therapeutics that can target these mechanisms. We are interested in the following questions. (1) How do neuroinflammation and activation of glial cells (microglia and astrocytes) regulate pain and spinal cord synaptic plasticity via neuro-glia
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