Intrathecal bone marrow stromal cells inhibit neuropathic pain via TGF-β secretion
Abstract
(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.
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https://hdl.handle.net/10161/10285Published Version (Please cite this version)
10.1172/JCI80883Publication Info
Chen, 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.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Gang Chen
Assistant Professor in Anesthesiology
Ru-Rong Ji
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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