Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury

Zhang,Xuesong; Chen,Chao; Ma,Shengzhong; Wang,Yan; Zhang,Xuelian; Su,Xiaojing

doi:10.3892/mmr.2015.3330

Inhibition of monocyte chemoattractant peptide-1 decreases secondary spinal cord injury

Authors:
- Xuesong Zhang
- Chao Chen
- Shengzhong Ma
- Yan Wang
- Xuelian Zhang
- Xiaojing Su
View Affiliations

Affiliations: Spine Department, General Hospital of PLA, Beijing 100853, P.R. China, Spine Department, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China, Endocrine Department, China-Japan Friendship Hospital, Beijing 100029, P.R. China
Published online on: February 11, 2015 https://doi.org/10.3892/mmr.2015.3330
Pages: 4262-4266

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

Previous studies have suggested that impairment secondary to mechanical injury is a major cause of irreversible damage to the spinal cord. Inflammatory chemokines have been shown to play an important role in the pathological and physiological consequences of secondary spinal cord injury (SCI). The aim of the present study was to evaluate how changes in the expression levels of the cellular chemokine, monocyte chemoattractant peptide-1 (MCP-1), and the chemotaxis of inflammatory cells (monocytes and macrophages) are involved in the process of SCI. RNA interference methods were used to study the mechanisms that protect residual neurons after SCI in an attempt to explore novel, early interventions for managing SCI. Our results suggested that inhibiting inflammation alleviates nerve cell injury caused by apoptosis and provides a potentially important approach for the future treatment of secondary SCI.

View Figures

View References

1	Fehlings MG and Perrin RG: The role and timing of early decompression for cervical spinal cord injury: update with a review of recent clinical evidence. Injury. 36(Suppl 2): B13–B26. 2005. View Article : Google Scholar : PubMed/NCBI
2	Barinaga M: New view of spinal cord injury. Science. 274:14661996. View Article : Google Scholar : PubMed/NCBI
3	Li GL, Farooque M and Olsson Y: Changes of Fas and Fas ligand immunoreactivity after compression trauma to rat spinal cord. Acta Neuropathol. 100:75–81. 2000. View Article : Google Scholar : PubMed/NCBI
4	Emery E, Aldana P, Bunge MB, et al: Apoptosis after traumatic human spinal cord injury. J Neurosurg. 89:911–920. 1998. View Article : Google Scholar : PubMed/NCBI
5	Whalley K, O’Neill P and Ferretti P: Changes in response to spinal cord injury with development: vascularization, hemorrhage and apoptosis. Neuroscience. 137:821–832. 2006. View Article : Google Scholar
6	McTigue DM, Tani M, Krivacic K, et al: Selective chemokine mRNA accumulation in the rat spinal cord after contusion injury. J Neurosci Res. 53:368–376. 1998. View Article : Google Scholar : PubMed/NCBI
7	Pan JZ, Ni L, Sodhi A, Aguanno A, Young W and Hart RP: Cytokine activity contributes to induction of inflammatory cytokine mRNAs in spinal cord following contusion. J Neurosci Res. 68:315–322. 2002. View Article : Google Scholar : PubMed/NCBI
8	Stammers AT, Liu J and Kwon BK: Expression of inflammatory cytokines following acute spinal cord injury in a rodent model. J Neurosci Res. 90:782–790. 2012. View Article : Google Scholar : PubMed/NCBI
9	Gourmala NG, Buttini M, Limonta S, Sauter A and Boddeke HW: Differential and time-dependent expression of monocyte chemoattractant protein-1 mRNA by astrocytes and macrophages in rat brain: effects of ischemia and peripheral lipopolysaccharide administration. J Neuroimmunol. 74:35–44. 1997. View Article : Google Scholar : PubMed/NCBI
10	Miyagishi R, Kikuchi S, Takayama C, Inoue Y and Tashiro K: Identification of cell types producing RANTES, MIP-1 alpha and MIP-1 beta in rat experimental autoimmune encephalomyelitis by in situ hybridization. J Neuroimmunol. 77:17–26. 1997. View Article : Google Scholar : PubMed/NCBI
11	Glabinski AR, Balasingam V, Tani M, et al: Chemokine monocyte chemoattractant protein-1 is expressed by astrocytes after mechanical injury to the brain. J Immunol. 156:4363–4368. 1996.PubMed/NCBI
12	Bartholdi D and Schwab ME: Expression of pro-inflammatory cytokine and chemokine mRNA upon experimental spinal cord injury in mouse: an in situ hybridization study. Eur J Neurosci. 9:1422–1438. 1997. View Article : Google Scholar : PubMed/NCBI
13	Lee SC, Liu W, Dickson DW, Brosnan CF and Berman JW: Cytokine production by human fetal microglia and astrocytes. Differential induction by lipopolysaccharide and IL-1 beta. J Immunol. 150:2659–2667. 1993.PubMed/NCBI
14	Thompson WL and Van Eldik LJ: Inflammatory cytokines stimulate the chemokines CCL2/MCP-1 and CCL7/MCP-3 through NFkB and MAPK dependent pathways in rat astrocytes [corrected]. Brain Res. 1287:47–57. 2009. View Article : Google Scholar : PubMed/NCBI
15	Majumder S, Zhou LZ and Ransohoff RM: Transcriptional regulation of chemokine gene expression in astrocytes. J Neurosci Res. 45:758–769. 1996. View Article : Google Scholar : PubMed/NCBI
16	Lee YL, Shih K, Bao P, Ghirnikar RS and Eng LF: Cytokine chemokine expression in contused rat spinal cord. Neurochem Int. 36:417–425. 2000. View Article : Google Scholar : PubMed/NCBI
17	Wang J, Zheng Q, Zhao M and Guo X: Neurocyte apoptosis and expressions of caspase-3 and Fas after spinal cord injury and their implication in rats. J Huazhong Univ Sci Technolog Med Sci. 26:709–712. 2006. View Article : Google Scholar
18	Adjan VV, Hauser KF, Bakalkin G, et al: Caspase-3 activity is reduced after spinal cord injury in mice lacking dynorphin: differential effects on glia and neurons. Neuroscience. 148:724–736. 2007. View Article : Google Scholar : PubMed/NCBI