Document Detail


Interaction of NG2(+) glial progenitors and microglia/macrophages from the injured spinal cord.
MedLine Citation:
PMID:  19780197     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Spinal cord contusion produces a central lesion surrounded by a peripheral rim of residual white matter. Despite stimulation of NG2(+) progenitor cell proliferation, the lesion remains devoid of normal glia chronically after spinal cord injury (SCI). To investigate potential cell-cell interactions of the predominant cells in the lesion at 3 days after injury, we used magnetic activated cell sorting to purify NG2(+) progenitors and OX42(+) microglia/macrophages from contused rat spinal cord. Purified NG2(+) cells from the injured cord grew into spherical masses when cultured in defined medium with FGF2 plus GGF2. The purified OX42(+) cells did not form spheroids and significantly reduced sphere growth by NG2(+) cells in co-cultures. Conditioned medium from these OX42(+) cells, unlike that from normal peritoneal macrophages or astrocytes also inhibited growth of NG2(+) cells, suggesting inhibition by secreted factors. Expression analysis of freshly purified OX42(+) cells for a panel of six genes for secreted factors showed expression of several that could contribute to inhibition of NG2(+) cells. Further, the pattern of expression of four of these, TNFalpha, TSP1, TIMP1, MMP9, in sequential coronal tissue segments from a 2 cm length of cord centered on the injury epicenter correlated with the expression of Iba1, a marker gene for OX42(+) cells, strongly suggesting a potential regional influence by activated microglia/macrophages on NG2(+) cells in vivo after SCI. Thus, the nonreplacement of lost glial cells in the central lesion zone may involve, at least in part, inhibitory factors produced by microglia/macrophages that are concentrated within the lesion.
Authors:
Junfang Wu; Soonmoon Yoo; Donna Wilcock; Judith M Lytle; Philberta Y Leung; Carol A Colton; Jean R Wrathall
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Glia     Volume:  58     ISSN:  1098-1136     ISO Abbreviation:  Glia     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-01-15     Completed Date:  2010-03-08     Revised Date:  2014-09-20    
Medline Journal Info:
Nlm Unique ID:  8806785     Medline TA:  Glia     Country:  United States    
Other Details:
Languages:  eng     Pagination:  410-22     Citation Subset:  IM    
Copyright Information:
2009 Wiley-Liss, Inc.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens / metabolism*
Astrocytes / physiology
Calcium-Binding Proteins / metabolism
Cells, Cultured
Coculture Techniques
Culture Media, Conditioned
Female
Macrophages / physiology*
Matrix Metalloproteinase 9 / metabolism
Microfilament Proteins
Microglia / physiology*
Neuroglia / physiology*
Proteoglycans / metabolism*
Rats
Spinal Cord Injuries / physiopathology*
Stem Cells / physiology*
Thrombospondin 1 / metabolism
Tissue Inhibitor of Metalloproteinase-1 / metabolism
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
R01 NS035647/NS/NINDS NIH HHS; R01 NS035647/NS/NINDS NIH HHS; R01 NS035647-11/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Aif1 protein, rat; 0/Antigens; 0/Calcium-Binding Proteins; 0/Culture Media, Conditioned; 0/Microfilament Proteins; 0/Proteoglycans; 0/Thrombospondin 1; 0/Tissue Inhibitor of Metalloproteinase-1; 0/Tumor Necrosis Factor-alpha; 0/chondroitin sulfate proteoglycan 4; EC 3.4.24.35/Matrix Metalloproteinase 9
Comments/Corrections

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