Targeting the peroxisome proliferator-activated receptors (PPARs) in spinal cord injury

2011 ◽  
Vol 15 (8) ◽  
pp. 943-959 ◽  
Author(s):  
Emanuela Esposito ◽  
Salvatore Cuzzocrea
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Peroxisome Proliferator ◽  
Cord Injury ◽  
Peroxisome Proliferator Activated Receptors

scholarly journals Decrease of PPARδin Type-1-Like Diabetic Rat for Higher Mortality after Spinal Cord Injury

PPAR Research ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Cheng-Chia Tsai ◽  
Kung-Shing Lee ◽  
Sheng-Hsien Chen ◽  
Li-Jen Chen ◽  
Keng-Fan Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Mortality Rate ◽  
Survival Rates ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Peroxisome Proliferator ◽  
Survival Times ◽  
Cord Injury ◽  
Peroxisome Proliferator Activated Receptors

Changes in the peroxisome proliferator-activated receptors-δ(PPARδ) expression in rats after spinal cord injury (SCI) have been previously reported. Diabetic animals show a higher mortality after SCI. However, the relationship between the progress of diabetes and PPARδin SCI remains unknown. In the present study, we used compressive SCI in streptozotocin-(STZ-) induced diabetic rats. GW0742, a PPARδagonist, was used to evaluate its merit in STZ rats after SCI. Changes in PPARδexpression were detected by Western blot. Survival rates were also estimated. A lower expression of PPARδin spinal cords of STZ-diabetic rats was observed. In addition, the survival times in two-week induction diabetes were longer than those in eight-week induction group, which is consistent with the expression of PPARδin the spinal cord. Moreover, GW0742 significantly increased the survival time of STZ rats. Furthermore, their motor function and pain response were attenuated by GSK0660, a selective PPARδantagonist, but were enhanced by GW0742. In conclusion, the data suggest that higher mortality rate in STZ-diabetic rats with SCI is associated with the decrease of PPARδexpression. Thus, change of PPARδexpression with the progress of diabetes seems responsible for the higher mortality rate after SCI.

scholarly journals RAR/RXR and PPAR/RXR Signaling in Spinal Cord Injury

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-14 ◽  
Author(s):  
Sabien van Neerven ◽  
Jörg Mey
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Peroxisome Proliferator ◽  
Inflammatory Reactions ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors ◽  
X Receptors ◽  
Physiological Reactions

The retinoid acid receptors (RAR) and peroxisome proliferator-activated receptors (PPAR) have been implicated in the regulation of inflammatory reactions. Both receptor families contain ligand-activated transcription factors which form heterodimers with retinoid X receptors (RXR). We review data that imply RAR/RXR and PPAR/RXR pathways in physiological reactions after spinal cord injury. Experiments show how RAR signaling may improve axonal regeneration and modulate reactions of glia cells. While anti-inflammatory properties of PPAR are well documented in the periphery, their possible roles in the central nervous system have only recently become evident. Due to its anti-inflammatory function this transcription factor family promises to be a useful target after spinal cord or brain lesions.

Evidence for the Role of Peroxisome Proliferator-Activated Receptor-β/δ in the Development of Spinal Cord Injury

2010 ◽  
Vol 333 (2) ◽  
pp. 465-477 ◽  
Author(s):  
Irene Paterniti ◽  
Emanuela Esposito ◽  
Emanuela Mazzon ◽  
Maria Galuppo ◽  
Rosanna Di Paola ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cord Injury

scholarly journals Potential Therapeutic Targets for PPAR after Spinal Cord Injury

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Dana M. McTigue
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Traumatic Injury ◽  
Therapeutic Targets ◽  
Great Promise ◽  
Peroxisome Proliferator ◽  
Cns Injury ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cord Injury

Traumatic injury to the spinal cord results in multiple anatomical, physiological, and functional deficits as a result of local neuronal and glial cell death as well as loss of descending and ascending axons traversing the injury site. The many different mechanisms thought to contribute to protracted secondary cell death and dysfunction after spinal cord injury (SCI) are potential therapeutic targets. Agents that bind and activate the transcription factor peroxisome proliferator-activated receptor- (PPAR-) show great promise for minimizing or preventing these deleterious cascades in other models of CNS disorders. This review will summarize the major secondary injury cascades occurring after SCI and discuss data from experimental CNS injury and disease models showing the exciting potential for PPAR therapies after SCI.

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