Early microvascular reactions and blood–spinal cord barrier disruption are instrumental in pathophysiology of spinal cord injury and repair: novel therapeutic strategies including nanowired drug delivery to enhance neuroprotection

2010 ◽  
Vol 118 (1) ◽  
pp. 155-176 ◽  
Author(s):  
Hari Shanker Sharma
Keyword(s):  
Drug Delivery ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Therapeutic Strategies ◽  
Barrier Disruption ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier ◽  
Injury And Repair ◽  
Novel Therapeutic Strategies ◽  
Novel Therapeutic

scholarly journals Gallic acid attenuates blood spinal cord barrier disruption by inhibiting Jmjd3 expression and activation after spinal cord injury

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S359-S360
Author(s):  
Chan Sol Park ◽  
Jee Youn Lee ◽  
Hae Young Choi ◽  
Tae Young Yune
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Gallic Acid ◽  
Barrier Disruption ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier

Propitious Therapeutic Modulators to Prevent Blood-Spinal Cord Barrier Disruption in Spinal Cord Injury

2016 ◽  
Vol 54 (5) ◽  
pp. 3578-3590 ◽  
Author(s):  
Hemant Kumar ◽  
Alexander E. Ropper ◽  
Soo-Hong Lee ◽  
Inbo Han
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Barrier Disruption ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier

scholarly journals Role of hypoxia-induced VEGF in blood-spinal cord barrier disruption in chronic spinal cord injury

2015 ◽  
Vol 18 (5) ◽  
pp. 293-295 ◽  
Author(s):  
Hou-Qing Long ◽  
Guang-Sheng Li ◽  
Xing Cheng ◽  
Jing-Hui Xu ◽  
Fo-Bao Li
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Chronic Spinal Cord Injury ◽  
Barrier Disruption ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier

scholarly journals Neutrophil Extracellular Traps Exacerbate Secondary Injury via Promoting Neuroinflammation and Blood–Spinal Cord Barrier Disruption in Spinal Cord Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhou Feng ◽  
Lingxia Min ◽  
Liang Liang ◽  
Beike Chen ◽  
Hui Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Transient Receptor Potential ◽  
Neutrophil Extracellular Traps ◽  
Transient Receptor Potential Vanilloid ◽  
Barrier Disruption ◽  
Extracellular Traps ◽  
Secondary Damage ◽  
Cord Injury ◽  
Blood Spinal Cord Barrier

As the first inflammatory cell recruited to the site of spinal cord injury (SCI), neutrophils were reported to be detrimental to SCI. However, the precise mechanisms as to how neutrophils exacerbate SCI remain largely obscure. In the present study, we demonstrated that infiltrated neutrophils produce neutrophil extracellular traps (NETs), which subsequently promote neuroinflammation and blood–spinal cord barrier disruption to aggravate spinal cord edema and neuronal apoptosis following SCI in rats. Both inhibition of NETs formation by peptidylarginine deiminase 4 (PAD4) inhibitor and disruption of NETs by DNase 1 alleviate secondary damage, thus restraining scar formation and promoting functional recovery after SCI. Furthermore, we found that NETs exacerbate SCI partly via elevating transient receptor potential vanilloid type 4 (TRPV4) level in the injured spinal cord. Therefore, our results indicate that NETs might be a promising therapeutic target for SCI.

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