Newly Formed Endothelial Cells Regulate Myeloid Cell Activity Following Spinal Cord Injury via Expression of CD200 Ligand

Abstract Background: The permeability of blood-spinal cord barrier (BSCB) is mainly determined by the junction complex between adjacent endothelial cells, including tight junctions (TJ) and adhesion junctions (AJ), which can be severely damaged after spinal cord injury (SCI). Exercise training is a recognized method for the treatment of SCI. The destruction of the BSCB mediated by matrix metalloproteinase (MMP) leads to inflammation, neurotoxin production, and apoptosis of neurons. The failure of effective regeneration of new blood vessels is also an important reason for delayed recovery after SCI. We introduced water treadmill training (TT) for the first time, which can help SCI rats successfully exercise and measured the effect of TT in promoting recovery after SCI and possible mechanisms involved.Methods: Sprague-Dawley (200–250g) rats were randomly divided into three groups: Sham operated, SCI, and SCI + TT. Animals were sacrificed 7 d or 14 d post-surgery. The degree of neurological deficit as assessed by the Basso-Beattie-Bresnahan motor rating scale, tissue water content, BSCB permeability, apoptosis, protein expression and ultrastructure of vascular endothelial cells were assessed, Western blot, immunofluorescence and transmission electron microscopy. Results: Our experiments showed that TT reduced the permeability of BSCB and decreased tissue structural damage. TT improved functional recovery significantly when compared with the SCI group; TJ and AJ proteins expression increased significantly after TT training and training reduced apoptosis induced by SCI. TT can promote angiogenesis and the expression of MMP-2 and MMP-9 was significantly inhibited by TT.Conclusions: In this study, the results indicate that TT promotes functional recovery for the following reasons: (1) TT protects residual BSCB structure from further damage; (2) it promotes vascular regeneration; and (3) it inhibits the expression of MMP-2/9 to mitigate BSCB damage.

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Selenium-Binding Protein 1 (SELENBP1) as Biomarker for Adverse Clinical Outcome After Traumatic Spinal Cord Injury

Frontiers in Neuroscience ◽

10.3389/fnins.2021.680240 ◽

2021 ◽

Vol 15 ◽

Author(s):

Julian Seelig ◽

Raban Arved Heller ◽

Patrick Haubruck ◽

Qian Sun ◽

Jochen Georg Klingenberg ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Spinal Injury ◽

Cell Damage ◽

Cell Activity ◽

Mechanical Trauma ◽

Specific Cell ◽

Traumatic Spinal Cord Injury ◽

Cord Injury ◽

Sensory Functions

Graphical AbstractThe pathophysiology of traumatic spinal cord injury (TSCI) can be divided into two major phases. (A) The mechanical trauma is followed within minutes by a secondary phase consisting of local complex and intertwined acute responses, intercellular signaling and cell activity regulating pathways. Inflammatory processes, oxidative stress and hypoxia, leading to cell damage and death, and specific cell contents are released into the circulation (B). The motor and sensory deficits upon TSCI are assessed by using the American Spinal Injury Association (ASIA) impairment scale (AIS), ranging from AIS A as a complete absence of any motor and sensory functions under the lesion site, to AIS E with complete preservation of motor and sensory functions. (C) The concentrations of serum SELENBP1 were elevated in patients classified as AIS A as compared to less severely affected patients classified as AIS B, C or D. A cut-off was deduced [(SELENBP1) > 30.2 μg/L], reliably predicting whether a patient belongs to the group showing neurological recovery (G1) or not (G0) within 3 months after the trauma. The figure was created by using https://biorender.com.

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305. Effects of moderate spinal cord injury on the expression of a barrier marker in endothelial cells of the testis and in the prostate of rats

Reproduction Fertility and Development ◽

10.1071/srb05abs305 ◽

2005 ◽

Vol 17 (9) ◽

pp. 130

Author(s):

M. N. Ghabriel ◽

J. J. Lu ◽

W. H. Lim ◽

B. P. Setchell

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Endothelial Cells ◽

Ventral Prostate ◽

Slight Reduction ◽

Brain Endothelial Cells ◽

Adult Rats ◽

Cord Injury ◽

The Central Nervous System ◽

Endothelial Barrier Antigen

It was recently shown that the endothelial barrier antigen (EBA), previously thought to be specific to endothelial cells in the central nervous system, was also present in endothelial cells in the testis and in epithelial cells in the dorsolateral prostate of adult rats.1 In the present study, we examined the effect of moderate spinal cord injury (SCI), produced by compression for 5 min of the cord at T 10/11. There was a slight reduction in EBA in the testis and prostate 24 h after SCI, and this became more obvious after 3days. EBA was completely absent from the prostate and testis at 1 week. By 2 and 4 weeks some expression of EBA returned, and at these times EBA was also detected in the ventral prostate. Brain endothelial cells remained positive throughout. We cannot yet say whether these changes are due directly to interference with the nerve supply, or involve changes in androgen status. (1)Ghabriel MN, Lu JJ, Hermanis G, Zhu C, Setchell BP (2002) Reproduction 123, 389–397.

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M1 macrophages impair tight junctions between endothelial cells after spinal cord injury

Brain Research Bulletin ◽

10.1016/j.brainresbull.2021.12.019 ◽

2022 ◽

Author(s):

Yang Luo ◽

Fei Yao ◽

Xuyang Hu ◽

Yiteng Li ◽

Yihao Chen ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Endothelial Cells ◽

Tight Junctions ◽

M1 Macrophages ◽

Cord Injury

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ADAM8 is selectively up-regulated in endothelial cells and is associated with angiogenesis after spinal cord injury in adult mice

The Journal of Comparative Neurology ◽

10.1002/cne.21902 ◽

2009 ◽

Vol 512 (2) ◽

pp. 243-255 ◽

Cited By ~ 35

Author(s):

Edward T. Mahoney ◽

Richard L. Benton ◽

Melissa A. Maddie ◽

Scott R. Whittemore ◽

Theo Hagg

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Endothelial Cells ◽

Adult Mice ◽

Cord Injury

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Aquaporins and Their Regulation after Spinal Cord Injury

Cells ◽

10.3390/cells7100174 ◽

2018 ◽

Vol 7 (10) ◽

pp. 174 ◽

Cited By ~ 2

Author(s):

Andrea Halsey ◽

Alex Conner ◽

Roslyn Bill ◽

Ann Logan ◽

Zubair Ahmed

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Endothelial Cells ◽

Membrane Proteins ◽

Water Movement ◽

Ependymal Cells ◽

Negative Effects ◽

Cord Injury ◽

Spinal Cord Edema

After injury to the spinal cord, edema contributes to the underlying detrimental pathophysiological outcomes that lead to worsening of function. Several related membrane proteins called aquaporins (AQPs) regulate water movement in fluid transporting tissues including the spinal cord. Within the cord, AQP1, 4 and 9 contribute to spinal cord injury (SCI)-induced edema. AQP1, 4 and 9 are expressed in a variety of cells including astrocytes, neurons, ependymal cells, and endothelial cells. This review discusses some of the recent findings of the involvement of AQP in SCI and highlights the need for further study of these proteins to develop effective therapies to counteract the negative effects of SCI-induced edema.

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