Delayed neuronal damage related to microglia proliferation after mild spinal cord compression injury

Morino, Tadao; Ogata, Tadanori; Horiuchi, Hideki; Takeba, Jun; Okumura, Hideo; Miyazaki, Tsuyoshi; Yamamoto, Haruyasu

doi:10.1016/s0168-0102(03)00095-6

Cited by 47 publications

(33 citation statements)

References 21 publications

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“…The proliferated microglia were positively stained by anti-TNF-a and anti-iNOS antibodies. 9 We concluded that the delayed motor dysfunction is related to microglial proliferation via its inflammatory responses. Since inflammatory responses continue several days after CNS damage, inhibitory therapy for such delayed mechanisms, including microglial proliferation, should be effective even after the acute phase in SCI.…”

Section: Discussionmentioning

confidence: 85%

“…[6][7][8] Previously, we developed a model for mild spinal cord compression injuries using rats. 9 In this model, microglia proliferated and were activated after spinal cord compression. The proliferated microglia produced TNF-a and iNOS.…”

Section: Introductionmentioning

confidence: 88%

“…9 Under general anesthesia using halothane, the rat's tenth and eleventh vertebral lamina were removed carefully without any damage to the spinal cord. Direct compression on the eleventh vertebral level was performed using a 20 g weight.…”

Section: Animalsmentioning

confidence: 99%

“…A decrease in the standing frequency reflects the severity of motor dysfunction of the hind limbs induced by thoracic spinal cord damage. 9 The standing frequency was measured for 1 h. Measurements were taken 24, 48 and 72 h after the spinal cord compression in a dark, silent room to prevent the influence of noise and light. Results were expressed as percentages of the average value from the sham rats (mean±s.e.m.).…”

Section: Evaluation Of the Rat Behaviormentioning

confidence: 99%

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Microglia inhibition is a target of mild hypothermic treatment after the spinal cord injury

et al. 2008

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Study Design: A basic study using a spinal cord injury (SCI) model in rats. Objectives: The effect of mild hypothermic treatment on histological changes and motor function after a rat spinal cord compression injury was assessed. Methods: Mild spinal cord compression was performed at the eleventh thoracic vertebral level by a 20 g weight for 20 min. Rats in the mild hypothermic model were kept at a body temperature of 33 1C and rats in the normothermic group were kept at 37 1C for 1 h from beginning of compression. Motor function was evaluated by measuring the frequency of standing. Microglia were stained by isolectin B4 and observed in the compressed portion of the spinal cord. The amount of tumor necrosis factor-a (TNF-a) in the compressed spinal cord was measured by the ELISA method. Results: In the normothermic rats, microglia proliferated up to 72 h after the compression. Proliferation was substantially inhibited at 48 and 72 h after compression in the hypothermic rats. The motor function of the hypothermic rats improved at 48 and 72 h after the compression, whereas no improvement was seen in the normothermic rats. The amount of TNF-a in the compressed portion of the spinal cord was lower in hypothermic rats compared with normothermic rats throughout the experiment. Conclusions: These results suggest that hypothermic treatment is effective for the amelioration of delayed motor dysfunction via inhibition of microglial inflammatory responses.

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Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 88%

Section: Animalsmentioning

confidence: 99%

Section: Evaluation Of the Rat Behaviormentioning

confidence: 99%

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Microglia inhibition is a target of mild hypothermic treatment after the spinal cord injury

et al. 2008

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“…After a compression injury, microglial proliferation and activation in the spinal cord tissue occur up to 72 h after compression. 11 Grabits et al 20 reported that PGE1 protected the spinal cord when they applied it 1 h after aortic occlusion. These reports indicate that not only acute, but also delayed neuronal degradation caused by pathological inflammatory responses to spinal cord ischemia can be prevented by the application of PGE1.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E1 analog increases spinal cord blood flow at the point of compression during and after experimental spinal cord injury

et al. 2009

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Study design: An in vivo study using a spinal cord compression model in rats. Objectives: To evaluate the effect of prostaglandin E1 (PGE1) on the change in thoracic spinal cord blood flow and on hind-limb motor function. Background: Until now, effect of PGE1 on spinal cord blood flow at the point of compression has not been tested. Methods: Our newly developed blood flow measurement system was a combination of a noncontacttype Laser Doppler system and a spinal cord compression device. The rat thoracic spinal cord was exposed and spinal cord blood flow at the point of compression was measured before, during and after compression. The functioning of the animals' hind-limbs was evaluated by the BBB Scale and by measuring the frequency of voluntary standing. Results: During the compression period, spinal cord blood flow was significantly higher in the PGE1-treated rats than in the control rats, which did not receive PGE1. After decompression, the spinal cord blood flow rapidly recovered to about 60% of the precompression level in the control rats. When the animals were treated with PGE1, blood flow after decompression reached about 90% of the precompression level. Twenty-gram compression for 40 mins induced motor deficiencies in the rat hind-limbs. The application of PGE1 significantly improved motor function of the rat hind-limbs after spinal cord injury. Conclusions: The application of PGE1 increased spinal cord blood flow during and after spinal cord compression, and improved motor function after the spinal cord injury.

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Advances in Biomaterial‐Based Spinal Cord Injury Repair

Shen

Fan

You

et al. 2021

Adv Funct Materials

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Spinal cord injury (SCI) often leads to the loss of motor and sensory functions and is a major challenge in neurological clinical practice. Understanding the pathophysiological changes and the inhibitory microenvironment is crucial to enable the identification of potential mechanisms for functional restoration and to provide guidance for the development of efficient treatment and repair strategies. To date, the implantation of specifically functionalized biomaterials in the lesion area has been shown to help promote axon regeneration and facilitate neuronal circuit generation by remolding SCI microenvironments. Moreover, structural and functional restoration of the spinal cord through the transplantation of naive spinal cord tissue grafts from adult donors, artificial spinal cord-like tissue developed from tissue engineering, and 3D printing will open up new avenues for SCI treatment. This review focuses on the dynamic pathophysiological changes in SCI microenvironments, biomaterials for SCI repairs, strategies for restoring spinal cord structure and function, experimental animal models, regenerative mechanisms, and clinical studies for SCI repair. The current status, recent advances, challenges, and prospects of scaffold-based SCI repair from basic to clinical settings are summarized and discussed, to provide a reference that will help to guide the future exploration and development of spinal cord regeneration strategies.

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Delayed neuronal damage related to microglia proliferation after mild spinal cord compression injury

Cited by 47 publications

References 21 publications

Microglia inhibition is a target of mild hypothermic treatment after the spinal cord injury

Microglia inhibition is a target of mild hypothermic treatment after the spinal cord injury

Prostaglandin E1 analog increases spinal cord blood flow at the point of compression during and after experimental spinal cord injury

Advances in Biomaterial‐Based Spinal Cord Injury Repair

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