Effects of Therapeutic Hypothermia on Apoptosis and Autophagy After Spinal Cord Injury in Rats

Seo, Jun-Yeong; Kim, Young-Hoon; Kim, Jang-Woon; Kim, Shin Il; Ha, Kee-Yong

doi:10.1097/brs.0000000000000845

Cited by 42 publications

(26 citation statements)

References 20 publications

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“…Accumulating evidence has demonstrated that autophagy activation is elevated in the central nervous system under stressed conditions (Park et al, 2015;Li et al, 2015a;Villamil-Ortiz and Cardona-Gomez, 2015;Yang et al, 2015). As shown in the previous studies, autophagy plays an important role in spinal cord injury (Baba et al, 2009;Seo et al, 2015;Fujita et al, 2015); however, its expression change and mechanism after spinal cord I/R injury are largely unknown. Furthermore, the role of autophagy in ischemic injury remains controversial.…”

Section: Introductionmentioning

confidence: 85%

Role of autophagy in the bimodal stage after spinal cord ischemia reperfusion injury in rats

Fang

Bao

et al. 2016

Neuroscience

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Section: Introductionmentioning

confidence: 85%

Role of autophagy in the bimodal stage after spinal cord ischemia reperfusion injury in rats

Fang

Bao

et al. 2016

Neuroscience

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“…Although adequate surgical decompression is the preferred treatment for SCI and results in favorable outcomes, SCI patients experience unpredictable and disastrous postoperative complications [25,26]. A series of studies have indicated that SERCA2 has significant protective effects on the heart, liver, and other tissues by reducing endoplasmic reticulum stress and apoptosis [27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Exendin-4 Plays a Protective Role in a Rat Model of Spinal Cord Injury Through SERCA2

Sun

Liu

Kong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Current therapies for spinal cord injury (SCI) have limited efficacy, and identifying a therapeutic target is a pressing need. Sarcoplasmic/endoplasmic reticulum Ca²⁺ ATPase 2 (SERCA2) plays an important role in regulating calcium homeostasis, which has been shown to inhibit apoptosis. Exendin-4 has been shown to inhibit the apoptosis of nerve cells in SCI, which can also improve SERCA2 expression. In this study, we sought to determine whether exendin-4 plays a protective role in a rat model of SCI via SERCA2. Methods: To investigate the effects of exendin-4 on SCI, a rat model of SCI was induced by a modified version of Allen’s method. Spinal cord tissue sections from rats and western blot analysis were used to examine SERCA2 expression after treatment with the long-acting glucagon-like peptide 1 receptor exendin-4 or the SERCA2 antagonist 5(6)-carboxyfluorescein diacetate N-succinimidyl ester (CE). Locomotor function was evaluated using the Basso Beattie Bresnahan locomotor rating scale and slanting board test. Results: Cell apoptosis was increased with CE treatment and decreased with exendin-4 treatment. Upregulation of SERCA2 in female rats with SCI resulted in an improvement of motor function scores and histological changes. Conclusion: These findings suggest that exendin-4 plays a protective role in a rat model of SCI through SERCA2 via inhibition of apoptosis. Existing drugs targeting SERCA2 may be an effective therapeutic strategy for the treatment of SCI.

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“…These results suggest that the protective effect of hormones on spinal cord neurons may occur through inhibition of autophagy in spinal cord neurons, thereby reducing autophagic cell death. Seo et al suggested that the treatment of spinal cord injury using a high dose of hormone could reduce the level of autophagy and apoptosis in injured spinal cord neurons to reduce spinal cord injury [26].…”

Section: Discussionmentioning

confidence: 99%

Effects of Dexamethasone on Autophagy and Apoptosis in Acute Spinal Cord Injury

Wang

Zhou

Zheng

et al. 2017

J Spine

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Objectives: To investigate the effects of dexamethasone on autophagy and apoptosis in spinal cord neurons. Methods:We established an in vitro model of spinal cord injury and given different concentrations of dexamethasone at 24 hours after injury. Then we used western blot, MTT, flow cytometry, RT-PCR to detect the level of apoptosis. Western blotting was used to evaluate the expression of LC3. The TEM was used to observe the ultrastructure of the autophagosome. After we give the autophagy inhibitor (3-MA) and autophagy activator (Rapamycin). The autophagy and apoptosis were observed by western blot, flow cytometry, and RT-PCR Results:The results of MTT showed that 10 -6 M dexamethasone could increase the activity after cell injury. Meanwhile, flow cytometry, RT-PCR and western blot showed that 10 -6 M decreased the apoptosis level. Similarly, autolysosome can be observed after treatment with dexamethasone by electron microscope. At the same time the expression of LC3 protein and beclin-1 gene expression increased. Give autophagy activator (Rapamycin) can increase the level of autophagy, reduce cell apoptosis. In contrast, the autophagy inhibitor (3-MA) inhibits autophagy and increases apoptosis. Conclusion:In conclusion, our observations indicate that dexamethasone inhibited the level of autophagy in the injured nerve cells in a dose-dependent manner. High doses of dexamethasone protected the damaged spinal cord neurons by inhibiting apoptosis, but a protective effect from low hormone concentrations was not obvious.

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Effects of Therapeutic Hypothermia on Apoptosis and Autophagy After Spinal Cord Injury in Rats

Abstract: N/A.

Cited by 42 publications

References 20 publications

Role of autophagy in the bimodal stage after spinal cord ischemia reperfusion injury in rats

Role of autophagy in the bimodal stage after spinal cord ischemia reperfusion injury in rats

Exendin-4 Plays a Protective Role in a Rat Model of Spinal Cord Injury Through SERCA2

Effects of Dexamethasone on Autophagy and Apoptosis in Acute Spinal Cord Injury

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