Induction of Autophagy and Autophagic Cell Death in Damaged Neural Tissue After Acute Spinal Cord Injury in Mice

Spine ◽  
2011 ◽  
Vol 36 (22) ◽  
pp. E1427-E1434 ◽  
Author(s):  
Haruo Kanno ◽  
Hiroshi Ozawa ◽  
Akira Sekiguchi ◽  
Seiji Yamaya ◽  
Eiji Itoi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Neural Tissue ◽  
Acute Spinal Cord Injury ◽  
Autophagic Cell Death ◽  
Cord Injury

scholarly journals Changes in Expression of Receptor-Interacting Protein Kinase 1 in Secondary Neural Tissue Damage Following Spinal Cord Injury

2020 ◽  
Vol 15 ◽  
pp. 263310552090640
Author(s):  
Haruo Kanno ◽  
Hiroshi Ozawa ◽  
Kyoichi Handa ◽  
Taishi Murakami ◽  
Eiji Itoi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Tissue Damage ◽  
Time Course ◽  
Apoptotic Cell ◽  
Neural Tissue ◽  
Apoptotic Cell Death ◽  
Neural Cells ◽  
Cord Injury

Introduction: Necroptosis is a form of programmed cell death that is different from apoptotic cell death. Receptor-interacting protein kinase 1 (RIPK1) plays a particularly important function in necroptosis execution. This study investigated changes in expression of RIPK1 in secondary neural tissue damage following spinal cord injury in mice. The time course of the RIPK1 expression was also compared with that of apoptotic cell death in the lesion site. Methods and Materials: Immunostaining for RIPK1 was performed at different time points after spinal cord injury. The protein expressions of RIPK1 were determined by western blot. The RIPK1 expressions in various neural cells were investigated using immunohistochemistry. To investigate the time course of apoptotic cell death, TUNEL-positive cells were counted at the different time points. To compare the incidence of necroptosis and apoptosis, the RIPK1-labeled sections were co-stained with TUNEL. Results: The RIPK1 expression was significantly upregulated in the injured spinal cord. The upregulation of RIPK1 expression was observed in neurons, astrocytes, and oligodendrocytes. The increase in RIPK1 expression started at 4 hours and peaked at 3 days after injury. Time course of the RIPK1 expression was similar to that of apoptosis detected by TUNEL. Interestingly, the increased expression of RIPK1 was rarely observed in the TUNEL-positive cells. Furthermore, the number of RIPK1-positive cells was significantly higher than that of TUNEL-positive cells. Conclusions: This study demonstrated that the expression of RIPK1 increased in various neural cells and peaked at 3 days following spinal cord injury. The temporal change of the RIPK1 expression was analogous to that of apoptosis at the lesion site. However, the increase in RIPK1 expression was barely seen in the apoptotic cells. These findings suggested that the RIPK1 might contribute to the pathological mechanism of the secondary neural tissue damage after spinal cord injury.

Spinal cord injury induces upregulation of Beclin 1 and promotes autophagic cell death

2009 ◽  
Vol 33 (2) ◽  
pp. 143-148 ◽  
Author(s):  
Haruo Kanno ◽  
Hiroshi Ozawa ◽  
Akira Sekiguchi ◽  
Eiji Itoi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Autophagic Cell Death ◽  
Beclin 1 ◽  
Cord Injury

Anti-Apoptotic Effect of Insulin in the Control of Cell Death and Neurologic Deficit after Acute Spinal Cord Injury in Rats

2007 ◽  
Vol 24 (9) ◽  
pp. 1502-1512 ◽  
Author(s):  
Xing-Huo Wu ◽  
Shu-Hua Yang ◽  
De-Yu Duan ◽  
Heng-Hui Cheng ◽  
Yu-Ting Bao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Neurologic Deficit ◽  
Acute Spinal Cord Injury ◽  
Cord Injury ◽  
Apoptotic Effect

scholarly journals MP Resulting in Autophagic Cell Death of Microglia through Zinc Changes against Spinal Cord Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Dingding Li ◽  
Guannan Wang ◽  
Donghe Han ◽  
Jing Bi ◽  
Chenyuan Li ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Death ◽  
Motor Neurons ◽  
Neuroprotective Effect ◽  
Pulse Therapy ◽  
Autophagic Cell Death ◽  
Cord Injury

Methylprednisolone pulse therapy (MPPT), as a public recognized therapy of spinal cord injury (SCI), is doubted recently, and the exact mechanism of MP on SCI is unclear. This study sought to investigate the exact effect of MP on SCI. We examined the effect of MP in a model of SCI in vivo and an LPS induced model in vitro. We found that administration of MP produced an increase in the Basso, Beattie, and Bresnahan scores and motor neurons counts of injured rats. Besides the number of activated microglia was apparently reduced by MP in vivo, and Beclin-1 dependent autophagic cell death of microglia was induced by MP in LPS induced model. At the same time, MP increases cellular zinc concentration and level of ZIP8, and TPEN could revert effect of MP on autophagic cell death of microglia. Finally, we have found that MP could inhibit NF-κβin LPS induced model. These results show that the MP could result in autophagic cell death of microglia, which mainly depends on increasing cellular labile zinc, and may be associated with inhibition of NF-κβ, and that MP can produce neuroprotective effect in SCI.

Vasopressor support in managing acute spinal cord injury: current knowledge

2019 ◽  
Vol 63 (3) ◽  
Author(s):  
John K. Yue ◽  
Rachel E. Tsolinas ◽  
John F. Burke ◽  
Hansen Deng ◽  
Pavan S. Upadhyayula ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Current Knowledge ◽  
Acute Spinal Cord Injury ◽  
Vasopressor Support ◽  
Cord Injury
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