Transplantation of Olfactory Ensheathing Cells in Spinal Cord Injury

Velasquez, Johana Tello; Ekberg, Jenny; John, James St

doi:10.1007/978-3-319-11481-1_13

Cited by 4 publications

(5 citation statements)

References 151 publications

(199 reference statements)

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“…It can lead to severe motor, sensory and autonomic dysfunction [3]. Moreover, traumatic SCI can cause several devastating symptoms, including chronic pain and paralysis [4,5]. Despite great efforts made to improve the functional outcome, current effective treatment for SCI is limited [6].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

Guo

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Spinal cord injury (SCI) is a grievous neurology-related disorder that causes many devastating symptoms. This research planned to dig the function and latent mechanisms of long noncoding RNA (lncRNA) ANRIL on hydrogen peroxide (H 2 O 2)-disposed injury in PC-12 cells. The PC-12 cells were disposed with H 2 O 2 for 24 h to construct the SCI model. H 2 O 2-disposed PC-12 cells was assessed by detecting cell viability, migration, invasion, apoptosis and autophagy. The level of ANRIL in H 2 O 2-disposed PC-12 cells was analysed, afterwards, the impacts of ANRIL silencing on H 2 O 2-disposed PC-12 cell injury was determined. The regulatory association between ANRIL and miR-499a, between miR-499a and PDCD4, as well as PDCD4 and PI3K/Akt/mTOR/p70S6K signals were investigated. H 2 O 2 produced PC-12 cell injury and promoted the level of ANRIL. Silencing of ANRIL inhibited H 2 O 2-disposed PC-12 cell injury through promoting cell viability, migration, invasion and inhibiting apoptosis and autophagy. Moreover, miR-499a was upregulated after silencing of ANRIL, and inhibition of miR-499a reversed the effects of silencing of ANRIL on H 2 O 2-disposed PC-12 cell injury. Also, PDCD4 was a target of miR-499a. Furthermore, ANRIL silencing alleviated the H 2 O 2-disposed injury in PC-12 cells possible by activating PI3K/Akt/mTOR/p70S6K signals, which was mediated by miR-499a/PDCD4 axis. Our results indicate that high level of ANRIL may sharpen the degree of SCI via targeting miR-499a/PDCD4 axis to regulate the briskness of PI3K/Akt/mTOR/p70S6K signals.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

Guo

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…1,2 Traumatic SCI can have several devastating consequences, such as chronic pain and paralysis. 3,4 Bone loss caused by SCI is refractory to interventions. 5 Moreover, the key mechanisms governing the cellular response to injury are largely known.…”

Section: Introductionmentioning

confidence: 99%

“…Spinal cord injury (SCI) is a serious neurological disease characterized by loss of nervous tissue and the consequent deficit of sensory and motor functions . Traumatic SCI can have several devastating consequences, such as chronic pain and paralysis . Bone loss caused by SCI is refractory to interventions .…”

Section: Introductionmentioning

confidence: 99%

Retracted: Downregulation of long noncoding RNA Sox2ot protects PC‐12 cells from hydrogen peroxide–induced injury in spinal cord injury via regulating the miR‐211‐myeloid cell leukemia‐1 isoform2 axis

Yin

Zheng

Zhuang

et al. 2018

J of Cellular Biochemistry

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This study aimed to investigate the effects and possible mechanisms of long noncoding RNA (lncRNA) Sox2 overlapping transcript (Sox2ot) on hydrogen peroxide (H O )-induced injury in pheochromocytoma (PC-12) cells. PC-12 cells were treated with H O to cell injury. The cells were transfected with short-hairpin RNA directed against Sox2ot (sh-Sox2ot), small interfering RNA directed against myeloid cell leukemia-1 (MCL-1) isoform2 (si-MCL-1), a miR-211 mimic, a miR-211 inhibitor, and their negative controls. Under different transfected treatments, cell viability, migration, invasion, and apoptosis as well as the expressions of apoptosis- and autophagy-related proteins were investigated. Besides, the regulatory relationships between Sox2ot and miR-211, miR-211 and MCL-1, as well as between MCL-1 and the protein kinase B (Akt)/mammalian target of the rapamycin (mTOR)/p70 ribosomal S6 protein kinase (p70S6K) signaling pathway were explored. Suppression of Sox2ot inhibited H O -induced PC-12 cell injury by increasing cell viability, migration, invasion, and decreasing apoptosis and autophagy. Moreover, suppression of Sox2ot increased miR-211 expression and alleviated H O -induced injury in PC-12 cells possibly via upregulation of miR-211. Furthermore, MCL-1 isoform2 was identified as a direct target of miR-211 and could be negatively regulated by miR-211. Suppression of miR-211 aggravated H O -induced cell injury by regulation of MCL-1 isoform2. Besides, inhibition of miR-211 suppressed the activation of the Akt/mTOR/p70S6K signaling pathway in H O -treated PC-12 cells, which was reversed after knockdown of MCL-1 isoform2 at the same time. Our findings indicate that downregulation of Sox2ot may protect PC-12 cells from H O -induced injury in SCI via targeting the miR-211/MCL-1 isoform2 axis. MCL-1 isoform2 may further regulate the activation of the Akt/mTOR/p70S6K pathway to mediate H O -induced injury. The Sox2ot-miR-211-MCL-1 isoform2 axis may be a promising therapeutic strategy for SCI.

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“…Internal to the glomerular layer are, from outside inwards, the external plexiform, mitral, internal plexiform, and granule cell layers (Au, Treloar, & Greer, 2002;Mombaerts et al, 1996;Royal & Key, 1999). OECs are present in both the inner and the outer NFL but have distinct properties and expression profile depending on anatomical location (Tello Velasquez, Ekberg, & St John, 2015;Windus et al, 2010).…”

Section: Which Cells Form the Glia Limitans Of The Olfactory Bulb?mentioning

confidence: 99%

“…Internal to the glomerular layer are, from outside inwards, the external plexiform, mitral, internal plexiform, and granule cell layers (Au, Treloar, & Greer, ; Mombaerts et al, ; Royal & Key, ). OECs are present in both the inner and the outer NFL but have distinct properties and expression profile depending on anatomical location (Tello Velasquez, Ekberg, & St John, ; Windus et al, ). Internal to the inner NFL, the glomerular layer is populated by astrocytes (Bailey & Shipley, ; Chiu & Greer, ) that express glial fibrillary acidic protein (GFAP); however, unlike most other astrocyte populations do not express S100β (Windus et al, ) (Figure g–k).…”

Section: Introductionmentioning

confidence: 99%

Novel insights into the glia limitans of the olfactory nervous system

Nazareth

Chen

Shelper

et al. 2019

J of Comparative Neurology

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Olfactory ensheathing cells (OECs) are often described as being present in both the peripheral and the central nervous systems (PNS and CNS). Furthermore, the olfactory nervous system glia limitans (the glial layer defining the PNS–CNS border) is considered unique as it consists of intermingling OECs and astrocytes. In contrast, the glia limitans of the rest of the nervous system consists solely of astrocytes which create a distinct barrier to Schwann cells (peripheral glia). The ability of OECs to interact with astrocytes is one reason why OECs are believed to be superior to Schwann cells for transplantation therapies to treat CNS injuries. We have used transgenic reporter mice in which glial cells express DsRed fluorescent protein to study the cellular constituents of the glia limitans. We found that the glia limitans layer of the olfactory nervous system is morphologically similar to elsewhere in the nervous system, with a similar low degree of intermingling between peripheral glia and astrocytes. We found that the astrocytic layer of the olfactory bulb is a distinct barrier to bacterial infection, suggesting that this layer constitutes the PNS–CNS immunological barrier. We also found that OECs interact with astrocytes in a similar fashion as Schwann cells in vitro. When cultured in three dimensions, however, there were subtle differences between OECs and Schwann cells in their interactions with astrocytes. We therefore suggest that glial fibrillary acidic protein–reactive astrocyte layer of the olfactory bulb constitutes the glia limitans of the olfactory nervous system and that OECs are primarily “PNS glia.”

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Transplantation of Olfactory Ensheathing Cells in Spinal Cord Injury

Cited by 4 publications

References 151 publications

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

Retracted: Downregulation of long noncoding RNA Sox2ot protects PC‐12 cells from hydrogen peroxide–induced injury in spinal cord injury via regulating the miR‐211‐myeloid cell leukemia‐1 isoform2 axis

Novel insights into the glia limitans of the olfactory nervous system

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