Effects of Nogo-A receptor antagonist on the regulation of the Wnt signaling pathway and neural cell proliferation in newborn rats with hypoxic ischemic encephalopathy

Wang, Yongxiang; Gu, Jiaxiang; Feng, Xinmin; Wang, Hua; Tao, Yajun; Wang, Jingcheng

doi:10.3892/mmr.2013.1579

Cited by 5 publications

(3 citation statements)

References 20 publications

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“…Studies have indicated that increased TGF-β signaling after stroke is neuroprotective and likely to be an important target for future stroke therapies [ 19 , 20 ]. WNT signaling can enhance neurogenesis and improve neurological function after ischemic injury [ 21 , 22 ]; it also has anti-inflammatory effects [ 23 ] and is neuroprotective in stroke [ 24 ]. Besides, Atherosclerosis_Role of ZNF202, Regulation of metabolism_Bile acids, regulation of glucose, and lipid metabolism via FXR, Neurophysiological process_HTR1A receptor signaling in neuronal cells, are also pathways that play important roles in neuroprotection [ 25 – 28 ].…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling Confirms the Dosage-Dependent Additive Neuroprotective Effects of Jasminoidin in a Mouse Model of Ischemia-Reperfusion Injury

Wang

et al. 2018

BioMed Research International

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Recent evidence demonstrates that a double dose of Jasminoidin (2·JA) is more effective than Jasminoidin (JA) in cerebral ischemia therapy, but its dosage-effect mechanisms are unclear. In this study, the software GeneGo MetaCore was used to perform pathway analysis of the differentially expressed genes obtained in microarrays of mice belonging to four groups (Sham, Vehicle, JA, and 2·JA), aiming to elucidate differences in JA and 2·JA's dose-dependent pharmacological mechanism from a system's perspective. The top 10 enriched pathways in the 2·JA condition were mainly involved in neuroprotection (70% of the pathways), apoptosis and survival (40%), and anti-inflammation (20%), while JA induced pathways were mainly involved in apoptosis and survival (60%), anti-inflammation (20%), and lipid metabolism (20%). Regarding shared pathways and processes, 3, 1, and 3 pathways overlapped between the Vehicle and JA, Vehicle and 2·JA, and JA and 2·JA conditions, respectively; for the top ten overlapped processes these numbers were 3, 0, and 4, respectively. The common pathways and processes in the 2·JA condition included differentially expressed genes significantly different from those in JA. Seven representative pathways were only activated by 2·JA, such as Gamma-Secretase regulation of neuronal cell development. Process network comparison indicated that significant nodes, such as alpha-MSH, ACTH, PKR1, and WNT, were involved in the pharmacological mechanism of 2·JA. Function distribution was different between JA and 2·JA groups, indicating a dosage additive mechanism in cerebral ischemia treatment. Such systemic approach based on whole-genome multiple pathways and networks may provide an effective and alternative approach to identify alterations underlining dosage-dependent therapeutic benefits of pharmacological compounds on complex disease processes.

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Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling Confirms the Dosage-Dependent Additive Neuroprotective Effects of Jasminoidin in a Mouse Model of Ischemia-Reperfusion Injury

Wang

et al. 2018

BioMed Research International

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“…Yang et al [ 16 ] found that Nogo-A silencing could promote the recovery of demyelinating disease. Wang et al [ 17 ] found that neurite outgrowth inhibition by Nogo-A was closely related with Wnt pathways, c-Jun, and c-Myc. Some scholars believed that Nogo-A is also involved in neuronal differentiation, apoptosis, and generation of free radicals [ 18 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Nogo-A Silencing on TNF-αand IL-6 Secretion and TH Downregulation in Lipopolysaccharide-Stimulated PC12 Cells

Zhong

Fan

Yan

et al. 2015

BioMed Research International

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Parkinson's disease (PD) is a common degenerative disease that lacks efficient treatment. Myelin-associated neurite outgrowth inhibitor A (Nogo-A) is relevant with inhibition of nerve regeneration and may play vital role in pathogenesis of PD. The study aimed to establish the shRNA expression plasmids of Nogo-A gene and explore the regulatory effects of Nogo-A silencing on the expression of inflammation factor tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) as well as tyrosine hydroxylase (TH) in lipopolysaccharide- (LPS-) stimulated rat PC12 cells. The results showed that both mRNA and protein levels of Nogo-A in pGenesil-nogoA-shRNA group were downregulated. The viabilities of PC12 cells decreased with increase of LPS concentrations. LPS significantly increased the supernatant TNF-alpha and IL-6 concentrations and reduced TH protein expression in PC12 cells, while silencing Nogo-A could block these effects. These results suggested that LPS can activate PC12 cells to secrete inflammatory cytokines and lower the TH expression, which can be regulated by Nogo-A gene silencing. Nogo-A silencing might provide new ideas for PD treatment in the future.

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“…Following SCI, the response of the host can generate an ischemic environment that can lead to cell death. Furthermore, this ischemic environment limits cell transplantation approaches that could be used to promote spinal cord regeneration (26). It has been widely accepted that apoptosis is the most common form of cell death following SCI.…”

Section: Discussionmentioning

confidence: 99%

Batroxobin protects against spinal cord injury in rats by promoting the expression of vascular endothelial growth factor to reduce apoptosis

Lin

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The host response to spinal cord injury (SCI) can lead to an ischemic environment that can induce cell death. Therapeutic interventions using neurotrophic factors have focused on the prevention of such reactions in order to reduce this cell death. Vascular endothelial growth factor (VEGF) is a potent angiogenic and vascular permeability factor. We hypothesized in this study that batroxobin would exhibit protective effects following SCI by promoting the expression of VEGF to reduce the levels of apoptosis in a rat model of SCI. Ninety adult female Sprague Dawley rats were divided randomly into sham injury (group I), SCI (group II) and batroxobin treatment (group III) groups. The Basso-Bettie-Bresnahan (BBB) scores, number of apoptotic cells and expression of VEGF were assessed at 1, 3, 5, 7, 14 and 28 days post-injury. The BBB scores were significantly improved in group III compared with those in group II between days 5 and 28 post-injury (P<0.05). At each time-point subsequent to the injury, the number of apoptotic cells in group III was reduced compared with that in group II. Compared with group II, treatment with batroxobin significantly increased the expression of VEGF from day 3 until 2 weeks post-SCI (P<0.05), while no significant difference was observed at day 28. These data suggest that batroxobin has multiple beneficial effects on SCI, indicating a potential clinical application.

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Effects of Nogo-A receptor antagonist on the regulation of the Wnt signaling pathway and neural cell proliferation in newborn rats with hypoxic ischemic encephalopathy

Cited by 5 publications

References 20 publications

Gene Expression Profiling Confirms the Dosage-Dependent Additive Neuroprotective Effects of Jasminoidin in a Mouse Model of Ischemia-Reperfusion Injury

Gene Expression Profiling Confirms the Dosage-Dependent Additive Neuroprotective Effects of Jasminoidin in a Mouse Model of Ischemia-Reperfusion Injury

Effects of Nogo-A Silencing on TNF-αand IL-6 Secretion and TH Downregulation in Lipopolysaccharide-Stimulated PC12 Cells

Batroxobin protects against spinal cord injury in rats by promoting the expression of vascular endothelial growth factor to reduce apoptosis

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