Suppression of lncRNA-ATB prevents amyloid-β-induced neurotoxicity in PC12 cells via regulating miR-200/ZNF217 axis

Wang, Jindong; Zhou, Tian-Tian; Wang, Tian; Wang, Bailing

doi:10.1016/j.biopha.2018.08.155

Cited by 51 publications

(38 citation statements)

References 33 publications

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“…Among these, long noncoding RNA (lncRNA) as a kind of ceRNA, could participate in the regulation of diseases and share the mechanism with ceRNA to regulate transcription of scar related genes (Zhu et al, ). Study on keloid show that lncRNA‐ATB competitively bound miR‐200c to inhibit the expression of ZNF217 in keloid fibroblasts from affecting the self‐secretion of TGF‐β2, which suggested that lncRNA‐ATB/miR‐200c/ZNF217/TGF‐β2 signaling pathway might be a new target to involved in regulating the formation (Wang, Zhou, Wang, & Wang, ; Zhu et al, ). Also, in keloid and HTS fibroblasts, lncRNA COL1A2‐AS1 adsorbed miR‐21 as a competitive endogenous RNA sponge to inhibit miR‐21‐induced Smad7 expression and thereby initiate antifibrinolysis.…”

Section: The Epigenetic Mechanism Regulating the Formation Of Myofibrmentioning

confidence: 99%

Molecular mechanism of myofibroblast formation and strategies for clinical drugs treatments in hypertrophic scars

Zhu

Hou

et al. 2019

Journal Cellular Physiology

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Hypertrophic scars (HTS) commonly occurred after burn and trauma. It was characterized by the excessive deposition of extracellular matrix with the inadequate remodeling, which could result in severe physiological and psychological problems.However, the effective available prevention and treatment measures were still limited. The main pathological feature of HTS was the excessive formation of myofibroblasts, and they persist in the repaired tissue. To better understand the mechanics of this process, this review focused on the characteristics and formation of myofibroblasts, the main effector cells in HTS. We summarized the present theories and opinions on myofibroblasts formation from the perspective of related signaling pathways and epigenetic regulation, such as DNA methylation, miRNA/lncRNA/ ceRNA action, histone modification, and so forth for a better understanding on the development of HTS. This information might assist in developing effective experimental and clinical treatment strategies. Additionally, we also summarized currently known clinical strategies for HTS treatment, including traditional drugs, molecular medicine, stem cells, and exosomes. K E Y W O R D S epigenetic mechanism, extracellular matrix, hypertrophic scars, myofibroblast, stem cells

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Section: The Epigenetic Mechanism Regulating the Formation Of Myofibrmentioning

confidence: 99%

Molecular mechanism of myofibroblast formation and strategies for clinical drugs treatments in hypertrophic scars

Zhu

Hou

et al. 2019

Journal Cellular Physiology

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“…On the other hand, the MMP can be defined as the ratio of JC-1 aggregation (OD 590 ) and monomer (OD 530 ) [35]. A higher ratio of JC-1 aggregation and monomer means a higher MMP.…”

Section: Resultsmentioning

confidence: 99%

Optimization of Degradation Conditions with PRG, a Polysaccharide from Phellinus ribis, by RSM and the Neuroprotective Activity in PC12 Cells Damaged by Aβ25–35

et al. 2019

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In the previous work, we found PRG, a polysaccharide from Phellinus ribis, exhibited neurotrophic activity. To obtain an active structural unit with lower molecular weight, PRG was degraded to prepare the degraded PRG (DPRG) using ascorbic acid and H2O2. The aim of the paper was to obtain DPRG by optimizing the degradation conditions using response surface methodology (RSM) and to study its protective effects of PC12 cells induced by Aβ25–35. The optimum conditions were as follows; the concentration of H2O2-Vc was 17 mM and degradation temperature was 50 °C; when degradation time was 1.6 h, the experimental response value of PC12 cell viability was 83.4 ± 0.15%, which was in accordance with the predicted value (83.5%). We also studied the protective effects of DPRG against the Aβ25–35-induced neurotoxicity and explored the underlying mechanism. The results showed that treatment with DPRG could attenuate PC12 cells death. The mechanism was relative to the inhibition of cell apoptosis by increasing the MMP level and decreasing the protein expression of cytochrome C (Cytc) in PC12 cells. In conclusion, DPRG with lower molecular weight was obtained successfully. It possessed neuroprotective properties and might be a candidate for neurodegenerative disease treatment.

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“…For example, Propofol was reported inducing neuroapoptosis in the hippocampus, with differential expression of 159 lncRNAs and 100 mRNAs (fold change ± 2.0, P < 0.05) 23 . Wang J indicated suppression of lncRNA-ATB prevents amyloid-β-induced neurotoxicity in PC12 cells via regulating miR-200/ZNF217 axis 24 . Pang X demonstrated Long non coding RNA SNHG16 reduced ketamine-induced neurotoxicity in human embryonic stem cell-derived neurons 25 .…”

Section: Discussionmentioning

confidence: 99%

Knockdown of LincRNA PADNA Promotes Bupivacaine-Induced Neurotoxicity by miR-194/FBXW7 Axis

Yuning

Chen

Tenghuan

et al. 2020

Preprint

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The aim of the study was to explore the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Mouse DRG neurons were cultured in vitro and treated with bupivacaine to establish the neurotoxicity model. Caspase3 activity, cell viability, tunel assay were analyzed to assess the role of lincRNA PADNA. Dual-luciferase reporter assay was used to determine the binding target of lincRNA PANDA. The expression of lincRNA PADNA was significantly increased with the increasing concentration of bupivacaine. Functional analysis revealed that knockdown of lincRNA PADNA accelerated the caspase3 activity and inhibited the cell viability. Western blot showed that knockdown of lincRNA PADNA promoted the occurrence of cleaved-caspase3. We also proved that lincRNA PADNA may bind with miR-194. Overexpression of miR-194 could rescued the function of lincRNA PADNA, suggesting that lincRNA PADNA may sponge miR-194. In addition, we provided new evidences that lincRNA PADNA/miR-194/FBXW7 axis play an important role in the neurotoxicity process. We performed comprehensive experiments to verify the function and mechanism of lincRNA PADNA in bupivacaine-induced neurotoxicity. Our study provided new evidences and clues for prevention of neurotoxicity.

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Suppression of lncRNA-ATB prevents amyloid-β-induced neurotoxicity in PC12 cells via regulating miR-200/ZNF217 axis

Cited by 51 publications

References 33 publications

Molecular mechanism of myofibroblast formation and strategies for clinical drugs treatments in hypertrophic scars

Molecular mechanism of myofibroblast formation and strategies for clinical drugs treatments in hypertrophic scars

Optimization of Degradation Conditions with PRG, a Polysaccharide from Phellinus ribis, by RSM and the Neuroprotective Activity in PC12 Cells Damaged by Aβ25–35

Knockdown of LincRNA PADNA Promotes Bupivacaine-Induced Neurotoxicity by miR-194/FBXW7 Axis

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