Silencing of <scp>miR</scp>‐497‐5p inhibits cell apoptosis and promotes autophagy in Parkinson's disease by upregulation of <scp>FGF2</scp>

Zhu, Wenjie; Hui, Zhang; Gao, Jun; Yun, Xu

doi:10.1002/tox.23344

Cited by 20 publications

(10 citation statements)

References 46 publications

(49 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…23,35 Former studies have proven the promoting role of miR-497-5p in neuronal apoptosis induced by MPP + and ketamine (an anesthetic). 24,36 Herein, it was found that miR-497-5p level in SH-SY5Y cells was upregulated by BV treatment in a dose-dependent manner. In addition, further investigation demonstrated that SNHG12 negatively regulated miR-497-5p and alleviated BVinduced neuronal damage in SH-SY5Y cells through interaction with miR-497-5p.…”

Section: Discussionmentioning

confidence: 92%

LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497–5p to upregulate NLRX1

Sun

Yuan

2022

Hum Exp Toxicol

View full text Add to dashboard Cite

Long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) has been reported to participate in the regulation of various nervous system disorders. Bupivacaine (BV), a commonly used local anesthetic, could generate neurotoxicity in neurons. This work intended to investigate the role and specific mechanism of SNHG12 in BV-induced neurotoxicity. In this study, we established an in vitro cell model of BV-induced neurotoxicity by exposing human neuroblastoma cells (SH-SY5Y) to BV. It was found that SNHG12 and NLRX1 levels were gradually downregulated, while miR-497–5p enrichment was upregulated accordingly with the increase of BV concentration. As indicated by functional assays, SNHG12 overexpression promoted cell viability but inhibited cell apoptosis and oxidative stress in BV-treated SH-SY5Y cells. In addition, it was identified that SNHG12 directly targeted miR-497–5p and attenuated BV-induced neurotoxicity via interaction with miR-497–5p. Besides, it was confirmed that SNHG12 could upregulate NLRX1 expression by absorbing miR-497–5p. Moreover, miR-497–5p decreased cell viability and induced cell apoptosis and oxidative stress, which was partly reversed by NLRX1 upregulation. In conclusion, our findings indicated that SNHG12 might relieve BV-associated neurotoxicity by upregulating NLRX1 via miR-497–5p in vitro, providing novel clues and biomarkers for the treatment and prevention of BV-associated neurotoxicity.

show abstract

Section: Discussionmentioning

confidence: 92%

LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497–5p to upregulate NLRX1

Sun

Yuan

2022

Hum Exp Toxicol

View full text Add to dashboard Cite

show abstract

“…Aberrant expression of miR-497-5p is mainly seen in different types of cancer [41], diabetic nephropathy [42], Parkinson's disease [43], preeclampsia [44], and metabolic syndrome [45]. In particular, Zhao et al have found that miR-497-5p can promote osteoblast differentiation in osteoporosis [46].…”

Section: Discussionmentioning

confidence: 99%

Circular RNA MELK Promotes Chondrocyte Apoptosis and Inhibits Autophagy in Osteoarthritis by Regulating MYD88/NF‐κB Signaling Axis through MicroRNA‐497‐5p

Zhang

Huang

et al. 2022

Contrast Media & Molecular Imaging

View full text Add to dashboard Cite

Osteoarthritis (OA) is a rheumatic disease and its pathogenesis involves the dysregulation of noncoding RNAs. Therefore, the regulatory mechanism of circular RNA MELK (circMELK) was specified in this work. OA human cartilage tissue was collected, and circMELK, miR-497-5p, and myeloid differentiation factor 88 (MYD88) expression were examined. Human chondrocytes were stimulated with interleukin- (IL-) 1β and interfered with vectors altering circMELK, miR-497-5p, and MyD88 expression to observe their effects on cell viability, cell cycle and apoptosis, autophagy, and inflammation. The binding relationship between RNAs was verified. The data presented that OA cartilage tissues presented raised circMELK and MYD88 and inhibited miR-497-5p expression. IL-1β suppressed cell viability, prevented cell cycle, and induced apoptosis, autophagy, and inflammation of chondrocytes. Functionally, IL-1β-induced changes of chondrocytes could be attenuated by suppressing circMELK or overexpressing miR-497-5p. circMELK acted as a sponge of miR-497-5p while miR-497-5p was a regulator of MYD88. MYD88 restricted the effect of overexpressing miR-497-5p on IL-1β-stimulated chondrocytes. MYD88 triggered nuclear factor-kappaB (NF-κB) pathway activation. Shortly, CircMELK promotes chondrocyte apoptosis and inhibits autophagy in OA by regulating MYD88/NF-κB signaling axis through miR-497-5p. Our study proposes a new molecular mechanism for the development of OA.

show abstract

“…Immunoblots were visualized using the ECL amplification system. Western blot data were quantified using ImageJ software, and relative intensities were calculated to the value of β‐actin 28,29 …”

Section: Methodsmentioning

confidence: 99%

Garcinol protects SH‐SY5Y cells against MPP+‐induced cell death by activating DJ‐1/SIRT1 and PGC‐1α mediated antioxidant pathway in sequential stimulation of p‐AMPK mediated autophagy

Lee

Kumar

Huang

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

Parkinson's disease (PD), a chronic and progressive neurodegenerative disease, can reduce the population of dopaminergic neurons in the substantia nigra. The cause of this neuronal death remains unclear. 1-Methyl-4-phenylpyridinium ion (MPP+) is a potent neurotoxin that can destroy dopaminergic (DA) neurons and promote PD. Garcinol, a polyisoprenylated benzophenone derivative, was extracted from Garcinia indica and is an important active compound it has been used as an anticancer, antioxidant, and anti-inflammatory, agent and it can suppress reactive oxygen species (ROS) mediated cell death in a PD model. Human neuroblastoma (SH-SY5Y) cells (1 Â 10 5 cells) were treated with MPP+ (1 mM) for 24 h to induce cellular ROS production. The formation of ROS was suppressed by pretreatment with different

show abstract

Silencing of miR‐497‐5p inhibits cell apoptosis and promotes autophagy in Parkinson's disease by upregulation of FGF2

Cited by 20 publications

References 46 publications

LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497–5p to upregulate NLRX1

LncRNA SNHG12 ameliorates bupivacaine-induced neurotoxicity by sponging miR-497–5p to upregulate NLRX1

Circular RNA MELK Promotes Chondrocyte Apoptosis and Inhibits Autophagy in Osteoarthritis by Regulating MYD88/NF‐κB Signaling Axis through MicroRNA‐497‐5p

Garcinol protects SH‐SY5Y cells against MPP+‐induced cell death by activating DJ‐1/SIRT1 and PGC‐1α mediated antioxidant pathway in sequential stimulation of p‐AMPK mediated autophagy

Contact Info

Product

Resources

About