Small Interfering RNA–Mediated Suppression of Fas Modulate Apoptosis and Proliferation in Rat Intervertebral Disc Cells

Park, Jong-Beom; Park, Chanjoo

doi:10.4184/asj.2017.11.5.686

Cited by 3 publications

(3 citation statements)

References 18 publications

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“…B. Park and C. Park [ 38 ] found that Fas siRNA might be a powerful therapeutic approach for disc degeneration by suppression of harmful gene expression. The characteristic of IDD is that the dysfunctional FASL reduce the expression level of FASL and unbalance the interaction between NP cells and immune cells, leading to the expression of certain regulatory factors that may play a role in this process [ 33 ], such as hsa_circ_0001658 and hsa-miR-181c-5p in this study.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS

Meng

2021

Computational and Mathematical Methods in Medicine

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Background and Purpose. Intervertebral disc degeneration (IDD) is the main cause of low back pain, but its pathogenesis has not been studied clearly. Circular RNA is a type of noncoding RNA (ncRNA). In this study, we studied the potential role of circular RNA in the pathogenesis of IDD. Methods. We obtained microarray data (GSE116726, GSE67566) from Gene Expression Omnibus database, and differential expression level of ncRNA in nucleus pulposus (NP) tissues of IDD patients was analyzed. The potential circRNA-miRNA-mRNA regulatory network was analyzed by starBase. The effect of the interaction between hsa_circ_0001658, hsa-miR-181c-5p, and FAS on the proliferation and apoptosis of human neural progenitor cells (hNPCs) was studied. Results. hsa_circ_0001658 was significantly upregulated ( logFC > 2.0 and adj . P . Val < 0.01 ) in the NP tissues of IDD patients, and hsa-miR-181c-5p expression was downregulated ( logFC < − 2.0 and adj . P . Val < 0.01 ). Silencing of hsa-miR-181c-5p or overexpression of hsa_circ_0001658 inhibited the proliferation of hNPCs and promoted their apoptosis. hsa_circ_0001658 acted as a sponge of hsa-miR-181c-5p. hsa-miR-181c-5p downregulated the expression of Fas cell surface death receptor (FAS), promoted the proliferation, and inhibited the apoptosis of hNPCs. hsa_circ_0001658 functioned in hNPCs through targeting hsa-miR-181c-5p/FAS. Conclusion. Circular RNA hsa_circ_0001658 inhibits IDD development by regulating hsa-miR-181c-5p/FAS. It is expected to be a potential target for the therapy of IDD.

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Section: Discussionmentioning

confidence: 99%

Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS

Meng

2021

Computational and Mathematical Methods in Medicine

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“…The RT-PCR experimental method used in this study was the same as described in a previous paper [ 10 ]. Briefly, total RNA was extracted from NP cells and tissues using TRIzol regent (Invitrogen, Grand Island, NY, USA) following the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

Inhibitory Effect of Insulin Treatment on Apoptosis of Intervertebral Disc Cells in a Streptozotocin-Induced Diabetic Rat Model

2023

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Study Design: Experimental study using a streptozotocin (STZ)-induced diabetic rat model. Purpose: This study aims to investigate whether insulin treatment could attenuate disc cell apoptosis and matrix degradation in a STZ-induced diabetic rat model.Overview of Literature: Diabetes is a significant risk factor for disc degeneration due to excessive apoptosis of disc cells and matrix degradation. However, no studies were noted to demonstrate the inhibitory effect of insulin treatment on the apoptosis of disc cells and matrix degradation in diabetic patients.Methods: Rats were allocated randomly into one of three groups: control, STZ, and STZ-insulin. Diabetes was induced by a single intraperitoneal injection of STZ (65 mg/kg) in the STZ and STZ-insulin groups. The blood glucose level was consistently above 400 mg/ dL in the STZ and STZ-insulin groups 2 weeks after STZ injection. After 2 weeks of STZ injection, the STZ-insulin group was administered insulin treatment (1.5 unit/100 g) daily for up to 4 weeks. Blood glucose of the STZ-insulin rats significantly decreased to normal levels 4 weeks after insulin treatment. The rats were sacrificed 6 weeks after STZ injection, and disc cells and tissues were harvested to investigate the expression of apoptosis markers and matrix metalloproteinases (MMPs).Results: Fas and caspase-8, -9, and -3 expressions were significantly increased in the STZ group, along with increased expressions of MMP-2 and -3. On the contrary, insulin treatment significantly decreased the expressions of Fas, caspase-8, -9, and -3 as well as MMP-2 and -3 in the STZ-insulin group.Conclusions: The results of the current study demonstrated that insulin treatment attenuates excessive apoptosis of disc cells and matrix degradation in the diabetic rat model. Accordingly, strict blood glucose control should be recommended to prevent disc degeneration in diabetic patients.

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“…In the early stage of apoptosis, Fas downregulation can reduce apoptosis and induce proliferation, resulting in enhanced IVD cell viability. Fas siRNA may be an effective method for treating IDD 84 . In addition, it has been reported that RNA interference is a promising method of local IDD therapy 85 .…”

Section: The Death Receptor Pathway and Iddmentioning

confidence: 99%

Targeted therapy for intervertebral disc degeneration: inhibiting apoptosis is a promising treatment strategy

Zhang¹,

Hu²,

Peng³

et al. 2021

Int. J. Med. Sci.

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Intervertebral disc (IVD) degeneration (IDD) is a multifactorial pathological process associated with low back pain (LBP). The pathogenesis is complicated, and the main pathological changes are IVD cell apoptosis and extracellular matrix (ECM) degradation. Apoptotic cell loss leads to ECM degradation, which plays an essential role in IDD pathogenesis. Apoptosis regulation may be a potential attractive therapeutic strategy for IDD. Previous studies have shown that IVD cell apoptosis is mainly induced by the death receptor pathway, mitochondrial pathway, and endoplasmic reticulum stress (ERS) pathway. This article mainly summarizes the factors that induce IDD and apoptosis, the relationship between the three apoptotic pathways and IDD, and potential therapeutic strategies. Preliminary animal and cell experiments show that targeting apoptotic pathway genes or drug inhibition can effectively inhibit IVD cell apoptosis and slow IDD progression. Targeted apoptotic pathway inhibition may be an effective strategy to alleviate IDD at the gene level. This manuscript provides new insights and ideas for IDD therapy.

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Small Interfering RNA–Mediated Suppression of Fas Modulate Apoptosis and Proliferation in Rat Intervertebral Disc Cells

Cited by 3 publications

References 18 publications

Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS

Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS

Inhibitory Effect of Insulin Treatment on Apoptosis of Intervertebral Disc Cells in a Streptozotocin-Induced Diabetic Rat Model

Targeted therapy for intervertebral disc degeneration: inhibiting apoptosis is a promising treatment strategy

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