p66shc siRNA-Encapsulated PLGA Nanoparticles Ameliorate Neuropathic Pain Following Spinal Nerve Ligation

Shin, Nara; Shin, Hyo Jung; Yi, Yoon Young; Beom, Jaewon; Lee, Wonhyung; Lee, Choong‐Hyun; Kim, Dong Ho

doi:10.3390/polym12051014

Cited by 17 publications

(13 citation statements)

References 44 publications

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“… 45 , 46 P66shc has been shown to participate in the regulation of mitochondrial homeostasis in NP cells and play an important role in IVDD. 47 (Figure 2 ).…”

Section: Relationships Between Mitochondria and Rosmentioning

confidence: 99%

“…Moderate levels of mitochondrial ROS can activate the antioxidant compensation mechanism, protecting organelles from the harmful effects of ROS and ultimately achieving metabolic balance. 47 However, when external conditions change, increased ROS production can induce mitochondrial membrane depolarization. Oxidative stress is induced when excessive ROS production outpaces antioxidant defenses.…”

Section: Relationships Between Mitochondria and Rosmentioning

confidence: 99%

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Mitochondrial Dysfunction in Oxidative Stress‐Mediated Intervertebral Disc Degeneration

Wang

Zheng

Zhou

et al. 2022

Orthopaedic Surgery

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Intervertebral disc degeneration (IVDD) is the most common contributor to low back pain (LBP). Recent studies have found that oxidative stress and reactive oxygen species (ROS) play an important role in IVDD. As a by‐product of aerobic respiration, ROS is mainly produced in the mitochondria by the electron transport chain and other mitochondrial located proteins. With the excessive accumulation of ROS, mitochondria are also the primary target of ROS attack in disc cells. A disrupted balance between intracellular ROS production and antioxidant capacity will lead to oxidative stress, which is the key contributor to cell apoptosis, cell senescence, excessive autophagy, and mitochondrial dysfunction. As the pivotal ingredient of oxidative stress, mitochondrial dysfunction manifests as imbalanced mitochondrial dynamics and dysregulated mitophagy. Mitochondria can alter their own dynamics through the process of fusion and fission, so that disabled mitochondria can be separated from the mitochondrial pool. Moreover, mitophagy participates by clearing these dysfunctional mitochondria. Abnormality in any of these processes either increases the production or decreases the clearance of ROS, leading to a vicious cycle that results in the death of intervertebral disc cells in large quantities, combined with degradation of the extracellular matrix and overproduction of matrix metalloproteinase. In this review, we explain the changes in mitochondrial morphology and function during oxidative stress‐mediated IVDD and highlight the important role of mitochondria in this process. Eventually, we summarize the IVDD therapeutic strategies targeting mitochondrial dysfunction based on current understanding of the role of oxidative stress in IVDD.

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“… 45 , 46 P66shc has been shown to participate in the regulation of mitochondrial homeostasis in NP cells and play an important role in IVDD. 47 (Figure 2 ).…”

Section: Relationships Between Mitochondria and Rosmentioning

confidence: 99%

Section: Relationships Between Mitochondria and Rosmentioning

confidence: 99%

Mitochondrial Dysfunction in Oxidative Stress‐Mediated Intervertebral Disc Degeneration

Wang

Zheng

Zhou

et al. 2022

Orthopaedic Surgery

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“… 142 Intrathecal treatments with C‐X3‐C motif chemokine receptor 1 (CX3CR1), p38, p66shc siRNA encapsulated PLGA nanoparticles, or forkhead box P3 (Foxp3) plasmid‐encapsulated PLGA nanoparticles inhibit microglial activation and hyperalgesia in SNL rats. 141 , 143 , 144 , 145 …”

Section: Challenges and Considerations In Delivering Mirna‐and Lncrna...mentioning

confidence: 99%

The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review

Jiang

Wang

et al. 2022

Clinical Laboratory Analysis

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Background Non‐coding RNAs (ncRNAs) are involved in neuropathic pain development. Herein, we systematically searched for neuropathic pain‐related ncRNAs expression changes, including microRNAs (miRNAs), long non‐coding RNAs (lncRNAs), and circular non‐coding RNAs (circRNAs). Methods We searched two databases, PubMed and GeenMedical, for relevant studies. Results Peripheral nerve injury or noxious stimuli can induce extensive changes in the expression of ncRNAs. For example, higher serum miR‐132‐3p, ‐146b‐5p, and ‐384 was observed in neuropathic pain patients. Either sciatic nerve ligation, dorsal root ganglion (DRG) transaction, or ventral root transection (VRT) could upregulate miR‐21 and miR‐31 while downregulating miR‐668 and miR‐672 in the injured DRG. lncRNAs, such as early growth response 2‐antisense‐RNA (Egr2‐AS‐RNA) and Kcna2‐AS‐RNA, were upregulated in Schwann cells and inflicted DRG after nerve injury, respectively. Dysregulated circRNA homeodomain‐interacting protein kinase 3 (circHIPK3) in serum and the DRG, abnormally expressed lncRNAs X‐inactive specific transcript (XIST), nuclear enriched abundant transcript 1 (NEAT1), small nucleolar RNA host gene 1 (SNHG1), as well as ciRS‐7, zinc finger protein 609 (cirZNF609), circ_0005075, and circAnks1a in the spinal cord were suggested to participate in neuropathic pain development. Dysregulated miRNAs contribute to neuropathic pain via neuroinflammation, autophagy, abnormal ion channel expression, regulating pain‐related mediators, protein kinases, structural proteins, neurotransmission excitatory–inhibitory imbalances, or exosome miRNA‐mediated neuron–glia communication. In addition, lncRNAs and circRNAs are essential in neuropathic pain by acting as antisense RNA and miRNA sponges, epigenetically regulating pain‐related molecules expression, or modulating miRNA processing. Conclusions Numerous dysregulated ncRNAs have been suggested to participate in neuropathic pain development. However, there is much work to be done before ncRNA‐based analgesics can be clinically used for various reasons such as conservation among species, proper delivery, stability, and off‐target effects.

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“…Results demonstrated that the NPs were less toxic and had a two-fold antioxidant activity compared to the pure drug. 60 Four similar studies investigated the benefit of PLGA NPs for alleviating pain in rat models of spinal nerve ligation (performed at L5) using Sprague-Dawley rats, by loading PLGA NPs with Foxp3 plasmid, 61 p66shc siRNA, 62 p38 siRNA 63 and encapsulating PLGA with CX3CR1 siRNA, 64 respectively. All four studies indicated that the use of the aforementioned PLGA NPs effectively reduced neuropathic pain in SNL-induced rats by reducing microglial activity and expression of proinflammatory mediators.…”

Section: Plga Nps In Tsci Modelsmentioning

confidence: 99%

Nanoparticles in traumatic spinal cord injury: therapy and diagnosis

Mousa¹,

Mohammad²,

Rezk³

et al. 2021

F1000Res

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Nanotechnology has been previously employed for constructing drug delivery vehicles, biosensors, solar cells, lubricants and as antimicrobial agents. The advancement in synthesis procedure makes it possible to formulate nanoparticles (NPs) with precise control over physico-chemical and optical properties that are desired for specific clinical or biological applications. The surface modification technology has further added impetus to the specific applications of NPs by providing them with desirable characteristics. Hence, nanotechnology is of paramount importance in numerous biomedical and industrial applications due to their biocompatibility and stability even in harsh environments. Traumatic spinal cord injuries (TSCIs) are one of the major traumatic injuries that are commonly associated with severe consequences to the patient that may reach to the point of paralysis. Several processes occurring at a biochemical level which exacerbate the injury may be targeted using nanotechnology. This review discusses possible nanotechnology-based approaches for the diagnosis and therapy of TSCI, which have a bright future in clinical practice.

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p66shc siRNA-Encapsulated PLGA Nanoparticles Ameliorate Neuropathic Pain Following Spinal Nerve Ligation

Cited by 17 publications

References 44 publications

Mitochondrial Dysfunction in Oxidative Stress‐Mediated Intervertebral Disc Degeneration

Mitochondrial Dysfunction in Oxidative Stress‐Mediated Intervertebral Disc Degeneration

The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review

Nanoparticles in traumatic spinal cord injury: therapy and diagnosis

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