Schwann cells-derived exosomal miR-21 participates in high glucose regulation of neurite outgrowth

Liu, Yu-pu; Tian, Mingyue; Yang, Yi-duo; Li, Han; Zhao, Tiantian; Zhu, Jing; Mou, Fang-fang; Cui, Guo-Hong; Guo, Hai-dong

doi:10.1016/j.isci.2022.105141

Cited by 11 publications

(8 citation statements)

References 60 publications

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“…For example, miR-21 has been shown to increase in response to spinal cord injury (SCI) and exerts various protective effects against SCI [ 11 ]. Notably, our previous study also demonstrated that the overexpressed miR-21 promoted neurite outgrowth [ 12 ]. Most importantly, miR-21 has been implicated in the mechanism through which EA promotes functional recovery and nerve regeneration after sciatic nerve injury (SNI) [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Electroacupuncture Promotes Nerve Regeneration and Functional Recovery Through Regulating lncRNA GAS5 Targeting miR-21 After Sciatic Nerve Injury

Tian,

Yang,

Qin

et al. 2023

Mol Neurobiol

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Although the benefits of electroacupuncture (EA) for peripheral nerve injury (PNI) are well accepted in clinical practice, the underlying mechanism remains incompletely elucidated. In our study, we observed that EA intervention led to a reduction in the expression of the long non-coding RNA growth-arrest-specific transcript 5 (GAS5) and an increased in miR-21 levels within the injured nerve, effectively promoting functional recovery and nerve regeneration following sciatic nerve injury (SNI). In contrast, administration of adeno-associated virus expressing GAS5 (AAV-GAS5) weakened the therapeutic effect of EA. On the other hand, both silencing GAS5 and introducing a miR-21 mimic prominently enhanced the proliferation activity and migration ability of Schwann cells (SCs), while also inhibiting SCs apoptosis. On the contrary, inhibition of SCs apoptosis was found to be mediated by miR-21. Additionally, overexpression of GAS5 counteracted the effects of the miR-21 mimic on SCs. Moreover, SCs that transfected with the miR-21 mimic promoted neurite growth in hypoxia/reoxygenation-induced neurons, which might be prevented by overexpressing GAS5. Furthermore, GAS5 was found to be widely distributed in the cytoplasm and was negatively regulated by miR-21. Consequently, the targeting of GAS5 by miR-21 represents a potential mechanism through which EA enhances reinnervation and functional restoration following SNI. Mechanistically, the GAS5/miR-21 axis can modulate the proliferation, migration, and apoptosis of SCs while potentially influencing the neurite growth of neurons.

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Section: Introductionmentioning

confidence: 99%

Electroacupuncture Promotes Nerve Regeneration and Functional Recovery Through Regulating lncRNA GAS5 Targeting miR-21 After Sciatic Nerve Injury

Tian,

Yang,

Qin

et al. 2023

Mol Neurobiol

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“…DPN is a highly prevalent complication of T2DM and severely affects the quality of patients. 3,4,7,8 Recent stud-ies have revealed that the gut microbiota is involved in the onset of T2DM by decreasing glucose tolerance and insulin resistance. 1 Parabacteroides species have been shown to regulate glycolipid metabolic.…”

Section: Discussionmentioning

confidence: 99%

“…[4][5][6] The mortality rate of DPN patients is approximately 25%−50% within 5-10 years. 7 DPN may cause a high risk of sensory dysfunction, pain, and falls and reduce the quality of patients. 8 Therefore, DPN poses a significant threat to public health.…”

Section: Introductionmentioning

confidence: 99%

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Tauroursodeoxycholic acid protects Schwann cells from high glucose–induced cytotoxicity by targeting NLRP3 to regulate cell migration and pyroptosis

Wang,

Li,

Zhang

et al. 2023

Biotech and App Biochem

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Diabetic peripheral neuropathy (DPN) is the most prevalent complication of type 2 diabetes mellitus (T2DM), and it seriously affects the quality of life of patients. Tauroursodeoxycholic acid (TUDCA) is a bile acid that plays a protective role against various diseases. However, the function of TUDCA in DPN progression needs to be elucidated. Hence, this study clarified the action of TUDCA on DPN development and explored its mechanism of action. Fecal samples were collected from 50 patients with T2DM or DPN. Schwann cells induced by high levels were constructed to simulate an uncontrolled diabetic state. Cell viability and migration were measured using the CCK‐8 and wound‐healing assays, respectively. Reactive oxygen species and pyroptosis were detected using flow cytometry. Parabacteroides goldsteinii and Parabacteroides distasonis levels were decreased in the feces of patients with DPN. TUDCA enhanced the viability and migration ability of high glucose‐stimulated Schwann cells. In addition, Schwann cell pyroptosis stimulated by high glucose levels was inhibited by TUDCA. Furthermore, the protective roles of TUDCA in cell viability, migration ability, and pyroptosis of Schwann cells stimulated by high glucose were suppressed by the overexpression of NLRP3. TUDCA enhanced cell viability and migration and suppressed pyroptosis in Schwann cells stimulated by high glucose levels by modulating NLRP3 expression. Thus, TUDCA may be a promising drug for DPN therapy.

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“…Schwann cells (SCs) are the critical glial cells due to their roles in the development, maintenance, function, and regeneration of nerves in the peripheral nervous system [ 1 , 2 , 3 ]. SCs are able to improve nerve regeneration after nerve injury through decreased expression of myelin-related protein and increased expression of cell adhesion molecules, neurotrophic factors, and cytokines [ 4 , 5 , 6 , 7 ]. These changes facilitate axonal regeneration by guiding distal nerve stump and basal lamina growth.…”

Section: Introductionmentioning

confidence: 99%

Improving Schwann Cell Differentiation from Human Adipose Stem Cells with Metabolic Glycoengineering

Wang

Liu

et al. 2023

Cells

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Schwann cells (SCs) are myelinating cells that promote peripheral nerve regeneration. When nerve lesions form, SCs are destroyed, ultimately hindering nerve repair. The difficulty in treating nerve repair is exacerbated due to SC’s limited and slow expansion capacity. Therapeutic use of adipose-derived stem cells (ASCs) is emerging in combating peripheral nerve injury due to these cells’ SC differentiation capability and can be harvested easily in large numbers. Despite ASC’s therapeutic potential, their transdifferentiation period typically takes more than two weeks. In this study, we demonstrate that metabolic glycoengineering (MGE) technology enhances ASC differentiation into SCs. Specifically, the sugar analog Ac5ManNTProp (TProp), which modulates cell surface sialylation, significantly improved ASC differentiation with upregulated SC protein S100β and p75NGFR expression and elevated the neurotrophic factors nerve growth factor beta (NGFβ) and glial cell-line-derived neurotrophic factor (GDNF). TProp treatment remarkably reduced the SC transdifferentiation period from about two weeks to two days in vitro, which has the potential to improve neuronal regeneration and facilitate future use of ASCs in regenerative medicine.

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Schwann cells-derived exosomal miR-21 participates in high glucose regulation of neurite outgrowth

Cited by 11 publications

References 60 publications

Electroacupuncture Promotes Nerve Regeneration and Functional Recovery Through Regulating lncRNA GAS5 Targeting miR-21 After Sciatic Nerve Injury

Electroacupuncture Promotes Nerve Regeneration and Functional Recovery Through Regulating lncRNA GAS5 Targeting miR-21 After Sciatic Nerve Injury

Tauroursodeoxycholic acid protects Schwann cells from high glucose–induced cytotoxicity by targeting NLRP3 to regulate cell migration and pyroptosis

Improving Schwann Cell Differentiation from Human Adipose Stem Cells with Metabolic Glycoengineering

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