MiR-139-5p alleviates neural cell apoptosis induced by spinal cord injury through targeting TRAF3

Zhang, Ziying; Shen, Lianfang; Yan, Yingying

doi:10.18388/abp.2020_5198

Cited by 4 publications

(4 citation statements)

References 36 publications

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“…Likewise, in the brain, TRAF3 promotes neuronal cell death partly through TAK1-MKK-JNK activation in both ischemia/reperfusion and subarachnoid hemorrhage injury models [24,28]. Zhang et al also showed that TRAF3 promoted neuronal apoptosis following spinal cord injury via thoracic vertebral contusion; however, whether this was also dependent on TAK1-MKK-JNK activation was not investigated in this study [29]. Here, we show that NR-TRAF3 regulates TLR4-specific immune activation by LPS endotoxin administration.…”

Section: Discussionmentioning

confidence: 72%

“…Notably, gene and protein databases report high Traf3 expression in the brain and retina [27]. However, studies regarding TRAF3 function in neuronal tissues have only recently begun to be investigated [24,28,29]. Further, to our knowledge, no retinal-specific mouse models have yet been developed and retinal TRAF3 function has not been explored.…”

Section: Introductionmentioning

confidence: 99%

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The Chx10-Traf3 Knockout Mouse as a Viable Model to Study Neuronal Immune Regulation

Gurley

Gmyrek

Hargis

et al. 2021

Cells

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Uncontrolled inflammation is associated with neurodegenerative conditions in central nervous system tissues, including the retina and brain. We previously found that the neural retina (NR) plays an important role in retinal immunity. Tumor necrosis factor Receptor-Associated Factor 3 (TRAF3) is a known immune regulator expressed in the retina; however, whether TRAF3 regulates retinal immunity is unknown. We have generated the first conditional NR-Traf3 knockout mouse model (Chx10-Cre/Traf3f/f) to enable studies of neuronal TRAF3 function. Here, we evaluated NR-Traf3 depletion effects on whole retinal TRAF3 protein expression, visual acuity, and retinal structure and function. Additionally, to determine if NR-Traf3 plays a role in retinal immune regulation, we used flow cytometry to assess immune cell infiltration following acute local lipopolysaccharide (LPS) administration. Our results show that TRAF3 protein is highly expressed in the NR and establish that NR-Traf3 depletion does not affect basal retinal structure or function. Importantly, NR-Traf3 promoted LPS-stimulated retinal immune infiltration. Thus, our findings propose NR-Traf3 as a positive regulator of retinal immunity. Further, the NR-Traf3 mouse provides a tool for investigations of neuronal TRAF3 as a novel potential target for therapeutic interventions aimed at suppressing retinal inflammatory disease and may also inform treatment approaches for inflammatory neurodegenerative brain conditions.

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Section: Discussionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

The Chx10-Traf3 Knockout Mouse as a Viable Model to Study Neuronal Immune Regulation

Gurley

Gmyrek

Hargis

et al. 2021

Cells

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“…20 Moreover, miR-139-5p also repressed the apoptosis and oxidative stress of neurons to alleviate nerve cell injury. 21,22 In PE-related studies, miR-139-5p was discovered to increase trophoblast cell proliferation, invasion and migration, so it might inhibit PE progression. 23,24 Consistent with these results, our results revealed that miR-139-5p mimic promoted trophoblast cell proliferation, invasion and angiogenesis to reverse the regulation of circ_0077109 on trophoblast cell function.…”

Section: Discussionmentioning

confidence: 99%

“…MiR‐139‐5p had been shown to act as a tumor suppressor to restrain cell proliferation and invasion in many cancers, such as lung adenocarcinoma 19 and hepatocellular carcinoma 20 . Moreover, miR‐139‐5p also repressed the apoptosis and oxidative stress of neurons to alleviate nerve cell injury 21,22 . In PE‐related studies, miR‐139‐5p was discovered to increase trophoblast cell proliferation, invasion and migration, so it might inhibit PE progression 23,24 .…”

Section: Discussionmentioning

confidence: 99%

Circ_0077109 sponges miR‐139‐5p and upregulates HOXD10 in trophoblast cells as potential mechanism for preeclampsia progression

Zhang

Liu

2022

American J Rep Immunol

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Background: One of the important reasons for the development of preeclampsia (PE) is the abnormal function of trophoblast cells. Many circular RNAs (circRNAs) have been confirmed to participate in the regulation of trophoblast cell function to mediate PE progression. However, whether circ_0077109 is involved in PE progression through regulating trophoblast cell function remains unclear.Methods: Quantitative real-time PCR was utilized for measuring the expression of circ_0077109, microRNA (miR)-139-5p and homeobox D10 (HOXD10). Trophoblast cell proliferation, apoptosis, invasion, and angiogenesis was assessed cell counting kit 8 assay, EdU assay, flow cytometry, transwell assay and tube formation assay. In addition, western blot analysis was used to determine protein expression. The interaction between miR-139-5p and circ_0077109 or HOXD10 was verified by dual-luciferase reporter assay and RIP assay. Results:Our results pointed out that circ_0077109 was a circRNA with upregulated expression in PE patients. Overexpression of circ_0077109 suppressed trophoblast cell proliferation, invasion, and angiogenesis, while increased apoptosis. MiR-139-5p was found to be sponged by circ_0077109, and its mimic reversed the suppressive effect of circ_0077109 on trophoblast cell function. HOXD10 was a target of miR-139-5p, and its overexpression inhibited trophoblast cell proliferation, invasion, and angiogenesis. MiR-139-5p inhibitor could repress trophoblast cell function, while this effect could be reversed by HOXD10 knockdown. Conclusion:In summary, we confirmed that circ_0077109 inhibited trophoblast cell function through the regulation of miR-139-5p/HOXD10 axis, which might be a potential target for PE treatment.

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Long non-coding RNA DHRS4 antisense RNA 1 inhibits ectopic endometrial cell proliferation, migration, and invasion in endometriosis by regulating microRNA-139-5p expression

Cui

Zhou²,

Lin

2022

Bioengineered

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Endometriosis is an estrogen-dependent chronic gynecological syndrome. Recent studies have shown that long non-coding RNAs participate in the pathogenesis and development of endometriosis. This study aimed to explore the mechanisms of DHRS4 antisense RNA 1 (DHRS4-AS1) in endometriosis. Dual-luciferase reporter assays were conducted to determine the relationship between DHRS4-AS1, microRNA (miR)-139-5p, and arrestin domain-containing 3 (ARRDC3). Furthermore, the expression of DHRS4-AS1 and miR-139-5p in ectopic endometrial stromal cells (EC-ESCs) and endometriosis tissues was examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Additionally, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, and Transwell assays were performed to evaluate the proliferation, apoptosis, and migration and invasion of EC-ESCs, respectively. Western blotting and RT-qPCR were further utilized to determine cleaved-Caspase 3, Caspase 3, and matrix metalloproteinase 9 (MMP-9) expression levels. Compared with the EN group, DHRS4-AS1 levels were lower and miR-139-5p levels were higher in EC-ESCs and tissues obtained from patients with endometriosis. Functional assays validated that DHRS4-AS1 targets miR-139-5p, with ARRDC3 being a downstream target of miR-139-5p. Rescue experiments demonstrated that DHRS4-AS1 inhibited EC-ESC proliferation, migration, and invasion, but promoted apoptosis, by targeting miR-139-5p in endometriosis. cleaved-Caspase3 expression level and the cleaved-Caspase 3/Caspase 3 ratio increased, while the expression levels of MMP-9 decreased, after transfection with DHRS4-AS1 overexpression plasmids; however, the effects induced by DHRS4-AS1 overexpression could be partially reversed by co-transfection with the miR-139-5p mimic. The current study demonstrates that the DHRS4-AS1/miR-139-5p/ARRDC3 axis participates in the regulation of EC-ESC function.

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MiR-139-5p alleviates neural cell apoptosis induced by spinal cord injury through targeting TRAF3

Cited by 4 publications

References 36 publications

The Chx10-Traf3 Knockout Mouse as a Viable Model to Study Neuronal Immune Regulation

The Chx10-Traf3 Knockout Mouse as a Viable Model to Study Neuronal Immune Regulation

Circ_0077109 sponges miR‐139‐5p and upregulates HOXD10 in trophoblast cells as potential mechanism for preeclampsia progression

Long non-coding RNA DHRS4 antisense RNA 1 inhibits ectopic endometrial cell proliferation, migration, and invasion in endometriosis by regulating microRNA-139-5p expression

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