Runx2 was Correlated with Neurite Outgrowth and Schwann Cell Differentiation, Migration After Sciatic Nerve Crush

Ding, Da-Zhi; Zhang, Peipei; Liu, Yuxi; Wang, Yi; Sun, Weiwei; Yu, Zhaohui; Cheng, Zhen; Wang, Youhua

doi:10.1007/s11064-018-2670-0

Cited by 11 publications

(11 citation statements)

References 32 publications

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“…[16][17][18][19] As reported by recent studies, the expression of RUNX2 in Schwann cells and axons increased after sciatic nerve crush. 16 RUNX2 over-expression accelerates progression of post-traumatic osteoarthritis in adult mice. 17 miR-203 affects traumatic heterotopic ossification via reducing RUNX2 expression.…”

Section: Discussionsupporting

confidence: 59%

“…RUNX2 has been reported as a multifunctional transcription factor for osteoblast differentiation in previous studies, which exerts its effect on mesenchymal stem cell chondrogenic differentiation. [16][17][18][19] As reported by recent studies, the expression of RUNX2 in Schwann cells and axons increased after sciatic nerve crush. 16 RUNX2 over-expression accelerates progression of post-traumatic osteoarthritis in adult mice.…”

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confidence: 59%

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MiR-30a-5p ameliorates LPS-induced inflammatory injury in human A549 cells and mice via targeting RUNX2

Yao

et al. 2020

Innate Immun

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In this study, we aim to investigate the role of miR-30a-5p in acute lung injury/acute respiratory distress syndrome (ALI/ARDS) using LPS-induced A549 cells and mice. We found cell viability was significantly declined accompanied by cell apoptosis and cell cycle arrest at G0/G1 phase in LPS-treated A549 cells. MiR-30a-5p was down-regulated by LPS treatment and miR-30a-5p significantly protected A549 cells from LPS-induced injury by increasing cell viability, reducing cell apoptosis, promoting cell cycle progression, and inhibiting inflammatory reactions. Dual-luciferase activity demonstrated that RUNX2 was a direct target for miR-30a-5p and its expression was negatively and directly regulated by miR-30a-5p. Over-expression of RUNX2 weakened the inhibitory effect of miR-30a-5p on inflammatory injury. In vivo, over-expression of miR-30a-5p alleviated LPS-induced inflammatory responses and lung injury in LPS-administrated mice. Besides, miR-30a-5p repressed LPS-elevated phosphorylation levels of the signal transducer and activator of transcription 3 (STAT3) and c-Jun N-terminal kinase (JNK), IκBα degradation, and NF-κB p65 phosphorylation. In conclusion, miR-30a-5p ameliorates LPS-induced inflammatory injury in A549 cells and mice via targeting RUNX2 and related signaling pathways, thereby influencing the progression of ARDS.

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Section: Discussionsupporting

confidence: 59%

supporting

confidence: 59%

MiR-30a-5p ameliorates LPS-induced inflammatory injury in human A549 cells and mice via targeting RUNX2

Yao

et al. 2020

Innate Immun

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“…In 5-FU-resistant colon cancer cell lines, the Wnt pathway is activated, thereby inhibiting the p53 pathway and enhancing cell survival. Consistent with the findings of previous studies, the present study confirmed the importance of NAMPT the resistance of CRC to 5-FU ( 45 ). The present study further demonstrated that visfatin promoted tumorigenesis and inhibited sensitivity to 5-FU via the SDF-1/CXCR4 axis.…”

Section: Discussionsupporting

confidence: 93%

“…It activates various signalling pathways to affect tumour proliferation, migration and prognosis. PI3K/Akt and extracellular signalling-regulated protein kinases 1 and 2 (ERK 1/2) are two key signalling pathways involved in cell signal transduction, colorectal cancer cell survival and 5-FU resistance ( 45 , 46 ). CSCs initiate heterogeneous tumours and repopulate metastatic outgrowths ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Visfatin inhibits colon cancer cell apoptosis and decreases chemosensitivity to 5‑FU by promoting the SDF‑1/CXCR4/Akt axis

et al. 2022

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5-Fluorouracil (5-FU) is the preferred chemotherapeutic drug used in the treatment of colon cancer; however, drug resistance affects its clinical efficacy. Visfatin, an adipokine that promotes tumour development, has the potential to increase resistance to chemotherapy. The present study aimed to verify the effects of visfatin on the sensitivity of colon cancer cells to 5-FU and to elucidate the potential mechanisms involved. Tissue microarrays (TMAs) were used to analyse visfatin differential expression in normal colon and colon cancer tissues, and the data were further validated in vitro . Cell Counting Kit-8, clone formation, caspase-3/7 activity assays, as well as other analyses were used to verify the effects of visfatin on sensitivity to 5-FU. TMA and correlation analyses were used to predict and verify the correlation between visfatin and stromal cell-derived factor-1 (SDF-1). Rescue experiments and PI3K/Akt inhibitors were used to verify the role of the visfatin/SDF-1/Akt axis in the sensitivity of colon cancer cells to 5-FU. Visfatin was found to be highly expressed in colon cancer tissues and cell lines. Moreover, visfatin knockdown increased apoptosis, reduced cell proliferation and enhanced the chemosensitivity of DLD-1 and SW48 cells to 5-FU. A positive correlation between visfatin and SDF-1 was observed, with the knockdown of visfatin enhancing cell sensitivity to 5-FU chemotherapy by targeting the SDF-1/C-X-C chemokine receptor type 4 (CXCR4) axis. Furthermore, the Akt signalling pathway downstream of SDF-1/CXCR4 proved to be critical in the decreased sensitisation of colon cancer cells to 5-FU induced by visfatin. On the whole, the present study demonstrates that visatin can potentially decrease colon cancer cell apoptosis, promote proliferation and decrease colon cancer cell sensitivity to 5-FU via the visfatin/SDF-1/Akt axis.

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“…Following SNC injury, levels of Runx2 significantly increase within 3 days, peak after 1 week, and then return to normal levels by 4 weeks. When Runx2 expression is inhibited, neurite outgrowth in PC12 cells stimulated with NGF for 3 days can be inhibited, and a decrease in NF200 expression, which is closely related to neurite outgrowth, is observed [6]. Chen et al have shown that Runx2 can reduce the inhibitory effect of high glucoseinduced osteoblast differentiation by regulating the PI3K/AKT/GSK3β/β-catenin pathway [5].…”

Section: Discussionmentioning

confidence: 99%

Identification of a miRNA biomarker for the large artery atherosclerosis subtype of acute ischemic stroke

Zhang¹,

Li²,

Feng³

et al. 2022

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Aim of the study: To identify miRNA biomarkers of arterial atherosclerosis subtypes in acute ischemic stroke. Material and methods: 40 participants recruited in our hospital from October 2017 to January 2018. There were 12 patients with acute ischemic stroke (AIS), 13 patients with atherosclerosis (AS) and 15 healthy subjects. They were divided into the AIS group, AS group and healthy control (HC) group. The miRNA expression levels of the AIS group, AS group and HC group were measured by miRNA microarray. Bioinformatics analysis was performed using the miRNA target prediction database. Results: The expression of 3 miRNAs,, was significantly different between the AIS and AS/HC groups. Genes targeted by miR-129-1-3p were involved in 12 pathways, of which axon guidance, retrograde endocannabinoid signalling and sphingolipid signalling pathways were associated with axonal and synaptic function. miR-129-1-3p mimics significantly decreased cortical neurite length and Runx2 levels, while miR-129-1-3p inhibitors promoted neurite growth and increased Runx2 expression. Conclusions: miR-129-1-3p may be a relevant biomarker for the diagnosis of stroke caused by large artery atherosclerosis and could represent a novel therapeutic target for stroke treatment.

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Runx2 was Correlated with Neurite Outgrowth and Schwann Cell Differentiation, Migration After Sciatic Nerve Crush

Cited by 11 publications

References 32 publications

MiR-30a-5p ameliorates LPS-induced inflammatory injury in human A549 cells and mice via targeting RUNX2

MiR-30a-5p ameliorates LPS-induced inflammatory injury in human A549 cells and mice via targeting RUNX2

Visfatin inhibits colon cancer cell apoptosis and decreases chemosensitivity to 5‑FU by promoting the SDF‑1/CXCR4/Akt axis

Identification of a miRNA biomarker for the large artery atherosclerosis subtype of acute ischemic stroke

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