MiR-128-3p directly targets VEGFC/VEGFR3 to modulate the proliferation of lymphatic endothelial cells through Ca2+ signaling

Zhou, Jie; He, Zhiyou; Guo, Le; Zeng, Junfeng; Liang, Pengfei; Ren, Lixia; Zhang, Minghua; Zhang, Pihong; Huang, Xiaoyuan

doi:10.1016/j.biocel.2018.05.006

Cited by 26 publications

(24 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, Chen et al found that inhibition of miR-128-3p could protect human cardiomyocytes from I/RI (42). Loss-of-function experiments in our study showed that downregulation of miRNA-128-3p promoted NSC proliferation and reduced the rate of apoptosis, which is consistent with previous reports that antagonism of miR-128-3p could remarkably improve the proliferation of lymphatic endothelial cells (43). Furthermore, miRNA-128-3p exhibited opposite regulatory effects to Nrf2 in oxidative stress.…”

Section: Discussionsupporting

confidence: 92%

Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

Theaflavin has been proven to own strong antioxidative capacity; however, the molecular mechanism underlying its protective effect against cerebral ischemia-reperfusion (I/R) injury remains unclear. Therefore, the present study was designed to elucidate the neuroprotective effects of theaflavin on cerebral I/R injury and its underlying molecular mechanisms. To investigate the effects of theaflavin on neurological function, neurogenesis, and oxidative stress, experiments were performed using a cerebral I/R injury rat model, and neural stem cells (NSCs) were subjected to oxygen-glucose deprivation and reoxygenation (OGD/R). Further, the expression profiles of miRNA-128-3p and the regulatory function of nuclear factor (erythroid-derived 2)-related factor 2 (Nrf2) were evaluated in these models. We found that theaflavin treatment significantly reduced infarct volume and neuronal injury, and thus improved the impaired memory and learning ability. Furthermore, theaflavin treatment significantly enhanced the increase in NSC proliferation, reduction in the apoptotic rate and inhibition of oxidative stress. Mechanistically, theaflavin targeted miRNA-128-3p and further activated the Nrf2 pathway to reduce oxidative stress. In summary, theaflavin has a strong ability to attenuate cerebral I/R injury through miRNA-128-3p-mediated recovery of the impaired antioxidant defense system, which suggests that it could be a potential drug candidate for ischemic stroke.

show abstract

Section: Discussionsupporting

confidence: 92%

Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…Lin et al showed that brain derived neurotrophic factor promoted VEGFC‐dependent lymphangiogenesis through inhibition of miR‐624‐3p in chondrosarcoma cells in vitro . A recent study revealed that VEGFC was a direct downstream target of miR‐128‐3p and modulated lymphatic endothelial cell proliferation . We discovered that the expression of VEGFC was negatively correlated with miR‐128‐3p expression in OS tissues and confirmed that VEGFC was a direct target of miR‐128‐3p in MG63 cells, which implied that there existed a ceRNA network among MIAT, miR‐128‐3p and VEGFC in OS.…”

Section: Discussionsupporting

confidence: 64%

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

et al. 2019

View full text Add to dashboard Cite

The aberrant expression of long non‐coding RNAs (lncRNAs) has been involved in the progression of many human tumors including osteosarcoma (OS). However, the biological function and the underlying mechanism of the lncRNA myocardial infarction‐associated transcript (MIAT) in OS remain unclear. In the present study, we found that lncRNA MIAT was significantly up‐regulated in both OS tissues and cell lines, and high expression of MIAT was positively associated with tumor size and lymph node metastasis of OS patients. In addition, knockdown of MIAT inhibited proliferation, migration, invasion and promoted apoptosis of OS cells in vitro. Moreover, the expression of MIAT was negatively associated with miR‐128‐3p but positively correlated with vascular endothelial growth factor C (VEGFC) in OS. Further mechanistic study revealed that lncRNA MIAT promoted OS progression by up‐regulating VEGFC via sponging miR‐128‐3p in vitro. Taken together, our results suggest that MIAT/miR‐128‐3p/VEGFC axis contributes to OS progression and may be used as a novel therapeutic target for OS. © 2019 IUBMB Life, 9999(9999):1–9, 2019

show abstract

“…miRNAs are post-transcriptional regulators that bind to the 3′-untranslated region (3′-UTR) of the target gene messenger RNA [17,18]. Our bioinformatics analysis demonstrated that FOXO4 was a putative target of miR-328-3p by harboring a miR-328-3p binding sequence in the 3′-UTR of its mRNA (Targetscan).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of microRNA-328-3p by hepatitis B virus contributes to THLE-2 cell injury by downregulating FOXO4

Ouyang

et al. 2020

J Transl Med

View full text Add to dashboard Cite

Background: Hepatitis B virus (HBV) remains a major cause of chronic hepatitis and hepatocellular carcinoma, and miRNAs play important roles in HBV pathogenesis. Our previous study has shown that miR-328-3p is upregulated in HBV-infected patients and serves as a potent predictor for the prognosis of HBV-related liver failure. Methods: Here, the role of miR-328-3p in modulating cell injury in HBV-infected liver cells THLE-2 was investigated in detail. MiR-328-3p expression was examined using qRT-PCR. The levels of pro-inflammatory cytokines were measured using ELISA. HBV RNA and HBV DNA levels were quantified. The interactions between STAT3 and miR-328-3p promoter as well as miR-328-3p and FOXO4 were analyzed using chromatin immunoprecipitation (CHIP) assay and luciferase reporter assay, respectively. THLE-2 cell injury was evaluated by examining cell viability and apoptosis. Results: HBV promoted expression of miR-328-3p through the STAT3 signal pathway and that increasingly expressed miR-328-3p downregulated its target FOXO4, leading to the promotion of cell injury in HBV-infected liver cells THLE-2. Conclusion: These data demonstrate that HBV-STAT3-miR-328-3p-FOXO4 regulation pathway may play an important role in the pathogenesis of HBV infection.

show abstract

MiR-128-3p directly targets VEGFC/VEGFR3 to modulate the proliferation of lymphatic endothelial cells through Ca2+ signaling

Cited by 26 publications

References 29 publications

Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress

Theaflavin attenuates cerebral ischemia/reperfusion injury by abolishing miRNA‑128‑3p‑mediated Nrf2 inhibition and reducing oxidative stress

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

Upregulation of microRNA-328-3p by hepatitis B virus contributes to THLE-2 cell injury by downregulating FOXO4

Contact Info

Product

Resources

About