MicroRNA-21 promotes proliferation of rat hepatocyte BRL-3A by targeting FASLG

Li, J.J.; Chan, Wai-Kit; Leung, WK; Wang, Y.; Xu, Cun-Shuan

doi:10.4238/2015.april.27.30

Cited by 15 publications

(15 citation statements)

References 28 publications

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“…FASLG is a type-II membrane protein that binds to and activates Fas-receptors, leading to cell apoptosis [50]. Multiple studies have proved that miR-21 promotes cell proliferation by targeting FASLG [51][52][53]. In our study, we proved that PGE1 down-regulates FASLG expression by increasing miR-21-5p expression in rat cardiomyocytes exposed to conditions that produce H/R injury.…”

Section: Discussionsupporting

confidence: 56%

Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis

et al. 2019

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Background: Prostaglandin-E1 (PGE1) is a potent vasodilator with anti-inflammatory and antiplatelet effects. However, the mechanism by which PGE1 contributes to the amelioration of cardiac injury remains unclear. Methods: The present study was designed to investigate how PGE1 protects against hypoxia/reoxygenation (H/R)-induced injuries by regulating microRNA-21-5p (miR-21-5p) and fas ligand (FASLG). Rat H9C2 cells and isolated primary cardiomyocytes were cultured under hypoxic conditions for 6 h (6H, hypoxia for 6 h), and reoxygenated for periods of 6 (6R, reoxygenation for 6 h), 12, and 24 h, respectively. Cells from the 6H/6R group were treated with various doses of PGE1; after which, their levels of viability and apoptosis were detected. Results: The 6H/6R treatment regimen induced the maximum level of H9C2 cell apoptosis, which was accompanied by the highest levels of Bcl-2-associated X protein (Bax) and cleaved-caspase-3 expression and the lowest level of B-cell lymphoma 2 (Bcl-2) expression. Treatment with PGE1 significantly diminished the cell cytotoxicity and apoptosis induced by the 6H/6R regimen, and also decreased expression of IL-2, IL-6, P-p65, TNF-α, and cleaved-caspase-3. In addition, we proved that PGE1 up-regulated miR-21-5p expression in rat cardiomyocytes exposed to conditions that produce H/R injury. FASLG was a direct target of miR-21-5p, and PGE1 reduced the ability of H/R-injured rat cardiomyocytes to undergo apoptosis by affecting the miR-21-5p/FASLG axis. In addition, we proved that PGE1 could protect primary cardiomyocytes against H/R-induced injuries. Conclusions: These results indicate that PGE1 exerts cardioprotective effects in H9C2 cells during H/R by regulating the miR-21-5p/FASLG axis.

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Section: Discussionsupporting

confidence: 56%

Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis

et al. 2019

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“…Usually, the combination of FASLG with Fas death receptor, induces the polymerization of Fas to form death-inducing signaling, and is complicated by recruiting the death domain adapter protein FADD, caspase-8, and caspase-2 [31,32]. Caspase-8 and caspase-2 are activated through autoproteolytic cleavage and subsequently cleave caspase-3, and then result in cytochrome C release from the mitochondria, ultimately triggering apoptosis [33,34]. Thus, we inferred that miR-149-5p suppression induced THP-1 cells apoptosis via targeting FASLG, subsequently regulating the expression of p-FADD and caspases.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of MicroRNA-149-5p Induces Apoptosis of Acute Myeloid Leukemia Cell Line THP-1 by Targeting Fas Ligand (FASLG)

Tian

Li²

2016

Med Sci Monit

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BackgroundThis study was aimed to reveal the role of miR-149-5p in acute myeloid leukemia (AML) cells apoptosis and the possible mechanism involved.Material/MethodsThe expression of miR-149-5p in leukemia cell lines, as well as the blood and bone marrow (BM) samples from leukemia patients, were monitored by reverse-transcription polymerase chain reaction (RT-PCR). AML cell line THP-1 was transfected with miR-149-5p mimic or inhibitor, and then cell apoptosis was determined using the APO Percentage assay kit. The target of miR-149-5p was predicted by using the microRNA.org database, and verified by RT-PCR, Western blot, and Dual-Luciferase reporter assays. Further, small interfering RNA (siRNA) against the target gene was co-transfected with miR-149-5p inhibitor, and then the cell apoptosis and the expression of apoptosis-related proteins were assessed.ResultsMiR-149-5p was significantly up-regulated in leukemia cell lines and samples from leukemia patients (P<0.01 or P<0.001), especially in THP-1 cells and samples from AML patients. Cell apoptosis was significantly decreased by miR-149-5p overexpression (P<0.01) and increased by miR-149-5p suppression (P<0.05). Fas Ligand (FASLG) was a direct target of miR-149-5p, and was negatively regulated by miR-149-5p. More importantly, the inductive effects of miR-149-5p suppression on cell apoptosis were abrogated by si-FASLG (P<0.01). Furthermore, the up-regulative effects of miR-149-5p suppression on the phosphorylated form of Fas-associated via death domain (p-FADD), caspase-8, caspase-2, caspase-3, and the cleaved forms of these caspases were abrogated by si-FASLG.ConclusionsInhibition of miR-149-5p can induce apoptosis in THP-1 cells. These inductive effects might be via targeting FASLG and activating FADD and caspases.

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“…MiR-21 functions as an inducer of cell proliferation [ 92 – 94 ]. Interestingly, transfection of human NP cells with miR-21 mimic dramatically increased Akt activity via targeting PTEN, leading to upregulation of cyclin D1 expression and subsequent cell proliferation [ 95 ].…”

Section: Roles Of the Pi3k/akt Pathway In The Pathogenesis Of Iddmentioning

confidence: 99%

The PI3K/Akt pathway: a critical player in intervertebral disc degeneration

et al. 2017

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Intervertebral disc degeneration (IDD) is thought to be the primary cause of low back pain, a severe public health problem worldwide. Current therapy for IDD aims to alleviate the symptoms and does not target the underlying pathological alternations within the disc. Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway protects against IDD, which is attributed to increase of ECM content, prevention of cell apoptosis, facilitation of cell proliferation, induction or prevention of cell autophagy, alleviation of oxidative damage, and adaptation of hypoxic microenvironment. In the current review, we summarize recent progression on activation and negative regulation of the PI3K/Akt signaling pathway, and highlight its impact on IDD. Targeting this pathway could become an attractive therapeutic strategy for IDD in the near future.

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MicroRNA-21 promotes proliferation of rat hepatocyte BRL-3A by targeting FASLG

Cited by 15 publications

References 28 publications

Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis

Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis

Inhibition of MicroRNA-149-5p Induces Apoptosis of Acute Myeloid Leukemia Cell Line THP-1 by Targeting Fas Ligand (FASLG)

The PI3K/Akt pathway: a critical player in intervertebral disc degeneration

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