Lycium barbarum polysaccharides protects H9c2 cells from hypoxia-induced injury by down-regulation of miR-122

Li, Qiaoju; Zhang, Zai-Wei; Hu, Li; Pan, Xiaoyu; Chen, Shasha; Cui, Zhiyuan; Ma, Jie; Zhou, Zhongxing; Xing, Bing

doi:10.1016/j.biopha.2018.11.012

Cited by 20 publications

(14 citation statements)

References 36 publications

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“…Importantly, reactive fibrosis at the infarct border zone and the remote uninjured myocardium, leads to chamber compliance alteration, increased ventricular stiffness and compromised cardiac output [22,47]. Replacement fibrosis refers to scar formation, a critical process for preventing bursting of the ventricular wall after ischemic insult during MI [22,60]. In addition, an elevated ratio between circulating miR-122-5p/miR-133b is a specific early prognostic biomarker in acute MI [57].…”

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

“…Therefore, miR-122 is emerging as a prognostic biomarker of infarct size and cardiac dysfunction in MI. Overexpression of miR-122 remarkably attenuated Lycium barbarum polysaccharide (LBP)-mediated protective activity in hypoxia-injured H9C2 cells, while the inhibition of miR-122 accelerated LBP-mediated protective activity [60]. Surprisingly, the LBP-induced activation of the phosphorylated extracellular signal-regulated kinase (ERK) and AMPK signaling pathways was attenuated by miR-122 overexpression and accelerated by miR-122 suppression [60].…”

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

“…Overexpression of miR-122 remarkably attenuated Lycium barbarum polysaccharide (LBP)-mediated protective activity in hypoxia-injured H9C2 cells, while the inhibition of miR-122 accelerated LBP-mediated protective activity [60]. Surprisingly, the LBP-induced activation of the phosphorylated extracellular signal-regulated kinase (ERK) and AMPK signaling pathways was attenuated by miR-122 overexpression and accelerated by miR-122 suppression [60]. An in vivo investigation revealed that, the administration of anti-miR-122 decreased infarct size and improved cardiac function in MI rats associated with improvements to the LVEF and left ventricular fractional shortening, indicating that miR-122 inhibition may have potential for the prevention and treatment of acute MI (Table 1; Fig.…”

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

“…An in vivo investigation revealed that, the administration of anti-miR-122 decreased infarct size and improved cardiac function in MI rats associated with improvements to the LVEF and left ventricular fractional shortening, indicating that miR-122 inhibition may have potential for the prevention and treatment of acute MI (Table 1; Fig. 3) [60]. Overexpression of miR-122 by miR-122 mimics inhibited cellular viability and promoted the apoptosis of CMs, while miR-122 knockdown promoted cell viability and inhibited apoptosis [61].…”

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

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Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases

et al. 2020

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Fibrotic diseases cause annually more than 800,000 deaths worldwide, where of the majority accounts for cardiovascular fibrosis, which is characterized by endothelial dysfunction, myocardial stiffening and reduced dispensability. MicroRNAs (miRs), small noncoding RNAs, play critical roles in cardiovascular dysfunction and related disorders. Intriguingly, there is a critical link among miR-122, cardiovascular fibrosis, sirtuin 6 (SIRT6) and angiotensin-converting enzyme 2 (ACE2), which was recently identified as a coreceptor for SARS-CoV2 and a negative regulator of the rennin-angiotensin system. MiR-122 overexpression appears to exacerbate the angiotensin II-mediated loss of autophagy and increased inflammation, apoptosis, extracellular matrix deposition, cardiovascular fibrosis and dysfunction by modulating the SIRT6-Elabela-ACE2, LGR4-β-catenin, TGFβ-CTGF and PTEN-PI3K-Akt signaling pathways. More importantly, the inhibition of miR-122 has proautophagic, antioxidant, anti-inflammatory, anti-apoptotic and antifibrotic effects. Clinical and experimental studies clearly demonstrate that miR-122 functions as a crucial hallmark of fibrogenesis, cardiovascular injury and dysfunction. Additionally, the miR-122 level is related to the severity of hypertension, atherosclerosis, atrial fibrillation, acute myocardial infarction and heart failure, and miR-122 expression is a risk factor for these diseases. The miR-122 level has emerged as an early-warning biomarker cardiovascular fibrosis, and targeting miR-122 is a novel therapeutic approach against progression of cardiovascular dysfunction. Therefore, an increased understanding of the cardiovascular roles of miR-122 will help the development of effective interventions. This review summarizes the biogenesis of miR-122; regulatory effects and underlying mechanisms of miR-122 on cardiovascular fibrosis and related diseases; and its function as a potential specific biomarker for cardiovascular dysfunction.

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Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

Section: Roles Of Mir-122 In Myocardial Infarctionmentioning

confidence: 99%

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Roles of MicroRNA-122 in Cardiovascular Fibrosis and Related Diseases

et al. 2020

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“…Therefore, miRNAs are potential biomarkers for the diagnosis, prognosis, prevention and treatment of non-small cell lung cancer. Many natural Chinese herbal ingredients have been found to regulate micro-RNAs, such as Lycium barbarum polysaccharides [13], Coptisine from Rhizoma Coptidis [14], resveratrol, curcumin and berberine [15].…”

Section: Introductionmentioning

confidence: 99%

6′-O-galloylpaeoniflorin regulates proliferation and metastasis of non-small cell lung cancer through AMPK/miR-299-5p/ATF2 axis

et al. 2020

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Background: Recent studies have shown 6'-O-galloylpaeoniflorin (GPF), a nature product extracted from the roots of paeoniflorin exerts anti-oxidant and anti-inflammatory activities. However, the effects of GPF on the proliferation and invasion in non-small cell lung cancer (NSCLC) cells have not been clarified. Methods: MTT assay was performed to determine the cytotoxicity of GPF treatment on NSCLC cells. Colony formation assay, cell scratch test and transwell assay were performed to determine the proliferation and invasion of NSCLC cells in vitro, respectively. An A549 cell xenograft mouse model was performed to confirm the growth of NSCLC cells in vivo. Western blotting was used to measure the levels of activating transcription factor 2 (ATF2), AMP-activated protein kinase (AMPK) and phosph-AMPK (p-AMPK). Luciferase assay was used to validate the binding of miR-299-5p on the 3' untranslated region (UTR) of ATF2. Results: Administration of GPF (50 or 100 μM) was significantly cytotoxic to A549 cells and H1299 cells, as well as inhibited the clonality, invasion and metastasis of NSCLC cells in vitro. GPF treatment also inhibited the tumor growth of NSCLC cell mouse xenografts in vivo. Exotic expression of miR-299-5p significantly inhibited the growth of NSCLC cells in vitro and in vivo. Downregulation of miR-299-5p expression attenuated the inhibition of the proliferation and metastasis of non-small cell lung cancer cells by GPF treatment. miR-299-5p significantly decreased ATF2 mRNA and protein levels in A549 cells (p < 0.05). Overexpression of ATF2 blocked the inhibitory effect of miR-299-5p on the proliferation and invasiveness of A549 cells. Conclusions: GPF regulates miR-299-5p/ATF2 axis in A549 cells via the AMPK signalling pathway, thereby inhibiting the proliferation and metastasis of non-small cell lung cancer cells.

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