Therapeutic Effects of Salvianolic Acid B on Angiotensin II–Induced Atrial Fibrosis by Regulating Atrium Metabolism via Targeting AMPK/FoxO1/miR-148a-3p Axis

Liu, Jie; Sun, Qijuan; Sun, Xiaotong; Wang, Qian; Zou, Guangchen; Wang, Dewei; Baoxiang, Zhuang; Juan, Zhaodong; Zhang, Rui; Zhang, Daoliang

doi:10.1007/s12265-022-10303-3

Cited by 6 publications

(4 citation statements)

References 49 publications

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“…Upregulated miR-148a-3p also opposed the IL-6-induced cytokine pathways and apoptotic cell death, as previously described in THP-1 macrophages stimulated with oxidized LDL [16]. Recently, upregulated miR-148a-3p has been associated with reduced oxidative stress in angiotensin II-activated atrial fibroblasts, retinal epithelial cells exposed to hyperglycemia, and both in vivo and in vitro ischemia/reperfusion models [55][56][57].…”

Section: Discussionsupporting

confidence: 61%

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

Anastasio,

Donisi,

Colloca

et al. 2024

IJMS

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In endothelial cells, miR-148a-3p is involved in several pathological pathways, including chronic inflammatory conditions. However, the molecular mechanism of miR-148a-3p in endothelial inflammatory states is, to date, not fully elucidated. To this end, we investigated the involvement of miR-148a-3p in mitochondrial dysfunction and cell death pathways in human aortic endothelial cells (teloHAECs) treated with interleukin-6 (IL-6), a major driver of vascular dysfunction. The results showed that during IL6-activated inflammatory pathways, including increased protein levels of sirtuin 7 (SIRT7) (p < 0.01), mitochondrial stress (p < 0.001), and apoptosis (p < 0.01), a decreased expression of miR-148a-3p was observed (p < 0.01). The employment of a miR-148a mimic counteracted the IL-6-induced cytokine release (p < 0.01) and apoptotic cell death (p < 0.01), and ameliorated mitochondria redox homeostasis and respiration (p < 0.01). The targeted relationship between miR-148a-3p and SIRT7 was predicted by a bioinformatics database analysis and validated via the dual-luciferase reporter assay. Mechanistically, miR-148a-3p targets the 3′ untranslated regions of SIRT7 mRNA, downregulating its expression (p < 0.01). Herein, these in vitro results support the role of the miR-148a-3p/SIRT7 axis in counteracting mitochondrial damage and apoptosis during endothelial inflammation, unveiling a novel target for future strategies to prevent endothelial dysfunction.

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Section: Discussionsupporting

confidence: 61%

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

Anastasio,

Donisi,

Colloca

et al. 2024

IJMS

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“…Numerous studies on miR-148a-3p have revealed various downstream effects of modulating the levels or activities of miR-148a-3p. In addition to the promotion of angiogenesis, miR-148a-3p also inhibits the progression of malignancies such as hepatocellular carcinoma, lung cancer, and myeloid leukemia, besides exerting antifibrotic effects in pulmonary, liver, and atrial fibrosis. ,− Moreover, miR-148a-3p inhibits the inflammatory response and attenuates apoptosis in atherosclerosis to delay its progression. , The miR-148a-3p may also exert effects on skin wound healing by mediating other downstream effects and activating other signaling pathways, which requires further in-depth research.…”

Section: Discussionmentioning

confidence: 99%

Enhancing Skin Injury Repair: Combined Application of PF-127 Hydrogel and hADSC-Exos Containing miR-148a-3p

Zhang,

Su,

Zhao

et al. 2024

ACS Biomater. Sci. Eng.

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The use of exosomes to relieve skin injuries has received considerable attention. The PluronicF-127 hydrogel (PF-127 hydrogel) is a novel biomaterial that can be used to carry biomolecules. This study sought to investigate the impact of exosomes originating from human mesenchymal stem cells (MSCs) developed from adipose tissue (hADSC-Exos) combined with a PF-127 hydrogel on tissue repair and explore the underlying mechanism using in vitro and in vivo experiments. miR-148a-3p is the most expressed microRNA (miRNA) in hADSC-Exos. We found that exosomes combined with the PF-127 hydrogel had a better efficacy than exosomes alone; moreover, miR-148a-3p knockdown lowered its efficacy. In vitro, we observed a significant increase in the tumor-like ability of HUVECs after exosome treatment, which was attenuated after miR-148a-3p knockdown. Furthermore, the effects of miR-148a-3p on hADSC-Exos were achieved through the prevention of PTEN and the triggering of phosphatidylinositol 3-kinase (PI3K)/Akt signaling. In conclusion, our results demonstrated that hADSC-Exos can promote angiogenesis and skin wound healing by delivering miR-148a-3p and have a better effect when combined with the PF-127 hydrogel, which may be an alternative strategy to promote wound healing.

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“…The search for targeted therapy in CRC aimed at interfering with critical cell mechanisms such as cell growth and proliferation, angiogenesis, migration, and differentiation focuses on miRNA's ability to penetrate cells and inhibit target pathway(s), preventing cancer growth and causing apoptosis [43][44][45][46]. The capacity of miR-148a-3p to induce mitochondrial injury and aberrant ROS production has been reported in different cell models [56][57][58]. The results of this study provided the first evidence that overexpression of miR-148a-3p caused mitochondrial dysfunction along with oxidative stress, resulting in mitochondrial impairment and membrane depolarization in SW480 and SW620 cells.…”

Section: Discussionmentioning

confidence: 99%

MiR-148a-3p Promotes Colorectal Cancer Cell Ferroptosis by Targeting SLC7A11

Martino,

Balestrieri,

Aragona

et al. 2023

Cancers

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Ferroptosis, an iron-dependent form of cell death, and dysregulated microRNA (miRNA) expression correlate with colorectal cancer (CRC) development and progression. The tumor suppressor ability of miR-148a-3p has been reported for several cancers. Nevertheless, the role of miR-148a-3p in CRC remains largely undetermined. Here, we aim at investigating the molecular mechanisms and regulatory targets of miR-148a-3p in the CRC cell death mechanism(s). To this end, miR-148a-3p expression was evaluated in SW480 and SW620 cells and normal colon epithelial CCD 841 CoN cells with quantitative real-time polymerase chain reaction (qRT-PCR). Data reported a reduction of miR-148a-3p expression in SW480 and SW620 cells compared to non-tumor cells (p < 0.05). Overexpression of miR-148a selectively inhibited CRC cell viability (p < 0.001), while weakly affecting normal CCD 841 CoN cell survival (p < 0.05). At the cellular level, miR-148a-3p mimics promoted apoptotic cell death via caspase-3 activation (p < 0.001), accumulation of mitochondrial reactive oxygen species (ROS) (p < 0.001), and membrane depolarization (p < 0.001). Moreover, miR-148a-3p overexpression induced lipid peroxidation (p < 0.01), GPX4 downregulation (p < 0.01), and ferroptosis (p < 0.01), as revealed by intracellular and mitochondrial iron accumulation and ACSL4/TFRC/Ferritin modulation. In addition, levels of SLC7A11 mRNA and protein, the cellular targets of miR-148a-3p predicted by bioinformatic tools, were suppressed by miR-148a-3p’s overexpression. On the contrary, the downregulation of miR-148a-3p boosted SLC7A11 gene expression and suppressed ferroptosis. Together, these in vitro findings reveal that miR-148a-3p can function as a tumor suppressor in CRC by targeting SLC7A11 and activating ferroptosis, opening new perspectives for the rationale of therapeutic strategies through targeting the miR-148a-3p/SLC7A11 pathway.

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Therapeutic Effects of Salvianolic Acid B on Angiotensin II–Induced Atrial Fibrosis by Regulating Atrium Metabolism via Targeting AMPK/FoxO1/miR-148a-3p Axis

Cited by 6 publications

References 49 publications

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

MiR-148a-3p/SIRT7 Axis Relieves Inflammatory-Induced Endothelial Dysfunction

Enhancing Skin Injury Repair: Combined Application of PF-127 Hydrogel and hADSC-Exos Containing miR-148a-3p

MiR-148a-3p Promotes Colorectal Cancer Cell Ferroptosis by Targeting SLC7A11

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