5′-tiRNA-Cys-GCA regulates VSMC proliferation and phenotypic transition by targeting STAT4 in aortic dissection

Zong, Tingyu; Yang, Yanyan; Lin, Xiaotong; Jiang, Shaoyan; Zhao, Hui; Liu, Meixin; Meng, Yuanyuan; Li, Yong; Zhao, Liang; Tang, Guozhang; Gong, Kun; Wang, Zhibin; Yu, Tao

doi:10.1016/j.omtn.2021.07.013

Cited by 33 publications

(19 citation statements)

References 56 publications

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“…Oxidative stress is an abnormal physiological phenomenon, and it is defined as "an imbalance between antioxidants and oxidants, resulting in the disruption of redox signaling and the corresponding molecular damage." To the best of our knowledge, it is associated with nearly all diseases such as cancers (Hayes et al, 2020), cardiovascular diseases (Dubois-Deruy et al, 2020), aortic dissection (Zong et al, 2021), atherosclerosis Xue et al, 2021), COVID-19 , drug-induced injuries , and diabetes (Zhang et al, 2020). The effective regulation or relief of oxidative stress can potentially prevent many diseases, and EVs play an important role in this process.…”

Section: Introductionmentioning

confidence: 99%

Extracellular Vesicles as Natural Delivery Carriers Regulate Oxidative Stress Under Pathological Conditions

Wang

et al. 2021

Front. Bioeng. Biotechnol.

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Extracellular vesicles are cellular secretory particles that can be used as natural drug delivery carriers. They have successfully delivered drugs including chemotherapeutics, proteins, and genes to treat various diseases. Oxidative stress is an abnormal physiological phenomenon, and it is associated with nearly all diseases. In this short review, we summarize the regulation of EVs on oxidative stress. There are direct effects and indirect effects on the regulation of oxidative stress through EVs. On the one hand, they can deliver antioxidant substances or oxides to recipient cells, directly relieving or aggravating oxidative stress. On the other hand, regulate factors of oxidative stress-related signaling pathways can be delivered to recipient cells by the mediation of EVs, realizing the indirect regulation of oxidative stress. To the best of our knowledge, however, only endogenous drugs have been delivered by EVs to regulate oxidative stress till now. And the heterogeneity of EVs may complicate the regulation of oxidative stress. Therefore, this short review aims to draw more attention to the EVs-based regulation of oxidative stress, and we hope excellent EVs-based delivery carriers that can deliver exogenous drugs to regulate oxidative stress can be exploited.

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Section: Introductionmentioning

confidence: 99%

Extracellular Vesicles as Natural Delivery Carriers Regulate Oxidative Stress Under Pathological Conditions

Wang

et al. 2021

Front. Bioeng. Biotechnol.

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“…Vascular endothelial cells (VECs) are the predominant cell type and generate a continuous inner monolayer of blood vessels, which are responsible for regulating inflammation and vascular homeostasis in healthy blood vessels (Coultas et al, 2005). Also, the attachment of monocytes to VECs is vital for the occurrence of atherosclerosis and inflammation (Rajendran et al, 2013;Yang et al, 2019;Li et al, 2021a;Li et al, 2021b;Zong et al, 2021). Herein we hypothesize that FD-based nanofibers would be able to exhibit favorable physicochemical properties to mediate VEC responses in engineering vascular tissues.…”

Section: Introductionmentioning

confidence: 99%

Preparation of Fucoidan-Based Electrospun Nanofibers and Their Interaction With Endothelial Cells

Chen

Zhu

Hao

et al. 2021

Front. Bioeng. Biotechnol.

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Sulfated polysaccharide fucoidan (FD) is widely applied in biomedical applications owing to its outstanding bioactivities. In addition to the biochemical features, the architecture of biomaterials plays a critical role in tissue repair and regeneration. Particularly, nanofibers have elicited great interest due to their extracellular matrix-like structure, high specific surface area, and favorable biological properties. Herein, chitosan-modified FD/ultra-high molecular weight polyethylene oxide (UHMWPEO) nanofibers are developed via green electrospinning and electrostatic interaction for studying their interaction with endothelial cells. The appropriate solvent is screened to dissolve FD. The electrospinnability of FD/UHMWPEO aqueous solutions is greatly dependent on the weight ratios of FD/UHMWPEO. The incorporation of UHMWPEO significantly improves the electrospinnability of solution and thermo-stability of nanofibers. Also, it is found that there is good miscibility or no phase separation in FD/UHMWPEO solutions. In vitro biological experiments show that the chitosan-modified FD/UHMWPEO nanofibers greatly facilitate the adhesion of endothelial cells and inhibit the attachment of monocytes. Thus, the designed FD-based nanofibers are promising bio-scaffolds in building tissue-engineered blood vessels.

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“…More studies have shown the regulatory role of ncRNA in health and disease (47,48). miRNA is a key regulator of cardiac phenotype that has caught the attention of basic scientists and clinicians (49)(50)(51).…”

Section: Discussionmentioning

confidence: 99%

miR-153-3p Targets βII Spectrin to Regulate Formaldehyde-Induced Cardiomyocyte Apoptosis

Yang

et al. 2021

Front. Cardiovasc. Med.

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Background: Formaldehyde (FA) is ubiquitous in the environment and can be transferred to the fetus through placental circulation, causing miscarriage and congenital heart disease (CHD). Studies have shown that βII spectrin is necessary for cardiomyocyte survival and differentiation, and its loss leads to heart development defects and cardiomyocyte apoptosis. Additionally, previous studies have demonstrated that miRNA is essential in heart development and remodeling. However, whether miRNA regulates FA-induced CHD and cardiomyocyte apoptosis remains unclear.Methods: Using commercially available rat embryonic cardiomyocytes and a rat model of fetal cardiomyocyte apoptosis. Real-time quantitative PCR (RT-qPCR) and Western blot were performed to examine the level of miR-153-3p, βII spectrin, caspase 7, cleaved caspase7, Bax, Bcl-2 expression in embryonic cardiomyocytes and a rat model of fetal cardiomyocyte apoptosis. Apoptotic cell populations were evaluated by flow cytometry and Tunel. Luciferase activity assay and RNA pull-down assay were used to detect the interaction between miR-153-3p and βII spectrin. Masson's trichrome staining detects the degree of tissue fibrosis. Fluorescence in situ hybridization (FISH) and Immunohistochemistry were used to detect the expression of miR-153-3p and βII spectrin in tissues.Results: Using commercially available rat embryonic cardiomyocytes and a rat model of fetal cardiomyocyte apoptosis, our studies indicate that miR-153-3p plays a regulatory role by directly targeting βII spectrin to promote cardiomyocyte apoptosis. miR-153-3p mainly regulates cardiomyocyte apoptosis by regulating the expression of caspase7, further elucidating the importance of apoptosis in heart development. Finally, the results with our animal model revealed that targeting the miR-153-3p/βII spectrin pathway effectively regulated FA-induced damage during heart development. Recovery experiments with miR-153-3p antagomir resulted in the reversal of FA-induced cardiomyocyte apoptosis and fetal cardiac fibrosis.Conclusion: This study investigated the molecular mechanism underpinning the role of βII spectrin in FA-induced CHD and the associated upstream miRNA pathway. The study findings suggest that miR-153-3p may provide a potential target for the clinical diagnosis and treatment of CHD.

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5′-tiRNA-Cys-GCA regulates VSMC proliferation and phenotypic transition by targeting STAT4 in aortic dissection

Cited by 33 publications

References 56 publications

Extracellular Vesicles as Natural Delivery Carriers Regulate Oxidative Stress Under Pathological Conditions

Extracellular Vesicles as Natural Delivery Carriers Regulate Oxidative Stress Under Pathological Conditions

Preparation of Fucoidan-Based Electrospun Nanofibers and Their Interaction With Endothelial Cells

miR-153-3p Targets βII Spectrin to Regulate Formaldehyde-Induced Cardiomyocyte Apoptosis

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