Angiotensin II-induced muscle atrophy via PPARγ suppression is mediated by miR-29b

Yang, Tingting; Sha, Zhao; Tang, Haifei; Hua, Xuejiao; Wang, Lijun; Wang, Zitong; Gao, Ziyu; Sluijter, Joost P.G.; Rowe, Glenn C.; Das, Saumya; Yang, Liming; Xiao, Junjie

doi:10.1016/j.omtn.2020.12.015

Cited by 21 publications

(25 citation statements)

References 42 publications

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“…miRNA can inhibit the expression of target genes in two ways by organizing mRNA translation or causing it to be explained by RISC [ 22 , 23 ]. In previous studies, it was found that miRNAs are involved in various regulatory pathways in skeletal muscle [ 24 , 25 , 26 , 27 , 28 , 29 , 30 ]. For example, miR-696 has been confirmed to be a physical-activity-dependent miRNA.…”

Section: Discussionmentioning

confidence: 99%

miR-27b-3p Attenuates Muscle Atrophy by Targeting Cbl-b in Skeletal Muscles

Yang

Wang

et al. 2022

Biomolecules

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As it is well known, muscle atrophy is a process in which protein degradation increases and protein synthesis decreases. This process is regulated by a variety of links. Among them, microRNAs play an essential role in this process, which has attracted widespread attention. In this paper, we find that miR-27b-3p and Cbl-b genes are significantly differentially expressed in the induced atrophy model. The dual-luciferase experiment and Western blot analysis confirmed that miR-27b-3p could regulate the expression of Cbl-b. In C2C12-differentiated myotubes, the overexpression of the Cbl-b gene showed that Cbl-b could upregulate the expression of MuRF-1 and Atrogin-1, which are related marker genes of muscle atrophy, at both the mRNA and protein levels, indicating that the Cbl-b gene can specifically affect muscle atrophy. The knockdown of the Cbl-b gene after C2C12-differentiated myotubes induced atrophy treatment can downregulate the expression of muscle-atrophy-related genes, indicating that manual intervention to downregulate the expression of Cbl-b has a certain alleviating effect on muscle atrophy. These data suggest that miR-27b-3p can regulate the expression of the Cbl-b gene and then exert a particular influence on muscle atrophy through the Cbl-b gene.

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Section: Discussionmentioning

confidence: 99%

miR-27b-3p Attenuates Muscle Atrophy by Targeting Cbl-b in Skeletal Muscles

Yang

Wang

et al. 2022

Biomolecules

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“…Luciferase reporter assays in AC16 cell were performed as described previously. 12 For analysis the target genes of miR-30d, the sequences and mutated sequences of 3’UTR of MAP4K4 and GRP78 were cloned into PGL3-basic vector. Luciferase reporter assays in HEK239 cell and H9C2 cell were performed as described previously.…”

Section: Methodsmentioning

confidence: 99%

“…Luciferase reporter assays in HEK239 cell and H9C2 cell were performed as described previously. 12 The sequences used in this study were listed in Table S4.…”

Section: Methodsmentioning

confidence: 99%

Targeting miR-30d reverses pathological cardiac hypertrophy

et al. 2022

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“… 5 miR-29b has been showed to promote many types of muscle atrophy including heart failure-induced muscle wasting via regulating target genes IGF-1, PI3K, and YY1. 50 , 51 Peroxisome proliferator activated receptor gamma (PPARγ) was found to inhibit AngII-induced muscle atrophy and improve muscle function by targeting and downregulating miR-29b; 51 , 52 similarly, inhibition of miR-29b by the CRISPR-Cas9 editing system significantly attenuated AngII-induced muscle atrophy in vivo . 53 It is noteworthy that several muscle-specific miRNAs, including miR-1, miR-133a, miR-133b, miR-208a, and miR-208b, have been found to be involved in the regulation of both cardiac and skeletal muscle functions.…”

Section: Ncrnas In Muscle Atrophy Induced By Heart Failurementioning

confidence: 99%

Non-coding RNA basis of muscle atrophy

Liu

Deng

Qiu

et al. 2021

Molecular Therapy - Nucleic Acids

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Muscle atrophy is a common complication of many chronic diseases including heart failure, cancer cachexia, aging, etc. Unhealthy habits and usage of hormones such as dexamethasone can also lead to muscle atrophy. However, the underlying mechanisms of muscle atrophy are not completely understood. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), play vital roles in muscle atrophy. This review mainly discusses the regulation of ncRNAs in muscle atrophy induced by various factors such as heart failure, cancer cachexia, aging, chronic obstructive pulmonary disease (COPD), peripheral nerve injury (PNI), chronic kidney disease (CKD), unhealthy habits, and usage of hormones; highlights the findings of ncRNAs as common regulators in multiple types of muscle atrophy; and summarizes current therapies and underlying mechanisms for muscle atrophy. This review will deepen the understanding of skeletal muscle biology and provide new strategies and insights into gene therapy for muscle atrophy.

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Angiotensin II-induced muscle atrophy via PPARγ suppression is mediated by miR-29b

Cited by 21 publications

References 42 publications

miR-27b-3p Attenuates Muscle Atrophy by Targeting Cbl-b in Skeletal Muscles

miR-27b-3p Attenuates Muscle Atrophy by Targeting Cbl-b in Skeletal Muscles

Targeting miR-30d reverses pathological cardiac hypertrophy

Non-coding RNA basis of muscle atrophy

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