Role of microRNAs on the Regulation of Mitochondrial Biogenesis and Insulin Signaling in Skeletal Muscle

Lima, Tanes I.; Araújo, Hygor N.; Menezes, Eveline Soares; Sponton, Carlos Henrique; Araújo, Michel Barbosa de; Bomfim, Lucas Henrique Montes; Queiroz, André Lima; Passos, Madla A.; Sousa, Thais Amaral e; Hirabara, Sandro Massao; Martins, Amanda Roque; Sampaio, Helena C.L.B.; Rodrigues, Alice Cristina; Curi, Rui; Carneiro, Everardo M.; Boschero, Antônio Carlos; Silveira, Leonardo R.

doi:10.1002/jcp.25645

Cited by 22 publications

(29 citation statements)

References 90 publications

(128 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Some miRNA species may also regulate mitochondrial metabolism and function by acting at multiple subcellular locations. A series of nuclear‐encoded miRNAs located in the cytoplasm specifically modulates mitochondrial metabolism and function in skeletal muscle [reviewed by our group (Russell et al., ; Tsitkanou, Della Gatta, & Russell, ) and others (Lima et al., ; Massart, Katayama, & Krook, )]. Of particular interest are miR‐494 (Yamamoto et al., ), miR‐23a (Russell et al., 2013; Wada et al., ), miR‐696 (Aoi et al., ) and miR‐542 (Garros et al., ).…”

Section: Mito‐myomirs: Potential Roles Of Mirnas In Skeletal Muscle Mmentioning

confidence: 99%

“…Overall, these results suggest that, in cardiac muscle, miR-181c might be partitioned in different cellular compartments to fine-tune the formation of the respiratory complexes.Some miRNA species may also regulate mitochondrial metabolism and function by acting at multiple subcellular locations. A series of nuclear-encoded miRNAs located in the cytoplasm specifically modulates mitochondrial metabolism and function in skeletal muscle [reviewed by our groupTsitkanou, Della Gatta, & Russell, 2016) and others(Lima et al, 2017;Massart, Katayama, & Krook, 2016)]. Of particular interest are miR-494(Yamamoto et al, 2012), miR-23aWada et al, 2015), miR-696(Aoi et al, 2010) and miR-542(Garros et al, 2017).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial regulation in skeletal muscle: A role for non‐coding RNAs?

Silver

Wadley

Lamon

2018

Experimental Physiology

View full text Add to dashboard Cite

Skeletal muscle is a highly metabolic tissue characterized by high mitochondrial abundance. As such, skeletal muscle homeostasis relies on the tight control of mitochondrial gene expression to ensure efficient mitochondrial function. Mitochondria retain a conserved genome from prokaryotic ancestors, and mitochondrial gene regulation relies on communication between mitochondrial- and nuclear-encoded transcripts. Small and long non-coding RNAs (ncRNAs) have regulatory roles in the modulation of gene expression. Emerging evidence demonstrates that regulatory ncRNAs, particularly microRNAs (miRNAs) and long ncRNAs (lncRNAs), localize within the mitochondria in diverse physiological and pathological states. These molecules present intriguing possibilities for the regulation of mitochondrial gene expression. Current research suggests that all known miRNAs are encoded by the nuclear genome but can target mitochondrial genes. Initial investigations demonstrate direct interactions between the muscle-enriched miR-1 and miR-181c and mitochondrial transcripts, suggesting advanced roles of miRNAs in mitochondrial gene regulation. This review draws evidence from the current literature to discuss the hypothesis that a level of ncRNA-mediated gene regulation, in particular miRNA-mediated gene regulation, takes place in the mitochondria. Although ncRNA-mediated regulation of the mitochondrial genome is a relatively unexplored field, it presents exciting possibilities to further our understanding of mitochondrial metabolism and human muscle physiology.

show abstract

Section: Mito‐myomirs: Potential Roles Of Mirnas In Skeletal Muscle Mmentioning

confidence: 99%

mentioning

confidence: 99%

Mitochondrial regulation in skeletal muscle: A role for non‐coding RNAs?

Silver

Wadley

Lamon

2018

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…Specific miRNAs were reported to be downregulated in skeletal muscle (miR‐1a, 133a, and 206) and visceral WAT (miR‐103) from high‐fat diet induced insulin resistant mice. Similarly, miRNAs have been proposed to play a role in insulin signaling (let‐7b, miR‐29b, miR‐23, and miR‐103), glucose uptake (miR‐223), and obesity (miR‐143) (Esau et al, ; Lima et al, ; Lu, Buchan, & Cook, ; Zampetaki et al, ).…”

Section: Introductionmentioning

confidence: 99%

Fenofibrate reverses changes induced by high‐fat diet on metabolism in mice muscle and visceral adipocytes

Frias

Rocha

Mendonça

et al. 2017

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

The effect of fenofibrate on the metabolism of skeletal muscle and visceral white adipose tissue of diet-induced obese (DIO) mice was investigated. C57BL/6J male mice were fed either a control or high-fat diet for 8 weeks. Fenofibrate (50 mg/Kg BW, daily) was administered by oral gavage during the last two weeks of the experimental period. Insulin-stimulated glucose metabolism in soleus muscles, glucose tolerance test, insulin tolerance test, indirect calorimetry, lipolysis of visceral white adipose tissue, expression of miR-103-3p in adipose tissue, and miR-1a, miR-133a/b, miR-206, let7b-5p, miR-23b-3p, miR-29-3p, miR-143-3p in soleus muscle, genes related to glucose and fatty acid metabolism in adipose tissue and soleus muscle, and proteins (phospho-AMPKα2, Pgc1α, Cpt1b), intramuscular lipid staining, and activities of fatty acid oxidation enzymes in skeletal muscle were investigated. In DIO mice, fenofibrate prevented weight gain induced by HFD feeding by increasing energy expenditure; improved whole body glucose homeostasis, and in skeletal muscle, increased insulin dependent glucose uptake, miR-1a levels, reduced intramuscular lipid accumulation, and phospho-AMPKα2 levels. In visceral adipose tissue of obese mice, fenofibrate decreased basal lipolysis rate and visceral adipocytes hypertrophy, and induced the expression of Glut-4, Irs1, and Cav-1 mRNA and miR-103-3p suggesting a higher insulin sensitivity of the adipocytes. The evidence is presented herein that beneficial effects of fenofibrate on body weight, glucose homeostasis, and muscle metabolism might be related to its action in adipose tissue. Moreover, fenofibrate regulates miR-1a-3p in soleus and miR-103-3p in adipose tissue, suggesting these microRNAs might contribute to fenofibrate beneficial effects on metabolism.

show abstract

“…Conversely, FoxO3a was significantly up-regulated when miR-155 inhibitor was transfected into HK2 cells subjected to H/R treatment, indicating that FoxO3a is a direct target of miR-155. Recently, miRNAs have emerged as important mediators of translational control and as regulators of a wide range of biological processes [17][18][19][20][21]. Over-expression of miRNAs is a common phenomenon that occurs in various diseases, and aberrantly expressed miRNAs often participate in the pathogenesis of specific diseases, including ischemic renal diseases.…”

Section: Mir-155 Directly Targets Foxo3a In Hk2 Cells During Hrimentioning

confidence: 99%

MiR-155 is Involved in Renal Ischemia-Reperfusion Injury via Direct Targeting of FoxO3a and Regulating Renal Tubular Cell Pyroptosis

Huang²,

梁英³

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Ischemia/reperfusion injury (IRI) plays a crucial role in renal transplantation and can cause renal failure associated with pyroptosis, a pro-inflammatory-induced programmed cell death. Small endogenous non-coding RNAs have been shown to be involved in renal ischemia/reperfusion injury. This study was performed to investigate which miRNAs regulate pyroptosis in response to renal ischemia/reperfusion injury and determine the mechanism underlying this regulation. Methods: An in vivo rat model of renal IRI was established, and the serum and kidneys were harvested 24 h after reperfusion to assess renal function and histological changes. For the in vitro study, the cultured human renal proximal tubular cell line HK-2 was subjected to 24 h of hypoxia (5% CO₂, 1% O₂, and 94% N2) followed by 12 h of reoxygenation (5% CO₂, 21% O₂, and 74% N₂). The mRNA expression levels were analyzed by real-time PCR, and the protein expression levels were analyzed using Western blot, immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA). Bioinformatics analyses were applied to predict miR-155 targets, which were then confirmed by a luciferase reporter assay. Results: We found that the levels of pyroptosis-related proteins, including caspase-1, caspase-11, IL-1β and IL-18, were significantly increased after renal ischemia/reperfusion injury. Similarly, hypoxia-reoxygenation injury (HRI) also induced pyroptosis in HK2 cells. Furthermore, our study revealed that miR-155 expression was substantially increased in the renal tissues of IRI rats and in HRI HK2 cells. Up-regulation of miR-155 promoted HK2 cell pyroptosis in HRI; conversely, knockdown of miR-155 attenuated this process. To understand the signaling mechanisms underlying the pro-pyroptotic activity of miR-155, we found that exogenous expression of miR-155 up-regulated the expression of caspase-1 as well as the pro-inflammatory cytokines IL-1β and IL-18. Moreover, miR-155 directly repressed FoxO3a expression and its downstream protein apoptosis repressor with caspase recruitment domain (ARC). Conclusions: Our study proposes a new signaling pathway of miR-155/FoxO3a/ARC leading to renal pyroptosis under ischemia/reperfusion injury conditions.

show abstract

Role of microRNAs on the Regulation of Mitochondrial Biogenesis and Insulin Signaling in Skeletal Muscle

Cited by 22 publications

References 90 publications

Mitochondrial regulation in skeletal muscle: A role for non‐coding RNAs?

Mitochondrial regulation in skeletal muscle: A role for non‐coding RNAs?

Fenofibrate reverses changes induced by high‐fat diet on metabolism in mice muscle and visceral adipocytes

MiR-155 is Involved in Renal Ischemia-Reperfusion Injury via Direct Targeting of FoxO3a and Regulating Renal Tubular Cell Pyroptosis

Contact Info

Product

Resources

About