Overload Induced Heat Shock Proteins (HSPs), MAPK and miRNA (miR-1 and miR133a) Response in Insulin-Resistant Skeletal Muscle

Katta, Anjaiah; Thulluri, Srinivasarao; Manne, Nandini D.P.K.; Addagarla, Hari S.; Arvapalli, Ravikumar; Nalabotu, Siva K.; Gadde, Muralikrishna; Rice, Kevin M.; Blough, Eric R.

doi:10.1159/000343363

Cited by 13 publications

(16 citation statements)

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“…miRNAs are short (ϳ20 -25 nucleotides) and noncoding RNA molecules, which repress gene expression by binding to the 3=-untranslated region of target mRNAs and either inhibit translation or promote cleavage of the transcript (1, 13). Recently, muscle-specific miRNAs miR-1, miR-133a, and miR206 have been shown to participate in the regulation of muscle mass (3,17,18,25,29). Some studies have reported that these miRNAs promote proliferation and differentiation of muscle cells (3,18,29), whereas miR-1 and miR-133a seem to be downregulated during skeletal muscle hypertrophy (17,25).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, muscle-specific miRNAs miR-1, miR-133a, and miR206 have been shown to participate in the regulation of muscle mass (3,17,18,25,29). Some studies have reported that these miRNAs promote proliferation and differentiation of muscle cells (3,18,29), whereas miR-1 and miR-133a seem to be downregulated during skeletal muscle hypertrophy (17,25). Furthermore, upregulations of miR-1 in dexamethasone-mediated muscle atrophy in mice and atrophic signals, which are integrated by miR-1, have been reported (19).…”

Section: Discussionmentioning

confidence: 99%

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AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C₂C₁₂skeletal muscle cells

Egawa

Ohno

Goto

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C2C12 skeletal muscle cells. Am J Physiol Endocrinol Metab 306: E344 -E354, 2014. First published December 17, 2013; doi:10.1152/ajpendo.00495.2013.-5=-AMP-activated protein kinase (AMPK) plays an important role as a negative regulator of skeletal muscle mass. However, the precise mechanism of AMPK-mediated regulation of muscle mass is not fully clarified. Heat shock proteins (HSPs), stress-induced molecular chaperones, are related with skeletal muscle adaptation, but the association between AMPK and HSPs in skeletal muscle hypertrophy is unknown. Thus, we investigated whether AMPK regulates hypertrophy by mediating HSPs in C2C12 cells. The treatment with AICAR, a potent stimulator of AMPK, decreased 72-kDa HSP (HSP72) expression, whereas there were no changes in the expressions of 25-kDa HSP, 70-kDa heat shock cognate, and heat shock transcription factor 1 in myotubes. Protein content and diameter were less in the AICARtreated myotubes in those without treatment. AICAR-induced suppression of myotube hypertrophy and HSP72 expression was attenuated in the siRNA-mediated AMPK␣ knockdown myotubes. AICAR increased microRNA (miR)-1, a modulator of HSP72, and the increase of miR-1 was not induced in AMPK␣ knockdown condition. Furthermore, siRNA-mediated HSP72 knockdown blocked AICARinduced inhibition of myotube hypertrophy. AICAR upregulated the gene expression of muscle Ring-finger 1, and this alteration was suppressed in either AMPK␣ or HSP72 knockdown myotubes. The phosphorylation of p70 S6 kinase Thr 389 was downregulated by AICAR, whereas this was attenuated in AMPK␣, but not in HSP72, knockdown myotubes. These results suggest that AMPK inhibits hypertrophy through, in part, an HSP72-associated mechanism via miR-1 and protein degradation pathways in skeletal muscle cells. microRNA; heat shock transcription factor 1; muscle rRing-finger 1; atrogin-1; acetyl-CoA carboxylase SKELETAL MUSCLE HAS A GREATER CAPACITY to adapt to various stimuli. Increased loading, such as resistance training and mechanical stretching, stimulates protein synthesis and reduces protein degradation, thereby inducing muscle hypertrophy (10). On the other hand, decrease of use, such as immobilization, denervation, aging, and/or various pathological conditions, attenuates protein synthesis and increases protein degradation, resulting in atrophy (12,32). Although the process of skeletal muscle adaptation to hypertrophic and atrophic stimuli has been studied, the molecular mechanism involved in this process is not fully understood yet.5=-AMP-activated protein kinase (AMPK) is well known as a sensor for cellular energy status and metabolic stress, such as muscle contraction, fasting, hypoxia, ischemia, and/or oxidative and osmotic stresses and as a signaling intermediary that controls the use of glucose and fatty acids in skeletal muscle (8,14,15). In addition, several studies in the past decade have suggested that AMPK plays an important rol...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C₂C₁₂skeletal muscle cells

Egawa

Ohno

Goto

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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“…The upregulation of miR-494 induced by TNFa desensitizes C2C12 muscle cells to the effects of insulin by inhibiting the pathway downstream of Akt, which was associated with the regulation of STXBP5 (an inhibitor of glucose transport) and SLC2A4 (the gene encoding GLUT4) expression . Katta et al (2013) demonstrated that miR-1 and miR-133 were associated with insulin resistance in insulin-resistant obese Zucker rats. Recently, several studies involving miRNA microarray analysis have been conducted using the GK diabetic model.…”

Section: Mirnas and Insulin Resistancementioning

confidence: 99%

Application of microRNAs in diabetes mellitus

Chen¹,

Lan²,

Roukos³

et al. 2014

Journal of Endocrinology

110

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MicroRNAs (miRNAs) are small molecules negatively regulating gene expression by diminishing their target mRNAs. Emerging studies have shown that miRNAs play diverse roles in diabetes mellitus. Type 1 diabetes (T1D) and T2D are two major types of diabetes. T1D is characterized by a reduction in insulin release from the pancreatic b-cells, while T2D is caused by islet b-cell dysfunction in response to insulin resistance. This review describes the miRNAs that control insulin release and production by regulating cellular membrane electrical excitability (ATP:ADP ratio), insulin granule exocytosis, insulin synthesis in b-cells, and b-cell fate and islet mass formation. This review also examines miRNAs involved the insulin resistance of liver, fat, and skeletal muscle, which change insulin sensitivity pathways (insulin receptors, glucose transporter type 4, and protein kinase B pathways). This review discusses the potential application of miRNAs in diabetes, including the use of gene therapy and therapeutic compounds to recover miRNA function in diabetes, as well as the role of miRNAs as potential biomarkers for T1D and T2D.

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“…26 Briefly, diaphragms were pulverized and then homogenized in Tissue Protein Extraction Reagent (Pierce) supplemented with 1 mM Dithiothreitol (DTT), protease, and phosphatase inhibitor cocktails (Sigma-Aldrich Co.). Lysates were sonicated on ice and centrifuged at 10,000× g at 4°C for 10 minutes.…”

Section: Immunoblot Analysismentioning

confidence: 99%

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

Asano¹,

Arvapalli²,

Manne³

et al. 2015

IJN

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The severe inflammation observed during sepsis is thought to cause diaphragm dysfunction, which is associated with poor patient prognosis. Cerium oxide (CeO 2 ) nanoparticles have been posited to exhibit anti-inflammatory and antioxidative activities suggesting that these particles may be of potential use for the treatment of inflammatory disorders. To investigate this possibility, Sprague Dawley rats were randomly assigned to the following groups: sham control, CeO 2 nanoparticle treatment only (0.5 mg/kg iv), sepsis, and sepsis+CeO 2 nanoparticles. Sepsis was induced by the introduction of cecal material (600 mg/kg) directly into the peritoneal cavity. Nanoparticle treatment decreased sepsis-associated impairments in diaphragmatic contractile ( P o ) function (sham: 25.6±1.6 N/cm 2 vs CeO 2 : 23.4±0.8 N/cm 2 vs Sep: 15.9±1.0 N/cm 2 vs Sep+CeO 2 : 20.0±1.0 N/cm 2 , P <0.05). These improvements in diaphragm contractile function were accompanied by a normalization of protein translation signaling (Akt, FOXO-1, and 4EBP1), diminished proteolysis (caspase 8 and ubiquitin levels), and decreased inflammatory signaling (Stat3 and iNOS). Histological analysis suggested that nanoparticle treatment was associated with diminished sarcolemma damage and diminished inflammatory cell infiltration. These data indicate CeO 2 nanoparticles may improve diaphragmatic function in the septic laboratory rat.

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Overload Induced Heat Shock Proteins (HSPs), MAPK and miRNA (miR-1 and miR133a) Response in Insulin-Resistant Skeletal Muscle

Cited by 13 publications

References 53 publications

AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C₂C₁₂skeletal muscle cells

AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C₂C₁₂skeletal muscle cells

Application of microRNAs in diabetes mellitus

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

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Overload Induced Heat Shock Proteins (HSPs), MAPK and miRNA (miR-1 and miR133a) Response in Insulin-Resistant Skeletal Muscle

Cited by 13 publications

References 53 publications

AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C2C12skeletal muscle cells

AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C2C12skeletal muscle cells

Application of microRNAs in diabetes mellitus

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

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Resources

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AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C₂C₁₂skeletal muscle cells

AICAR-induced activation of AMPK negatively regulates myotube hypertrophy through the HSP72-mediated pathway in C₂C₁₂skeletal muscle cells