KLF15 regulates slow myosin heavy chain expression through NFATc1 in C2C12 myotubes

Wang, Jie; Chen, Ting; Fu, Feng; Wei, Huan; Pang, Wei; Yang, Gongshe; Shen, Qingwu

doi:10.1016/j.bbrc.2014.03.091

Cited by 11 publications

(8 citation statements)

References 23 publications

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“…Moreover, four and a half LIM domains protein 3 (FHL3) may act as a transcriptional co‐activator of MHCIIa and MHCIIb or a co‐repressor of MHCI expression through selective interactions with the transcription factors MyoD and CREB (Zhang et al, ). Myocyte enhancer factor 2 (MEF2), serum response factor (SRF), and Kruppel‐like factor 15 (KLF15) are also transcription factors that differentially regulate MHC expression (Harrison et al, ; Wang et al, ). Alterations in their activities may also trigger the downregulation of myofibrillar gene expression, but this possibility remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of myofibrillar proteins in skeletal muscles of septic mice

et al. 2019

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Sepsis elicits skeletal muscle atrophy as a result of decreased total protein synthesis and/or increased total protein degradation. It is unknown how and whether sepsis differentially affects the expression of specific myofibrillar proteins in respiratory and limb muscles. In this study, we measured the effects of sepsis myofibrillar mRNAs and their corresponding protein levels in the diaphragm (DIA) and tibialis anterior (TA) muscles in a murine cecal ligation and perforation (CLP) model of sepsis. Male mice (C57/BL6j) underwent CLP‐induced sepsis. Sham‐operated mice were subjected to the same surgical procedures, except for CLP. Mice were euthanized 24, 48, or 96 h postsurgery. Transcript and protein levels of autophagy‐related genes, ubiquitin E3 ligases, and several myofibrillar genes were quantified. Sepsis elicited transient fiber atrophy in the DIA and prolonged atrophy in the TA. Atrophy was coincident with increased autophagy and ubiquitin E3 ligase expression. Myosin heavy chain isoforms decreased at 24 h in the DIA and across the time‐course in the TA, myosin light chain isoforms decreased across the time‐course in both muscles, and troponins T and C as well as tropomyosin decreased after 24 and 48 h in both the DIA and TA. α‐Actin and troponin I were unaffected by sepsis. Sepsis‐induced decreases in myofibrillar protein levels coincided with decreased mRNA expressions of these proteins, suggesting that transcriptional inhibition is involved. We hypothesize that sepsis‐induced muscle atrophy is mediated by decreased transcription and enhanced degradation of specific myofibrillar proteins, including myosin heavy and light chains, troponin C, troponin T, and tropomyosin.

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Section: Discussionmentioning

confidence: 99%

Differential regulation of myofibrillar proteins in skeletal muscles of septic mice

et al. 2019

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“…Within skeletal muscle it regulates lipid utilization (234), coordinates the transcriptional circuitry responsible for metabolism (234), mediates the metabolic ergogenic effects of glucocorticoids via metabolic programming (233), and affects exercise capacity (212,234). In addition to its metabolic role, KLF15 regulates myofiber typing (235), mTOR activity (233), and myofiber size (212). KLF15 displays a diurnal pattern of expression, and regulates branchedchain amino acid (BCAA) metabolism and utilization in a circadian fashion (236).…”

Section: Klf15-a Target Of Glucocorticoid Receptor In Skeletal Musclementioning

confidence: 99%

Growth Hormone(s), Testosterone, Insulin-Like Growth Factors, and Cortisol: Roles and Integration for Cellular Development and Growth With Exercise

et al. 2020

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Hormones are largely responsible for the integrated communication of several physiological systems responsible for modulating cellular growth and development. Although the specific hormonal influence must be considered within the context of the entire endocrine system and its relationship with other physiological systems, three key hormones are considered the "anabolic giants" in cellular growth and repair: testosterone, the growth hormone superfamily, and the insulin-like growth factor (IGF) superfamily. In addition to these anabolic hormones, glucocorticoids, mainly cortisol must also be considered because of their profound opposing influence on human skeletal muscle anabolism in many instances. This review presents emerging research on: (1) Testosterone signaling pathways, responses, and adaptations to resistance training; (2) Growth hormone: presents new complexity with exercise stress; (3) Current perspectives on IGF-I and physiological adaptations and complexity these hormones as related to training; and (4) Glucocorticoid roles in integrated communication for anabolic/catabolic signaling. Specifically, the review describes (1) Testosterone as the primary anabolic hormone, with an anabolic influence largely dictated primarily by genomic and possible non-genomic signaling, satellite cell activation, interaction with other anabolic signaling pathways, upregulation or downregulation of the androgen receptor, and potential roles in co-activators and transcriptional activity; (2) Differential influences of growth hormones depending on the "type" of the hormone being assayed and the magnitude of the physiological stress; (3) The exquisite regulation of IGF-1 by a family of binding proteins (IGFBPs 1-6), which can either stimulate or inhibit biological action depending on binding; and (4) Circadian patterning and newly discovered variants of glucocorticoid isoforms largely dictating glucocorticoid sensitivity and catabolic, muscle sparing, or pathological influence. The downstream integrated anabolic and catabolic mechanisms of these hormones not only affect the ability of skeletal muscle to generate force; they also have Kraemer et al. Anabolic and Catabolic Hormones and Exercise implications for pharmaceutical treatments, aging, and prevalent chronic conditions such as metabolic syndrome, insulin resistance, and hypertension. Thus, advances in our understanding of hormones that impact anabolic: catabolic processes have relevance for athletes and the general population, alike.

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“…KLF15 expression is low during development and robustly induced during postnatal maturation ( 87 ). Nonetheless, Klf15 knockdown does not interfere with muscle differentiation of C2C12 cells ( 89 ), and the skeletal muscle in Klf15 −/− mice exhibit no clear developmental defects ( 87 ). In addition, KLF15 controls expression of slow-type myosin heavy chain ( Myh7 ), suggesting it contributes to myofiber typing ( 89 ), though Klf15 −/− mice exhibit no changes in their fiber type compositions ( 87 ).…”

Section: Klfs In Skeletal Muscle Biology and Pathobiologymentioning

confidence: 99%

Krüppel-Like Factors in Metabolic Homeostasis and Cardiometabolic Disease

Oishi

Manabe

2018

Front. Cardiovasc. Med.

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Members of the Krüppel-like factor (KLF) family of transcription factors, which are characterized by the presence of three conserved Cys2/His2 zinc-fingers in their C-terminal domains, control a wide variety of biological processes. In particular, recent studies have revealed that KLFs play diverse and essential roles in the control of metabolism at the cellular, tissue and systemic levels. In both liver and skeletal muscle, KLFs control glucose, lipid and amino acid metabolism so as to coordinate systemic metabolism in the steady state and in the face of metabolic stresses, such as fasting. The functions of KLFs within metabolic tissues are also important contributors to the responses to injury and inflammation within those tissues. KLFs also control the function of immune cells, such as macrophages, which are involved in the inflammatory processes underlying both cardiovascular and metabolic diseases. This review focuses mainly on the physiological and pathological functions of KLFs in the liver and skeletal muscle. The involvement of KLFs in inflammation in these tissues is also summarized. We then discuss the implications of KLFs' control of metabolism and inflammation in cardiometabolic diseases.

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KLF15 regulates slow myosin heavy chain expression through NFATc1 in C2C12 myotubes

Cited by 11 publications

References 23 publications

Differential regulation of myofibrillar proteins in skeletal muscles of septic mice

Differential regulation of myofibrillar proteins in skeletal muscles of septic mice

Growth Hormone(s), Testosterone, Insulin-Like Growth Factors, and Cortisol: Roles and Integration for Cellular Development and Growth With Exercise

Krüppel-Like Factors in Metabolic Homeostasis and Cardiometabolic Disease

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