Fibromodulin and regulation of the intricate balance between myoblast differentiation to myocytes or adipocyte‐like cells

Lee, Eun Ju; Jan, Arif Tasleem; Baig, Mohammad Hassan; Ahmad, Khurshid; Malik, Adeel; Rabbani, Gulam; Kim, Taeyeon; Lee, Inkyu; Lee, Yong-Ho; Park, Soyoung; Choi, Inho

doi:10.1096/fj.201700665r

Cited by 40 publications

(31 citation statements)

References 47 publications

(57 reference statements)

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“…Microarray analysis was conducted with the Agilent Technologies mouse GE4X 44K (V2) chip to determine the differentially expressed genes in wild-type (TTR wt ) and TTR kd (TTR knockdown) cells as described previously [30]. Briefly, TTR wt and TTR kd cells were grown in serum (+) differentiation media for two days and RNAs were extracted, synthesized into cDNA with fluorescence using a Low RNA Input Linear Amplification kit (Agilent Technologies, CA, USA) according to the manufacturer's instructions.…”

Section: Microarray Analysismentioning

confidence: 99%

Transthyretin Maintains Muscle Homeostasis through the Novel Shuttle Pathway of Thyroid Hormones during Myoblast Differentiation

Lee

Shaikh

Choi

et al. 2019

Cells

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Skeletal muscle, the largest part of the total body mass, influences energy and protein metabolism as well as maintaining homeostasis. Herein, we demonstrate that during murine muscle satellite cell and myoblast differentiation, transthyretin (TTR) can exocytose via exosomes and enter cells as TTR- thyroxine (T4) complex, which consecutively induces the intracellular triiodothyronine (T3) level, followed by T3 secretion out of the cell through the exosomes. The decrease in T3 with the TTR level in 26-week-old mouse muscle, compared to that in 16-week-old muscle, suggests an association of TTR with old muscle. Subsequent studies, including microarray analysis, demonstrated that T3-regulated genes, such as FNDC5 (Fibronectin type III domain containing 5, irisin) and RXRγ (Retinoid X receptor gamma), are influenced by TTR knockdown, implying that thyroid hormones and TTR coordinate with each other with respect to muscle growth and development. These results suggest that, in addition to utilizing T4, skeletal muscle also distributes generated T3 to other tissues and has a vital role in sensing the intracellular T4 level. Furthermore, the results of TTR function with T4 in differentiation will be highly useful in the strategic development of novel therapeutics related to muscle homeostasis and regeneration.

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Section: Microarray Analysismentioning

confidence: 99%

Transthyretin Maintains Muscle Homeostasis through the Novel Shuttle Pathway of Thyroid Hormones during Myoblast Differentiation

Lee

Shaikh

Choi

et al. 2019

Cells

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“…Furthermore, two major SM ECM proteins, that is, collagen and laminin, are known to be associated with myopathies. In previous studies, we explored the roles of a small number of ECM proteins like fibromodulin, matrix gla proteins, and dermatopontin during different stages of myogenesis (Lee et al, 2016;Ahmad et al, 2017;Lee et al, 2018;Kim et al, 2019) and found fibromodulin, as well as dermatopontin, is involved in the vigorous recruitment of MSCs at sites of injury, and thus, aids SM regeneration Kim et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Cross-Talk Between Extracellular Matrix and Skeletal Muscle: Implications for Myopathies

et al. 2020

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Skeletal muscle (SM) comprises around 40% of total body weight and is among the most important plastic tissues, as it supports skeletal development, controls body temperature, and manages glucose levels. Extracellular matrix (ECM) maintains the integrity of SM, enables biochemical signaling, provides structural support, and plays a vital role during myogenesis. Several human diseases are coupled with dysfunctions of the ECM, and several ECM components are involved in disease pathologies that affect almost all organ systems. Thus, mutations in ECM genes that encode proteins and their transmembrane receptors can result in diverse SM diseases, a large proportion of which are types of fibrosis and muscular dystrophy. In this review, we present major ECM components of SMs related to muscle-associated diseases, and discuss two major ECM myopathies, namely, collagen myopathy and laminin myopathies, and their therapeutic managements. A comprehensive understanding of the mechanisms underlying these ECM-related myopathies would undoubtedly aid the discovery of novel treatments for these devastating diseases.

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“…In recent years, increasing studies have suggested FMOD as a crucial regulator of wound healing [ 12 , 17 , 25 – 28 ], which leads to the speculation that FMOD may also play a special role in the pathological progression of PVR, the process of wound healing in the eye. It is known that RPE plays critical roles in eye fibrosis, which raises the question that whether FMOD is associated with the abnormal activation of RPE.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway

et al. 2018

Journal of Ophthalmology

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Purpose Recent research has provided novel insight into the function of fibromodulin (FMOD) in wound healing and angiogenesis. The role of FMOD in initiation of proliferative vitreoretinopathy (PVR) has not been studied. This study investigated the effect of FMOD on human retinal pigment epithelial (RPE) cell, which plays an essential role in the progression of PVR, and the possible mechanisms. Methods Small interfering (si) RNA-based gene transfer technology was used to decrease FMOD expression and to study its effects on RPEs in vitro. Cell Counting Kit-8 assays, transwells, and flow cytometry analysis were used to measure cell proliferation, migration, cell cycle, and apoptosis. Western blot was used to measure expression of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), extracellular signal-related kinase 1/2 (ERK1/2), and phosphoinositide 3 kinase (PI3K/AKT). Results After transfection of RPEs with a FMOD-specific siRNA, cell proliferation and migration were inhibited to the percentage of 65% ± 5% and 39% ± 10%, respectively, compared to the control group. Depletion of FMOD induced cell cycle arrest and apoptosis in RPE cells. Downregulation of VEGF, VEGFR2, and phosphorylated AKT (p-AKT) were detected in transfected RPEs. Conclusion Depletion of FMOD selectively downregulated the expression of VEGF and VEGFR2 and inhibited the signaling pathway of AKT phosphorylation, which consequently inhibited the proliferation and migration of RPE Cell.

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Fibromodulin and regulation of the intricate balance between myoblast differentiation to myocytes or adipocyte‐like cells

Cited by 40 publications

References 47 publications

Transthyretin Maintains Muscle Homeostasis through the Novel Shuttle Pathway of Thyroid Hormones during Myoblast Differentiation

Transthyretin Maintains Muscle Homeostasis through the Novel Shuttle Pathway of Thyroid Hormones during Myoblast Differentiation

Cross-Talk Between Extracellular Matrix and Skeletal Muscle: Implications for Myopathies

Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway

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