Roles of chondroitin sulfate proteoglycan 4 in fibrogenic/adipogenic differentiation in skeletal muscle tissues

Takeuchi, S.; Nakano, Shinichi; Nakamura, Katsuyuki; Ozoe, Atsufumi; Chien, Peggie; Yoshihara, Hidehito; Hakuno, Fumihiko; Matsuwaki, Takashi; Saeki, Yasushi; Takahashi, Shin‐Ichiro; Yamanouchi, Keitaro; Nishihara, Masugi

doi:10.1016/j.yexcr.2016.08.023

Cited by 21 publications

(27 citation statements)

References 35 publications

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“…1A ), showing that senescence was induced in mesenchymal cells in the aged rats. Furthermore, immunohistochemical analysis of γH2AX and CSPG4, which was identified by our group to be expressed in the cells that have both fibrogenic and adipogenic potential like MPCs in the rat skeletal muscle [ 22 ], revealed the existence of double-positive cells ( Supplementary Fig. 1B ).…”

Section: Resultsmentioning

confidence: 99%

“…We previously showed that 2G11 cells exhibit fibrogenic potential [ 22 ]; here, to examine whether senescence affects this potential, we treated PMS-2G11 cells with TGFβ, which promotes fibrogenic differentiation [ 19 ], and measured the expression of the fibroblast markers Ctgf , Col1a1 , and Acta2 (also known as α-smooth muscle actin; α-SMA). As previously demonstrated, TGFβ treatment increased the expression of these 3 fibroblast markers in 2G11 cells ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, MPCs provide functional support to satellite cells and promote muscle regeneration [ 17 ]. We previously established the MPC clone 2G11 from rat skeletal muscle [ 21 ] and showed that 2G11 cells are fibro/adipogenic [ 20 , 22 ] and promote myotube formation by skeletal muscle progenitor cells [ 23 ]. Ageing causes a functional decrease in several cell types, but whether the fibro/adipogenic potential or the muscle-supportive effect of MPCs is perturbed in aged skeletal muscle remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress-mediated senescence in mesenchymal progenitor cells causes the loss of their fibro/adipogenic potential and abrogates myoblast fusion

Sugihara

Teramoto

Yamanouchi

et al. 2018

Aging

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Sarcopenia is the age-related loss of skeletal muscle mass and function. Skeletal muscle comprises diverse progenitor cells, including mesenchymal progenitor cells (MPCs), which normally support myogenic cell function but cause a decline in skeletal muscle function after differentiating into fibrous/adipose tissue. Cellular senescence is a form of persistent cell cycle arrest caused by cellular stress, including oxidative stress, and is accompanied by the acquisition of senescence-associated secretory phenotype (SASP). Here, we found γH2AX+ senescent cells appeared in the interstitium in skeletal muscle, corresponding in position to that of MPCs. H2O2 mediated oxidative stress in 2G11 cells, a rat MPC clone previously established in our laboratory, successfully induced senescence, as shown by the upregulation of p21 and SASP factors, including IL-6. The senescent 2G11 cells lost their fibro/adipogenic potential, but, intriguingly, coculture of myoblasts with senescent 2G11 cells abrogated the myotube formation, which coincided with the downregulation of myomaker, a muscle-specific protein involved in myogenic cell fusion; however, forced expression of myomaker could not rescue this abrogation. These results suggest that senescent MPCs in aged rat skeletal muscle lose their fibro/adipogenic potential, but differ completely from undifferentiated progenitor cells in that senescent MPCs suppress myoblast fusion and thereby potentially accelerate sarcopenia.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Oxidative stress-mediated senescence in mesenchymal progenitor cells causes the loss of their fibro/adipogenic potential and abrogates myoblast fusion

Sugihara

Teramoto

Yamanouchi

et al. 2018

Aging

Self Cite

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“…Ингибирование ХС и ГС воспалительного сигнального пути ФНОα/NF-kB уменьшает дистрофические изменения в хрящах [55] и мышцах (посредством ингибирования NF-kB в миофибриллах) [56]. Это замедляет апоптоз клеток хрящевой ткани, тем самым сохраняется объем хряща и улучшается дифференцировка миоцитов, способствуя увелечению массы мышц и, следовательно, их силы [57,58]. Влияние сульфатированных полисахаридных молекул на миогенную дифференцировку обсуждается с конца прошлого века [59].…”

Section: адекватное потребление калорий и белка -примени-unclassified

Chronic pain in older people: focus on sarcopenia

Наумов¹,

Мороз²,

Ховасова³

et al. 2019

Medicinskij sovet

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Наумов Антон Вячеславовичд.м.н., профессор кафедры болезней старения ФДПО Федерального государственного бюджетного образовательного учреждения высшего образования «Российский национальный исследовательский медицинский университет имени Н.И. Пирогова», заведующий лабораторией костно-мышечной системы Обособленного структурного подразделения «Российский геронтологический научно-клинический центр» Федерального государственного бюджетного образовательного учреждения высшего образования «Российский национальный исследовательский медицинский университет имени Н.И. Пирогова» Министерства здравоохранения Российской Федерации; старший научный сотрудник Федерального центра координации деятельности субъектов Российской Федерации по развитию организации оказания медицинской помощи по профилю «гериатрия»; тел.:

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“…Manuscript to be reviewed background such as tenocytes. CSPG4 binds FGF2 resulting in cell proliferation (Cattaruzza et al 2013;Takeuchi et al 2016) it also acts as a type VI collagen receptor and binds to perlecan (Tang et al 2018). Type VI collagen/CSPG4 regulate tenocyte behavior, play important roles in the assembly of tendon matrix, and have crucial roles in tendon repair processes (Sardone et al 2016 (Chun et al 2008).…”

Section: Ng2/cspg4 Is Another Transmembrane Proteoglycan Produced By mentioning

confidence: 99%

Peer Review #1 of "Achilles and tail tendons of perlecan exon 3 null heparan sulphate deficient mice display surprising improvement in tendon tensile properties and altered collagen fibril organisation compared to C57BL/6 wild type mice (v0.1)"

2018

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The aim of this study was to determine the role of the perlecan (Hspg2) heparan sulphate (HS) side chains on cell and matrix homeostasis in tail and Achilles tendons in 3 and 12 week old Hspg2 exon 3 null HS deficient (Hspg2 ∆3-/∆3-) and C57 BL/6 Wild Type (WT) mice. Perlecan has important cell regulatory and matrix organizational properties through HS mediated interactions with a range of growth factors and morphogens and with structural extracellular matrix glycoproteins which define tissue function and allow the resident cells to regulate tissue homeostasis. It was expected that ablation of the HS chains on perlecan would severely disrupt normal tendon organization and functional properties and it was envisaged that this study would better define the role of HS in normal tendon function and in tendon repair processes. Tail and Achilles tendons from each genotype were biomechanically tested (ultimate tensile stress [UTS], tensile modulus [TM]) and glycosaminoglycan (GAG) and collagen (hydroxyproline) compositional analyses were undertaken. Tenocytes were isolated from tail tendons from each mouse genotype and grown in monolayer culture. These cultures were undertaken in the presence of FGF-2 to assess the cell signaling properties of each genotype. Total RNA was isolated from 3-12 week old tail and Achilles tendons and qRT-PCR was undertaken to assess the expression of the following genes Vcan, Bgn, Dcn, Lum, Hspg2, Ltbp1, Ltbp2, Eln and Fbn1. Type VI collagen and perlecan were immunolocalised in tail tendon and collagen fibrils were imaged using transmission electron microscopy (TEM). FGF-2 stimulated tenocyte monolayers displayed elevated Adamts4, Mmp2, 3, 13 mRNA levels compared to WT mice.. Non stimulated tendon Col1A1,

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Roles of chondroitin sulfate proteoglycan 4 in fibrogenic/adipogenic differentiation in skeletal muscle tissues

Cited by 21 publications

References 35 publications

Oxidative stress-mediated senescence in mesenchymal progenitor cells causes the loss of their fibro/adipogenic potential and abrogates myoblast fusion

Oxidative stress-mediated senescence in mesenchymal progenitor cells causes the loss of their fibro/adipogenic potential and abrogates myoblast fusion

Chronic pain in older people: focus on sarcopenia

Peer Review #1 of "Achilles and tail tendons of perlecan exon 3 null heparan sulphate deficient mice display surprising improvement in tendon tensile properties and altered collagen fibril organisation compared to C57BL/6 wild type mice (v0.1)"

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