Low magnitude high frequency vibration promotes chondrogenic differentiation of bone marrow stem cells with involvement of β-catenin signaling pathway

Hou, Weiwei; Zhang, Denghui; Feng, Xiaoshan; Zhou, Yi

doi:10.1016/j.archoralbio.2020.104860

Cited by 13 publications

(12 citation statements)

References 40 publications

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“…In the cartilage, cell fate decision by GSK3β activity is also dependent on the context. For example, during endochondral ossification, GSK3β inactivation by cGMP-dependent protein kinase II promotes hypertrophy and terminal differentiation of chondrocytes [ 36 ], while GSK3β inactivation-activated β-catenin signaling promotes the chondrogenesis of bone marrow stem cells by rearranging the microfilament network upon stimulation by vibration [ 37 ]. GSK3β activity has also been suggested to serve as a checkpoint to maintain the mature chondrocytes in a healthy metabolic homeostasis status by finely tuning the overwork of β-catenin signaling [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3β Inactivation

Chang

Huang

Lee

et al. 2021

IJMS

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Osteoarthritis (OA) is still a recalcitrant musculoskeletal disease on account of its complex biochemistry and mechanical stimulations. Apart from stimulation by external mechanical forces, the regulation of intracellular mechanics in chondrocytes has also been linked to OA development. Recently, visfatin has received significant attention because of the clinical finding of the positive correlation between its serum/synovial level and OA progression. However, the precise mechanism involved is still unclear. This study determined the effect of visfatin on intracellular mechanics and catabolism in human primary chondrocytes isolated from patients. The intracellular stiffness of chondrocytes was analyzed by the particle-tracking microrheology method. It was shown that visfatin damages the microtubule and microfilament networks to influence intracellular mechanics to decrease the intracellular elasticity and viscosity via glycogen synthase kinase 3β (GSK3β) inactivation induced by p38 signaling. Further, microtubule network destruction in human primary chondrocytes is predominantly responsible for the catabolic effect of visfatin on the cyclooxygenase 2 upregulation. The present study shows a more comprehensive interpretation of OA development induced by visfatin through biochemical and biophysical perspectives. Finally, the role of GSK3β inactivation, and subsequent regulation of intracellular mechanics, might be considered as theranostic targets for future drug development for OA.

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Section: Discussionmentioning

confidence: 99%

Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3β Inactivation

Chang

Huang

Lee

et al. 2021

IJMS

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“…Various types of mechanical stimulation have been applied to enhance MSC chondrogenic differentiation in cartilage tissue engineering [ 122 ]. Hou et al demonstrated that low-magnitude high-frequency vibration enhanced the chondrogenic potential of rat BMSCs through activation of the Wnt/ β -catenin signaling pathway [ 123 ]. Xie et al revealed that proper tensile mechanical stimulation could improve the viscoelasticity and chondrogenic phenotype of rabbit BMSCs [ 124 ].…”

Section: Physical Stimulationmentioning

confidence: 99%

Recent Developed Strategies for Enhancing Chondrogenic Differentiation of MSC: Impact on MSC-Based Therapy for Cartilage Regeneration

Zha

Sun

et al. 2021

Stem Cells International

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Articular cartilage is susceptible to damage, but its self-repair is hindered by its avascular nature. Traditional treatment methods are not able to achieve satisfactory repair effects, and the development of tissue engineering techniques has shed new light on cartilage regeneration. Mesenchymal stem cells (MSCs) are one of the most commonly used seed cells in cartilage tissue engineering. However, MSCs tend to lose their multipotency, and the composition and structure of cartilage-like tissues formed by MSCs are far from those of native cartilage. Thus, there is an urgent need to develop strategies that promote MSC chondrogenic differentiation to give rise to durable and phenotypically correct regenerated cartilage. This review provides an overview of recent advances in enhancement strategies for MSC chondrogenic differentiation, including optimization of bioactive factors, culture conditions, cell type selection, coculture, gene editing, scaffolds, and physical stimulation. This review will aid the further understanding of the MSC chondrogenic differentiation process and enable improvement of MSC-based cartilage tissue engineering.

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“…While one aspect of SUN protein effects is centered around microtubule regulation of proliferation, SUN proteins also regulate mechanical response. Mechanical stimulation via low-intensity vibration (LIV), strain, and ECM activates mechanically sensitive biomolecular pathways such as Yes-associated-protein (YAP) and β-catenin /Wnt pathways [6,13,18,51,52], that in turn regulate both proliferation and differentiation [18,37,51,[53][54][55][56][57].…”

Section: Linc Complexmentioning

confidence: 99%

“…SUN proteins regulate mechanical response to strain and atomic force microscopy-induced cell deformation by restricting YAP [58] and β-catenin [16,59] entry into the nucleus by disrupting nuclear pore complex organization [60,61]. Additionally, SUN proteins are required for mechanoresponse and mechanoregulation of adipogensis in MSCs [37, [53][54][55][56] during low-intensity vibration (LIV). Interestingly, de-coupling of nesprins and SUN proteins also inhibits mechanoresponse to LIV [37, [53][54][55][56].…”

Section: Linc Complexmentioning

confidence: 99%

“…Additionally, SUN proteins are required for mechanoresponse and mechanoregulation of adipogensis in MSCs [37, [53][54][55][56] during low-intensity vibration (LIV). Interestingly, de-coupling of nesprins and SUN proteins also inhibits mechanoresponse to LIV [37, [53][54][55][56]. Decoupling of the LINC complex also decreases nuclear strain and deformation during microneedle manipulation indicating physical force transmission from the cytoskeleton into the nucleus is lost during loss of function of the LINC complex [48].…”

Section: Linc Complexmentioning

confidence: 99%

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Nuclear envelope mechanobiology: linking the nuclear structure and function

Goelzer

Ferguson

et al. 2021

Nucleus

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The nucleus, central to cellular activity, relies on both direct mechanical input as well as its molecular transducers to sense external stimuli and respond by regulating intra-nuclear chromatin organization that determines cell function and fate. In mesenchymal stem cells of musculoskeletal tissues, changes in nuclear structures are emerging as a key modulator of their differentiation and proliferation programs. In this review we will first introduce the structural elements of the nucleoskeleton and discuss the current literature on how nuclear structure and signaling are altered in relation to environmental and tissue level mechanical cues. We will focus on state-ofthe-art techniques to apply mechanical force and methods to measure nuclear mechanics in conjunction with DNA, RNA, and protein visualization in living cells. Ultimately, combining realtime nuclear deformations and chromatin dynamics can be a powerful tool to study mechanisms of how forces affect the dynamics of genome function.

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Low magnitude high frequency vibration promotes chondrogenic differentiation of bone marrow stem cells with involvement of β-catenin signaling pathway

Cited by 13 publications

References 40 publications

Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3β Inactivation

Effects of Visfatin on Intracellular Mechanics and Catabolism in Human Primary Chondrocytes through Glycogen Synthase Kinase 3β Inactivation

Recent Developed Strategies for Enhancing Chondrogenic Differentiation of MSC: Impact on MSC-Based Therapy for Cartilage Regeneration

Nuclear envelope mechanobiology: linking the nuclear structure and function

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