Activation of YAP regulates muscle fiber size in a PKC-dependent mechanism during chick in vitro myogenesis

Gomes, Geyse; Bagri, Kayo Moreira; Rosa, Ivone de Andrade; Jurberg, Arnon Dias; Mermelstein, Cláudia; Costa, Márcio Henrique Sá Netto

doi:10.1007/s10974-021-09608-8

Cited by 3 publications

(1 citation statement)

References 27 publications

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“…Aging and Disease • Volume 16, Number 1, February 2025 MST1/2 inhibition also increases myotube width, myoblast fusion, and myogenin expression in chick muscle cells, ultimately resulting in the formation of fully stratified myofibers with increased size [61]. In terms of osteogenesis, the deleting Yap and Taz reduces the number of osteoblasts and mineral apposition rates in mice, as well as decreases osteogenic gene induction in isolated osteoprogenitors [11].…”

Section: Yap/taz Dysregulation In Muscle Atrophy and Osteoporosismentioning

confidence: 99%

YAP/TAZ as Molecular Targets in Skeletal Muscle Atrophy and Osteoporosis

Kwon

2024

Aging and disease

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Skeletal muscles and bones are closely connected anatomically and functionally. Age-related degeneration in these tissues is associated with physical disability in the elderly and significantly impacts their quality of life. Understanding the mechanisms of age-related musculoskeletal tissue degeneration is crucial for identifying molecular targets for therapeutic interventions for skeletal muscle atrophy and osteoporosis. The Hippo pathway is a recently identified signaling pathway that plays critical roles in development, tissue homeostasis, and regeneration. The Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) are key downstream effectors of the mammalian Hippo signaling pathway. This review highlights the fundamental roles of YAP and TAZ in the homeostatic maintenance and regeneration of skeletal muscles and bones. YAP/TAZ play a significant role in stem cell function by relaying various environmental signals to stem cells. Skeletal muscle atrophy and osteoporosis are related to stem cell dysfunction or senescence triggered by YAP/TAZ dysregulation resulting from reduced mechanosensing and mitochondrial function in stem cells. In contrast, the maintenance of YAP/TAZ activation can suppress stem cell senescence and tissue dysfunction and may be used as a basis for the development of potential therapeutic strategies. Thus, targeting YAP/TAZ holds significant therapeutic potential for alleviating age-related muscle and bone dysfunction and improving the quality of life in the elderly.

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Section: Yap/taz Dysregulation In Muscle Atrophy and Osteoporosismentioning

confidence: 99%

YAP/TAZ as Molecular Targets in Skeletal Muscle Atrophy and Osteoporosis

Kwon

2024

Aging and disease

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Biology of Hippo signaling pathway: Skeletal muscle development and beyond

Qin,

Li,

et al. 2024

Journal of Integrative Agriculture

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12-O-tetradecanoylphorbol-13-acetate Reduces Activation of Hepatic Stellate Cells by Inhibiting the Hippo Pathway Transcriptional Coactivator YAP

Kim

Yoon

Kim

et al. 2022

Cells

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Although protein kinase C (PKC) regulates various biological activities, including cell proliferation, differentiation, migration, tissue remodeling, gene expression, and cell death, the antifibrotic effect of PKC in myofibroblasts is not fully understood. We investigated whether 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC activator, reduced the activation of hepatic stellate cells (HSCs) and explored the involvement of the Hippo pathway transcriptional coactivator YAP. We analyzed the effect of TPA on the proliferation and expression of α-smooth muscle actin (SMA) in the LX-2 HSC line. We also analyzed the phosphorylation of the Hippo pathway molecules YAP and LATS1 and investigated YAP nuclear translocation. We examined whether Gö 6983, a pan-PKC inhibitor, restored the TPA-inhibited activities of HSCs. Administration of TPA decreased the growth rate of LX-2 cells and inhibited the expression of α-SMA and collagen type I alpha 1 (COL1A1). In addition, TPA induced phosphorylation of PKCδ, LATS1, and YAP and inhibited the nuclear translocation of YAP compared with the control. These TPA-induced phenomena were mostly ameliorated by Gö 6983. Our results indicate that PKCδ exerts an antifibrotic effect by inhibiting the Hippo pathway in HSCs. Therefore, PKCδ and YAP can be used as therapeutic targets for the treatment of fibrotic diseases.

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Activation of YAP regulates muscle fiber size in a PKC-dependent mechanism during chick in vitro myogenesis

Cited by 3 publications

References 27 publications

YAP/TAZ as Molecular Targets in Skeletal Muscle Atrophy and Osteoporosis

YAP/TAZ as Molecular Targets in Skeletal Muscle Atrophy and Osteoporosis

Biology of Hippo signaling pathway: Skeletal muscle development and beyond

12-O-tetradecanoylphorbol-13-acetate Reduces Activation of Hepatic Stellate Cells by Inhibiting the Hippo Pathway Transcriptional Coactivator YAP

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