Piezo1 and IFT88 synergistically regulate mandibular condylar chondrocyte differentiation under cyclic tensile strain

Zhang, Zhuoyu; Sa, Guoliang; Wang, Zhuo; Wei, Zequan; Zheng, Li‐Wu; Zhang, Ruochen; Zhu, Xiashi; Yang, Xuewen

doi:10.1016/j.tice.2022.101781

Cited by 7 publications

(3 citation statements)

References 28 publications

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“…A recent study indicated that IFT88 determines the integrity of cilia and regulates the level of Piezo1. The authors confirmed the synergistic interaction between IFT88 and Piezo1 in regulating condylar chondrocyte differentiation under cyclic tensile strain ( Zhang et al, 2022a ). In addition, polycystin 2 was found to be an essential subunit for the ion channel located within the primary cilium; this subunit mainly conducts Na + and K + and is enhanced by Ca 2+ ( Liu X. et al, 2018 ).…”

Section: Elements In Mechanotransductionmentioning

confidence: 63%

“…On the basis of the findings of Servin-Vences et al, only Piezo1, and not Piezo2 or TRPV4, responds to stretch-activated currents ( Servin-Vences et al, 2017 ). Zhang et al confirmed that condylar chondrocytes respond to cyclic tensile strain (CTS) with 20% elongation of 0.1 Hz via Piezo1 followed by downregulation of sex-determining region Y-box 9 (SOX9) and COL2A1 ( Zhang et al, 2022a ). A recent study showed that in a unilateral anterior crossbite (UAC) rat model, Piezo1 was overexpressed in condylar cartilage, promoting progression of TMJOA through the Yes-associated protein (YAP)-matrix metalloproteinase 13 (MMP13)/a disintegrin and metalloproteinase with thrombospondin motif 5 (ADAMTS5) signaling pathway ( Feng et al, 2023 ).…”

Section: Elements In Mechanotransductionmentioning

confidence: 99%

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Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation

Liu,

Jia,

et al. 2024

Front. Pharmacol.

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The mechanical stress environment in the temporomandibular joint (TMJ) is constantly changing due to daily mandibular movements. Therefore, TMJ tissues, such as condylar cartilage, the synovial membrane and discs, are influenced by different magnitudes of mechanical stimulation. Moderate mechanical stimulation is beneficial for maintaining homeostasis, whereas abnormal mechanical stimulation leads to degeneration and ultimately contributes to the development of temporomandibular joint osteoarthritis (TMJOA), which involves changes in critical signaling molecules. Under abnormal mechanical stimulation, compensatory molecules may prevent degenerative changes while decompensatory molecules aggravate. In this review, we summarize the critical signaling molecules that are stimulated by moderate or abnormal mechanical loading in TMJ tissues, mainly in condylar cartilage. Furthermore, we classify abnormal mechanical stimulation-induced molecules into compensatory or decompensatory molecules. Our aim is to understand the pathophysiological mechanism of TMJ dysfunction more deeply in the ever-changing mechanical environment, and then provide new ideas for discovering effective diagnostic and therapeutic targets in TMJOA.

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Section: Elements In Mechanotransductionmentioning

confidence: 63%

Section: Elements In Mechanotransductionmentioning

confidence: 99%

Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation

Liu,

Jia,

et al. 2024

Front. Pharmacol.

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“…TRPV4 channels also mediate the thermo-mechanotransduction process in human CPCs [ 31 ]. In addition to TRPs, the mechanically activated cation channel Piezo1 also regulates chondrocyte differentiation [ 32 ].…”

Section: Ion Channels Involved In Progenitor Cell Differentiationmentioning

confidence: 99%

Ca2+-Activated K+ Channels in Progenitor Cells of Musculoskeletal Tissues: A Narrative Review

Takács

Kovács

Ebeid

et al. 2023

IJMS

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Musculoskeletal disorders represent one of the main causes of disability worldwide, and their prevalence is predicted to increase in the coming decades. Stem cell therapy may be a promising option for the treatment of some of the musculoskeletal diseases. Although significant progress has been made in musculoskeletal stem cell research, osteoarthritis, the most-common musculoskeletal disorder, still lacks curative treatment. To fine-tune stem-cell-based therapy, it is necessary to focus on the underlying biological mechanisms. Ion channels and the bioelectric signals they generate control the proliferation, differentiation, and migration of musculoskeletal progenitor cells. Calcium- and voltage-activated potassium (KCa) channels are key players in cell physiology in cells of the musculoskeletal system. This review article focused on the big conductance (BK) KCa channels. The regulatory function of BK channels requires interactions with diverse sets of proteins that have different functions in tissue-resident stem cells. In this narrative review article, we discuss the main ion channels of musculoskeletal stem cells, with a focus on calcium-dependent potassium channels, especially on the large conductance BK channel. We review their expression and function in progenitor cell proliferation, differentiation, and migration and highlight gaps in current knowledge on their involvement in musculoskeletal diseases.

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Intraflagellar transport protein 88 interacts with polycystin 2 to regulate mechanosensitive hedgehog signaling in mandibular condylar chondrocytes

Wang

Sa²,

Zheng³

et al. 2022

Archives of Oral Biology

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Piezo1 and IFT88 synergistically regulate mandibular condylar chondrocyte differentiation under cyclic tensile strain

Cited by 7 publications

References 28 publications

Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation

Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation

Ca2+-Activated K+ Channels in Progenitor Cells of Musculoskeletal Tissues: A Narrative Review

Intraflagellar transport protein 88 interacts with polycystin 2 to regulate mechanosensitive hedgehog signaling in mandibular condylar chondrocytes

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