The roles of Runx1 in skeletal development and osteoarthritis: A concise review

Liu, Yi; Huang, Chengdong; Bai, Mingru; Pi, Caixia; Zhang, Demao; Xie, Jing

doi:10.1016/j.heliyon.2022.e12656

Cited by 6 publications

(3 citation statements)

References 123 publications

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“…A previous study demonstrated that Runt-related transcription factor-1 (Runx1), renowned for its roles in hemopoiesis and leukaemia, possesses the ability to regulate crucial genes such as collagen type II (Col2a1) and X (Col10a1), SRY-box transcription factor 9 (Sox9), aggrecan (Acan), and matrix metalloproteinase 13 (MMP-13). Notably, the upregulation of Runx1 expression was found to enhance the overall homeostasis of the joint ( 20 ). Myeloid cell differentiation is an important part of cell differentiation.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics and systems biology approaches to identify potential common pathogeneses for sarcopenia and osteoarthritis

Yang,

Zhong,

et al. 2024

Front. Med.

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Sarcopenia, a geriatric syndrome characterized by progressive loss of muscle mass and strength, and osteoarthritis, a common degenerative joint disease, are both prevalent in elderly individuals. However, the relationship and molecular mechanisms underlying these two diseases have not been fully elucidated. In this study, we screened microarray data from the Gene Expression Omnibus to identify associations between sarcopenia and osteoarthritis. We employed multiple statistical methods and bioinformatics tools to analyze the shared DEGs (differentially expressed genes). Additionally, we identified 8 hub genes through functional enrichment analysis, protein–protein interaction analysis, transcription factor-gene interaction network analysis, and TF-miRNA coregulatory network analysis. We also discovered potential shared pathways between the two diseases, such as transcriptional misregulation in cancer, the FOXO signalling pathway, and endometrial cancer. Furthermore, based on common DEGs, we found that strophanthidin may be an optimal drug for treating sarcopenia and osteoarthritis, as indicated by the Drug Signatures database. Immune infiltration analysis was also performed on the sarcopenia and osteoarthritis datasets. Finally, receiver operating characteristic (ROC) curves were plotted to verify the reliability of our results. Our findings provide a theoretical foundation for future research on the potential common pathogenesis and molecular mechanisms of sarcopenia and osteoarthritis.

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Section: Discussionmentioning

confidence: 99%

Bioinformatics and systems biology approaches to identify potential common pathogeneses for sarcopenia and osteoarthritis

Yang,

Zhong,

et al. 2024

Front. Med.

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“…Chondrocytes are mechanosensitive cells that sense and respond to extracellular mechanical stimuli. Mechanical forces generated in the cartilage extracellular matrix with daily activities and disease progression change the cytoskeleton system, [80,81] promote focal adhesion assembly, [82] activate mechanical membrane signal receptors, [83] trigger the intracellular signaling cascade, [84,85] and ultimately determine the cell fate. [24,36,55] In this progress of mechanosensing and mechanotransduction, focal adhesions are regarded as bridges that link force sensing, cytoskeleton reorganization and chemical signal transduction.…”

Section: Discussionmentioning

confidence: 99%

Biomimetic Fibers Based on Equidistant Micropillar Arrays Determines Chondrocyte Fate via Mechanoadaptability

Zhou,

Yang,

Duan

et al. 2023

Adv Healthcare Materials

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It is recognized that the changes in the physical properties of extracellular matrix result in fine‐tuned cell responses including cell morphology, proliferation and differentiation. In this study, a novel patterned equidistant micropillar substrate based on polydimethylsiloxane (PDMS) was designed to mimic the collagen fiber‐like network of the cartilage matrix. By changing the component of the curing agent to an oligomeric base, we obtained micropillar substrates with the same topology but different stiffnesses and found that chondrocytes seeded onto the soft micropillar substrate maintain their phenotype by gathering type II collagen and aggrecan more effectively than those seeded onto the stiff micropillar substrate. Moreover, chondrocytes sensed and responded to micropillar substrates with different stiffnesses by altering the ECM‐cytoskeleton‐focal adhesion axis. We then found that the soft substrate‐preserved chondrocyte phenotype was dependent on the activation of Wnt/β‐catenin signaling at a high expression level. Finally, we indicated the changes in osteoid‐like region formation and cartilage phenotype loss in the stiffened sclerotic area of osteoarthritis mouse cartilage to validate the cell behavior changes triggered by micropillar substrates with different stiffnesses. This study provided the change in cell behaviors that are more similar to those of real chondrocytes at tissue level during the transition from a normal state to a state of osteoarthritis.This article is protected by copyright. All rights reserved

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“…A previous study demonstrated that Runt-related transcription factor-1 (Runx1), renowned for its roles in hemopoiesis and leukaemia, possesses the ability to regulate crucial genes such as collagen type II (Col2a1) and X (Col10a1), SRY-box transcription factor 9 (Sox9), aggrecan (Acan), and matrix metalloproteinase 13 (MMP-13). Notably, the upregulation of Runx1 expression was found to enhance the overall homeostasis of the joint (20). Myeloid cell differentiation is an important part of cell differentiation.…”

Section: Discussionmentioning

confidence: 99%

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The roles of Runx1 in skeletal development and osteoarthritis: A concise review

Cited by 6 publications

References 123 publications

Bioinformatics and systems biology approaches to identify potential common pathogeneses for sarcopenia and osteoarthritis

Bioinformatics and systems biology approaches to identify potential common pathogeneses for sarcopenia and osteoarthritis

Biomimetic Fibers Based on Equidistant Micropillar Arrays Determines Chondrocyte Fate via Mechanoadaptability

Table_1.DOCX

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