| Title | Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice |
| Author | |
| Corresponding Author | Wu, Xiaohao; Xiao, Guozhi |
| Publication Years | 2022-08-01
|
| DOI | |
| Source Title | |
| ISSN | 2152-5250
|
| Abstract | Osteoarthritis (OA) is the most common degenerative joint disease affecting the older populations globally. Phosphatidylinositol-4-phosphate 5-kinase type-1 gamma (Pip5k1c), a lipid kinase catalyzing the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2), is involved in various cellular processes, such as focal adhesion (FA) formation, cell migration, and cellular signal transduction. However, whether Pip5k1c plays a role in the pathogenesis of OA remains unclear. Here we show that inducible deletion of Pip5k1c in aggrecan-expressing chondrocytes (cKO) causes multiple spontaneous OA-like lesions, including cartilage degradation, surface fissures, subchondral sclerosis, meniscus deformation, synovial hy perplasia, and osteophyte formation in aged (15-month-old) mice, but not in adult (7-month-old) mice. Pip5k1c loss promotes extracellular matrix (ECM) degradation, chondrocyte hypertrophy and apoptosis, and inhibits chondrocyte proliferation in the articular cartilage of aged mice. Pip5k1c loss dramatically downregulates the expressions of several key FA proteins, including activated integrin beta 1, talin, and vinculin, and thus impairs the chondrocyte adhesion and spreading on ECM. Collectively, these findings suggest that Pip5k1c expression in chondrocytes plays a critical role in maintaining articular cartilage homeostasis and protecting against age-related OA. |
| Keywords | |
| URL | [Source Record] |
| Indexed By | |
| Language | English
|
| SUSTech Authorship | First
; Corresponding
|
| WOS Research Area | Geriatrics & Gerontology
|
| WOS Subject | Geriatrics & Gerontology
|
| WOS Accession No | WOS:000849338700001
|
| Publisher | |
| Data Source | Web of Science
|
| Citation statistics |
Cited Times [WOS]:1
|
| Document Type | Journal Article |
| Identifier | http://kc.sustech.edu.cn/handle/2SGJ60CL/395964 |
| Department | Department of Biochemistry 南方科技大学医学院 |
| Affiliation | 1.Southern Univ Sci & Technol, Sch Med, Guangdong Prov Key Lab Cell Microenvironm & Dis R, Dept Biochem,Shenzhen Key Lab Cell Microenvironm, Shenzhen, Peoples R China 2.Guangzhou Univ Chinese Med, Shenzhen Hosp Futian, Shenzhen, Guangdong, Peoples R China 3.Rush Univ, Dept Orthoped Surg, Med Ctr, Chicago, IL 60612 USA 4.Chinese Acad Sci, Res Ctr Human Tissues & Organs Degenerat, Inst Adv Technol, Shenzhen, Peoples R China |
| First Author Affilication | Department of Biochemistry; School of Medicine |
| Corresponding Author Affilication | Department of Biochemistry; School of Medicine |
| First Author's First Affilication | Department of Biochemistry; School of Medicine |
| Recommended Citation GB/T 7714 |
Qu, Minghao,Chen, Mingjue,Gong, Weiyuan,et al. Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice[J]. Aging and Disease,2022.
|
| APA |
Qu, Minghao.,Chen, Mingjue.,Gong, Weiyuan.,Huo, Shaochuan.,Yan, Qinnan.,...&Xiao, Guozhi.(2022).Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice.Aging and Disease.
|
| MLA |
Qu, Minghao,et al."Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice".Aging and Disease (2022).
|
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