Specific Deletion of β-Catenin in <i>Col2</i>-Expressing Cells Leads to Defects in Epiphyseal Bone

Wang, Tingyu; Li, Jun; Zhou, Guang Qian; Ma, Peter; Zhao, Yue; Wang, Baoli; Chen, Di

doi:10.7150/ijbs.23000

Cited by 6 publications

(6 citation statements)

References 26 publications

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“…Tibiae were harvested and fixed in 10% neutral‐buffered formalin for 3 days and decalcified for 14 days in 14% EDTA and then paraffin‐embedded. Three‐micrometer sections were cut and alcian blue/H&E orange G staining and tartrate‐resistant acid phosphatase (TRAP) staining were performed (Shu et al, ; B. Wang et al, ; Wang et al, ).…”

Section: Methodsmentioning

confidence: 99%

CHIP regulates skeletal development and postnatal bone growth

Wang

et al. 2020

Journal Cellular Physiology

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C terminus of Hsc70‐interacting protein (CHIP) is a chaperone‐dependent and U‐box containing E3 ubiquitin ligase. In previous studies, we found that CHIP regulates the stability of multiple tumor necrosis factor receptor‐associated factor proteins in bone cells. In Chip global knockout (KO) mice, nuclear factor‐κB signaling is activated, osteoclast formation is increased, osteoblast differentiation is inhibited, and bone mass is decreased in postnatal Chip KO mice. To determine the role of Chip in different cell types at different developmental stages, we created Chipflox/flox mice. We then generated Chip conditional KO mice ChipCMV and ChipOsxER and demonstrated defects in skeletal development and postnatal bone growth in Chip conditional KO mice. Our findings indicate that Chip conditional KO mice could serve as a critical reagent for further investigations of functions of CHIP in bone cells and in other cell types.

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Section: Methodsmentioning

confidence: 99%

CHIP regulates skeletal development and postnatal bone growth

Wang

et al. 2020

Journal Cellular Physiology

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“…Wnt signaling plays critical role in regulating MSC fate. Activation of Wnt signaling stimulates myogenesis and inhibits adipogenesis . It has been reported that Wnt signaling promotes the differentiation of adipose progenitor cells into fibroblastic cells rather than adipocytes .…”

Section: Wnt Signaling In Aging Adipose Tissuementioning

confidence: 99%

“…Activation of Wnt signaling stimulates myogenesis and inhibits adipogenesis. [149][150][151][152] It has been reported that Wnt signaling promotes the differentiation of adipose progenitor cells into fibroblastic cells rather than adipocytes. 138 Leptin is synthesized by mature adipocytes in response to changes in body fat mass and nutritional status.…”

Section: Wnt Signaling In Aging Adipose Tissuementioning

confidence: 99%

Wnt signaling in bone, kidney, intestine, and adipose tissue and interorgan interaction in aging

Chen

Xie

Shu

et al. 2018

Annals of the New York Academy of Sciences

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Over the last two decades, it has become increasingly apparent that Wnt signaling plays a critical role in development and adult tissue homeostasis in multiple organs and in the pathogenesis of many diseases. In particular, a crucial role for Wnt signaling in bone development and bone tissue homeostasis has been well recognized. Numerous genome-wide association studies confirmed the importance of Wnt signaling in controlling bone mass. Moreover, ample evidence suggests that Wnt signaling is essential for kidney, intestine, and adipose tissue development and homeostasis. Recent emerging evidence demonstrates that Wnt signaling may play a fundamental role in the aging process of those organs. New discoveries show that bone is not only the major reservoir for calcium and phosphate storage, but also the largest organ with multiple functions, including mineral and energy metabolism. The interactions among bone, kidney, intestine, and adipose tissue are controlled and regulated by several endocrine signals, including FGF23, klotho, sclerostin, osteocalcin, vitamin D, and leptin. Since the aging process is characterized by structural and functional decline in almost all tissues and organs, understanding the Wnt signaling-related interactions among bone, kidney, intestine, and adipose tissue in aging may shed light on the pathogenesis of age-related diseases.

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“… 30 Furthermore, Col2‐specific knockout of β‐catenin led to bone destruction in knee joint area, large numbers of osteoclasts and adipocytes were accumulated in the area underneath of growth plate. 31 In a study using Col2a1‐Wnt16 and Col2a1‐Cre;Wnt16 fl/fl mice as well as 3D chondrocyte pellet culture with technology of adenovirus Wnt16 manipulation, Tong and colleagues reveal that Wnt16 inhibit chondrocyte hypertrophy via activating PCP/JNK and cross‐talking with mTORC1‐PTHrP pathway. 32 Chen et al demonstrated that cyclin D1 stimulated proliferation and apoptosis of the chondrocyte through increasing the expression of Wnt3/β‐catenin rather than Wnt10a/β‐catenin signalling pathway.…”

Section: β‐Catenin Signalling In Oa Cartilagementioning

confidence: 99%

Signalling interaction between β‐catenin and other signalling molecules during osteoarthritis development

Feng,

Zhang,

et al. 2024

Cell Proliferation

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Osteoarthritis (OA) is the most prevalent disorder of synovial joint affecting multiple joints. In the past decade, we have witnessed conceptual switch of OA pathogenesis from a ‘wear and tear’ disease to a disease affecting entire joint. Extensive studies have been conducted to understand the underlying mechanisms of OA using genetic mouse models and ex vivo joint tissues derived from individuals with OA. These studies revealed that multiple signalling pathways are involved in OA development, including the canonical Wnt/β‐catenin signalling and its interaction with other signalling pathways, such as transforming growth factor β (TGF‐β), bone morphogenic protein (BMP), Indian Hedgehog (Ihh), nuclear factor κB (NF‐κB), fibroblast growth factor (FGF), and Notch. The identification of signalling interaction and underlying mechanisms are currently underway and the specific molecule(s) and key signalling pathway(s) playing a decisive role in OA development need to be evaluated. This review will focus on recent progresses in understanding of the critical role of Wnt/β‐catenin signalling in OA pathogenesis and interaction of β‐catenin with other pathways, such as TGF‐β, BMP, Notch, Ihh, NF‐κB, and FGF. Understanding of these novel insights into the interaction of β‐catenin with other pathways and its integration into a complex gene regulatory network during OA development will help us identify the key signalling pathway of OA pathogenesis leading to the discovery of novel therapeutic strategies for OA intervention.

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Specific Deletion of β-Catenin in Col2-Expressing Cells Leads to Defects in Epiphyseal Bone

Cited by 6 publications

References 26 publications

CHIP regulates skeletal development and postnatal bone growth

CHIP regulates skeletal development and postnatal bone growth

Wnt signaling in bone, kidney, intestine, and adipose tissue and interorgan interaction in aging

Signalling interaction between β‐catenin and other signalling molecules during osteoarthritis development

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