ArticleBone research2020
LIM domain proteins Pinch1/2 regulate chondrogenesis and bone mass in mice.
Article in Bone research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- LIMS2 downregulation is associated with tumor progression and immune landscape alterations in lung adenocarcinoma.Discover oncology · 2026Article
- The vinculin-β-catenin axis promotes bone formation and repair: an essential prerequisite for the anti-osteoporotic efficacy of sclerostin-neutralizing antibody.Science China. Life sciences · 2026Article
- Extracellular Vesicle-Mediated Nucleolin Transfer in Glioblastoma: A Targetable Axis Driving Blood-Tumour Barrier Formation.Journal of extracellular vesicles · 2026Article
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- Osteocytic vinculin controls bone mass by modulating Mef2c-driven sclerostin expression in mice.Bone research · 2025Article
- Bone-derived factors mediate crosstalk between skeletal and extra-skeletal organs.Bone research · 2025Review
- Targeting Piezo1 channel to alleviate intervertebral disc degeneration.Journal of orthopaedic translation · 2025Article
- Development of dual aptamers-functionalized c-MET PROTAC degraders for targeted therapy of osteosarcoma.Theranostics · 2025Article
- Pip5k1γ promotes anabolism of nucleus pulposus cells and intervertebral disc homeostasis by activating CaMKII-Ampk pathway in aged mice.Aging cell · 2024Article
- Targeting miR-29 mitigates skeletal senescence and bolsters therapeutic potential of mesenchymal stromal cells.Cell reports. Medicine · 2024Article
- Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024Review
- Gut microbial metabolite targets HDAC3-FOXK1-interferon axis in fibroblast-like synoviocytes to ameliorate rheumatoid arthritis.Bone research · 2024Article
- Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes.Journal of orthopaedic surgery and research · 2024Article
- The bone-liver interaction modulates immune and hematopoietic function through Pinch-Cxcl12-Mbl2 pathway.Cell death and differentiation · 2024Article
- Targeting Kindlin-2 in adipocytes increases bone mass through inhibiting FAS/PPARActa pharmaceutica Sinica. B · 2023Article
- Talin-1 inhibits Smurf1-mediated Stat3 degradation to modulate β-cell proliferation and mass in mice.Cell death & disease · 2023Article
- Loss of Pinch Proteins Causes Severe Degenerative Disc Disease-Like Lesions in Mice.Aging and disease · 2023Article
- Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice.Aging and disease · 2023Article
- A Simplified and Effective Approach for the Isolation of Small Pluripotent Stem Cells Derived from Human Peripheral Blood.Biomedicines · 2023Article
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The LIM domain-containing proteins Pinch1/2 regulate integrin activation and cell-extracellular matrix interaction and adhesion. Here, we report that deleting Pinch1 in limb mesenchymal stem cells (MSCs) and Pinch2 globally (double knockout; dKO) in mice causes severe chondrodysplasia, while single mutant mice do not display marked defects. Pinch deletion decreases chondrocyte proliferation, accelerates cell differentiation and disrupts column formation. Pinch loss drastically reduces Smad2/3 protein expression in proliferative zone (PZ) chondrocytes and increases Runx2 and Col10a1 expression in both PZ and hypertrophic zone (HZ) chondrocytes. Pinch loss increases sclerostin and Rankl expression in HZ chondrocytes, reduces bone formation, and increases bone resorption, leading to low bone mass. In vitro studies revealed that Pinch1 and Smad2/3 colocalize in the nuclei of chondrocytes. Through its C-terminal region, Pinch1 interacts with Smad2/3 proteins. Pinch loss increases Smad2/3 ubiquitination and degradation in primary bone marrow stromal cells (BMSCs). Pinch loss reduces TGF-β-induced Smad2/3 phosphorylation and nuclear localization in primary BMSCs. Interestingly, compared to those from single mutant mice, BMSCs from dKO mice express dramatically lower protein levels of β-catenin and Yap1/Taz and display reduced osteogenic but increased adipogenic differentiation capacity. Finally, ablating Pinch1 in chondrocytes and Pinch2 globally causes severe osteopenia with subtle limb shortening. Collectively, our findings demonstrate critical roles for Pinch1/2 and a functional redundancy of both factors in the control of chondrogenesis and bone mass through distinct mechanisms.
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