ArticleBone research2023
α-parvin controls chondrocyte column formation and regulates long bone development.
Article in Bone research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Palmitic Acid Inhibits the Proliferation and Hypertrophy of Antler Chondrocytes by Disrupting Mitochondria-Associated Endoplasmic Reticulum Membrane Function.Antioxidants (Basel, Switzerland) · 2026Article
- Transcriptome Analysis of Differentially Expressed Genes and Molecular Pathways Involved During Osteoclast Differentiation.Molecular biotechnology · 2026Article
- Single-cell technologies drive mechanistic insights and therapeutic translation in skeletal system research.iScience · 2026Review
- Effects of nutritional low phosphorus status caused by extremely low phosphorus diet during lactation and early childhood on endochondral ossification in offspring rats.Frontiers in nutrition · 2026Article
- Parvin is essential for indirect flight muscle (IFM) performance and Zasp52 localisation to the Z-disc in Drosophila melanogaster.Cell and tissue research · 2025Article
- Primary cilia in growth plates orchestrate long bone development.Fundamental research · 2025Article
- Fibroblasts as a ruler of the immune microenvironment: measurement and modulation in tissue homeostasis and disease.Frontiers in immunology · 2025Review
- Article
- N-cadherin and β1 integrin coordinately regulate growth plate cartilage architecture.Molecular biology of the cell · 2024Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endochondral ossification requires proper control of chondrocyte proliferation, differentiation, survival, and organization. Here we show that knockout of α-parvin, an integrin-associated focal adhesion protein, from murine limbs causes defects in endochondral ossification and dwarfism. The mutant long bones were shorter but wider, and the growth plates became disorganized, especially in the proliferative zone. With two-photon time-lapse imaging of bone explant culture, we provide direct evidence showing that α-parvin regulates chondrocyte rotation, a process essential for chondrocytes to form columnar structure. Furthermore, loss of α-parvin increased binucleation, elevated cell death, and caused dilation of the resting zones of mature growth plates. Single-cell RNA-seq analyses revealed alterations of transcriptome in all three zones (i.e., resting, proliferative, and hypertrophic zones) of the growth plates. Our results demonstrate a crucial role of α-parvin in long bone development and shed light on the cellular mechanism through which α-parvin regulates the longitudinal growth of long bones.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.