ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2011
Runx2 contributes to murine Col10a1 gene regulation through direct interaction with its cis-enhancer.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 73 citations in OpenAlex.
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- New Insights on the Therapeutic Potential of Runt-Related Transcription Factor 2 for Osteoarthritis: Evidence from Mendelian Randomization.Rheumatology and therapy · 2024Article
- A synthetic, closed-looped gene circuit for the autonomous regulation of RUNX2 activity during chondrogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
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- Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice.Aging and disease · 2023Article
- Emerging RUNX2-Mediated Gene Regulatory Mechanisms Consisting of Multi-Layered Regulatory Networks in Skeletal Development.International journal of molecular sciences · 2023Review
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Mef2a is a positive regulator ofAmerican journal of translational research · 2023Article
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- Runx2 regulates chromatin accessibility to direct the osteoblast program at neonatal stages.Cell reports · 2022Article
- Kindlin-2 preserves integrity of the articular cartilage to protect against osteoarthritis.Nature aging · 2022Article
- Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint.Journal of cellular and molecular medicine · 2021Review
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- Expression Profiling and Functional Analysis of CandidateFrontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
We have recently shown that a 150-bp Col10a1 distal promoter (-4296 to -4147 bp) is sufficient to direct hypertrophic chondrocyte-specific reporter (LacZ) expression in vivo. More recently, through detailed sequence analysis we identified two putative tandem-repeat Runx2 binding sites within the 3'-end of this 150-bp region (TGTGGG-TGTGGC, -4187 to -4176 bp). Candidate electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation, and transfection studies demonstrate that these putative Runx2 sites bind Runx2 and mediate upregulated Col10a1/reporter activity in vitro. Transgenic studies using the 5'-sequence without Runx2 sites were not able to drive the cell-specific LacZ reporter activity, suggesting the in vivo requirement of the Runx2 sites located in the 3'-end in mediating Col10a1/reporter expression. Indeed, mutating the Runx2 sites in the context of the 150-bp promoter abolishes its capacity to drive hypertrophic chondrocyte-specific reporter expression in transgenic mice. We have also generated multiple transgenic mouse lines using only the 3'-sequence containing the Runx2 sites to drive the LacZ gene. Interestingly, no hypertrophic chondrocyte-specific blue staining was observed in these transgenic mice. Together, our data support that Runx2 directly interacts with murine Col10a1 cis-enhancer. This interaction is required but not sufficient for cell-specific Col10a1 promoter activity in vivo. Additional cooperative/repressive elements within the 5'- or 3'-sequences of this 150-bp promoter are needed to work with Runx2 together to mediate cell-specific Col10a1 expression. Further delineation of these elements/factors has the potential to identify novel therapeutic targets for multiple skeletal disorders, including osteoarthritis, that show abnormal Col10a1 expression and altered chondrocyte maturation.
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