ArticleProceedings of the National Academy of Sciences of the United States of America2010
Alternate protein kinase A activity identifies a unique population of stromal cells in adult bone.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Guidelines on reporting epidemiological observational studies and their proper use in endocrine research.Hormones (Athens, Greece) · 2026Article
- Fibrous dysplasia in a patient with Carney complex.Hormones (Athens, Greece) · 2026Review
- Protein kinase A is a dependent factor and therapeutic target in mouse models of fibrous dysplasia.Nature communications · 2025Article
- Article
- Germline and Mosaic Variants in PRKACA and PRKACB Cause a Multiple Congenital Malformation Syndrome.American journal of human genetics · 2020Article
- PRKACB variants in skeletal disease or adrenocortical hyperplasia: effects on protein kinase A.Endocrine-related cancer · 2020Article
- Prkar1a haploinsufficiency ameliorates the growth hormone excess phenotype in Aip-deficient mice.Human molecular genetics · 2020Article
- Celecoxib treatment of fibrous dysplasia (FD) in a human FD cell line and FD-like lesions in mice with protein kinase A (PKA) defects.Molecular and cellular endocrinology · 2017Article
- Prkar1a gene knockout in the pancreas leads to neuroendocrine tumorigenesis.Endocrine-related cancer · 2017Article
- Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia.Endocrine-related cancer · 2016Article
- MEN1, MEN4, and Carney Complex: Pathology and Molecular Genetics.Neuroendocrinology · 2016Review
- Haploinsufficiency for either one of the type-II regulatory subunits of protein kinase A improves the bone phenotype of Prkar1a+/- mice.Human molecular genetics · 2015Article
- Review
- Germline PRKACA amplification causes variable phenotypes that may depend on the extent of the genomic defect: molecular mechanisms and clinical presentations.European journal of endocrinology · 2015Article
- Osteoblast-specific expression of the fibrous dysplasia (FD)-causing mutation Gsα(R201C) produces a high bone mass phenotype but does not reproduce FD in the mouse.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- DNAJB1-PRKACA is specific for fibrolamellar carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015Article
- Constitutive expression of Gsα(R201C) in mice produces a heritable, direct replica of human fibrous dysplasia bone pathology and demonstrates its natural history.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
- E pluribus unum? The main protein kinase A catalytic subunit (PRKACA), a likely oncogene, and cortisol-producing tumors.The Journal of clinical endocrinology and metabolism · 2014Article
- Clinical and molecular genetics of the phosphodiesterases (PDEs).Endocrine reviews · 2014Review
- Knockdown of PRKAR1A, the gene responsible for Carney complex, interferes with differentiation in osteoblastic cells.Molecular endocrinology (Baltimore, Md.) · 2014Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
Abstract
A population of stromal cells that retains osteogenic capacity in adult bone (adult bone stromal cells or aBSCs) exists and is under intense investigation. Mice heterozygous for a null allele of prkar1a (Prkar1a(+/-)), the primary receptor for cyclic adenosine monophosphate (cAMP) and regulator of protein kinase A (PKA) activity, developed bone lesions that were derived from cAMP-responsive osteogenic cells and resembled fibrous dysplasia (FD). Prkar1a(+/-) mice were crossed with mice that were heterozygous for catalytic subunit Calpha (Prkaca(+/-)), the main PKA activity-mediating molecule, to generate a mouse model with double heterozygosity for prkar1a and prkaca (Prkar1a(+/-)Prkaca(+/-)). Unexpectedly, Prkar1a(+/-)Prkaca(+/-) mice developed a greater number of osseous lesions starting at 3 months of age that varied from the rare chondromas in the long bones and the ubiquitous osteochondrodysplasia of vertebral bodies to the occasional sarcoma in older animals. Cells from these lesions originated from an area proximal to the growth plate, expressed osteogenic cell markers, and showed higher PKA activity that was mostly type II (PKA-II) mediated by an alternate pattern of catalytic subunit expression. Gene expression profiling confirmed a preosteoblastic nature for these cells but also showed a signature that was indicative of mesenchymal-to-epithelial transition and increased Wnt signaling. These studies show that a specific subpopulation of aBSCs can be stimulated in adult bone by alternate PKA and catalytic subunit activity; abnormal proliferation of these cells leads to skeletal lesions that have similarities to human FD and bone tumors.
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