ArticleThe Journal of biological chemistry2010
Microfibril-associated glycoprotein-1, an extracellular matrix regulator of bone remodeling.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Article
- Identification of food deprivation in salmonids using gill biomarkers.Conservation physiology · 2025Article
- Calcification of the elastic component: the impact on the cardiovascular system.Frontiers in cardiovascular medicine · 2025Review
- Microfibril-associated protein 2 interacts with LEF1/TCF7 and immune infiltration in uterine corpus endometrial carcinoma.Central-European journal of immunology · 2025Article
- The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.Cell research · 2024Review
- Multi-organ phenotypes in mice lacking latent TGFβ binding protein 2 (LTBP2).Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- Association between inflammatory bowel disease and osteoporosis in European and East Asian populations: exploring causality, mediation by nutritional status, and shared genetic architecture.Frontiers in immunology · 2024Article
- Review
- The role of microfibrillar-associated protein 2 in cancer.Frontiers in oncology · 2022Review
- Decreased Levels of Microfibril-Associated Glycoprotein (MAGP)-1 in Patients with Colon Cancer and Obesity Are Associated with Changes in Extracellular Matrix Remodelling.International journal of molecular sciences · 2021Article
- Identification of the growth factor-binding sequence in the extracellular matrix protein MAGP-1.The Journal of biological chemistry · 2020Article
- Fibrillin microfibrils and elastic fibre proteins: Functional interactions and extracellular regulation of growth factors.Seminars in cell & developmental biology · 2019Review
- Microfibril-associated glycoproteins MAGP-1 and MAGP-2 in disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Contribution of metabolic disease to bone fragility in MAGP1-deficient mice.Matrix biology : journal of the International Society for Matrix Biology · 2018Article
- Characterization of metabolic health in mouse models of fibrillin-1 perturbation.Matrix biology : journal of the International Society for Matrix Biology · 2016Article
- Differential regulation and synthetic lethality of exclusive RB1 and CDKN2A mutations in lung cancer.International journal of oncology · 2016Article
- Marrow Adipose Tissue Expansion Coincides with Insulin Resistance in MAGP1-Deficient Mice.Frontiers in endocrinology · 2016Article
- The microfibril-associated glycoproteins (MAGPs) and the microfibrillar niche.Matrix biology : journal of the International Society for Matrix Biology · 2015Review
- An insulin-sensitizing thiazolidinedione, which minimally activates PPARγ, does not cause bone loss.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
MAGP1 is an extracellular matrix protein that, in vertebrates, is a ubiquitous component of fibrillin-rich microfibrils. We previously reported that aged MAGP1-deficient mice (MAGP1Delta) develop lesions that are the consequence of spontaneous bone fracture. We now present a more defined bone phenotype found in MAGP1Delta mice. A longitudinal DEXA study demonstrated age-associated osteopenia in MAGP1Delta animals and muCT confirmed reduced bone mineral density in the trabecular and cortical bone. Further, MAGP1Delta mice have significantly less trabecular bone, the trabecular microarchitecture is more fragmented, and the diaphyseal cross-sectional area is significantly reduced. The remodeling defect seen in MAGP1Delta mice is likely not due to an osteoblast defect, because MAGP1Delta bone marrow stromal cells undergo osteoblastogenesis and form mineralized nodules. In vivo, MAGP1Delta mice exhibit normal osteoblast number, mineralized bone surface, and bone formation rate. Instead, our findings suggest increased bone resorption is responsible for the osteopenia. The number of osteoclasts derived from MAGP1Delta bone marrow macrophage cells is increased relative to the wild type, and osteoclast differentiation markers are expressed at earlier time points in MAGP1Delta cells. In vivo, MAGP1Delta mice have more osteoclasts lining the bone surface. RANKL (receptor activator of NF-kappaB ligand) expression is significantly higher in MAGP1Delta bone, and likely contributes to enhanced osteoclastogenesis. However, bone marrow macrophage cells from MAGP1Delta mice show a higher propensity than do wild-type cells to differentiate to osteoclasts in response to RANKL, suggesting that they are also primed to respond to osteoclast-promoting signals. Together, our findings suggest that MAGP1 is a regulator of bone remodeling, and its absence results in osteopenia associated with an increase in osteoclast number.
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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.