ArticleThe Journal of biological chemistry2015
WNT1-induced Secreted Protein-1 (WISP1), a Novel Regulator of Bone Turnover and Wnt Signaling.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Multi-ancestry genome-wide association analyses identify novel genetic mechanisms in rheumatoid arthritis.Nature genetics · 2022Pooled it
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- The WISP1/Src/MIF Axis Promotes the Malignant Phenotype of Non-Invasive MCF7 Breast Cancer Cells.Cells · 2026Article
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- A glucocorticoid spike derails muscle repair to heterotopic ossification after spinal cord injury.Cell reports. Medicine · 2024Article
- Repurposing Niclosamide to Modulate Renal RNA-Binding Protein HuR for the Treatment of Diabetic Nephropathy in db/db Mice.International journal of molecular sciences · 2024Article
- Sclerostin blockade inhibits bone resorption through PDGF receptor signaling in osteoblast lineage cells.JCI insight · 2024Article
- Osteoarthritis versus psoriasis arthritis: Physiopathology, cellular signaling, and therapeutic strategies.Genes & diseases · 2024Review
- Breast cancer remotely imposes a myeloid bias on haematopoietic stem cells by reprogramming the bone marrow niche.Nature cell biology · 2023Article
- Significance of CCNs in liver regeneration.Journal of cell communication and signaling · 2023Review
- Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023Review
- The regulation and functions of the matricellular CCN proteins induced by shear stress.Journal of cell communication and signaling · 2023Review
- HuR-dependent expression of Wisp1 is necessary for TGFβ-induced cardiac myofibroblast activity.Journal of molecular and cellular cardiology · 2023Article
- Analysis of CCN4/WISP1 Effects on Joint Tissues Using Gain- and Loss-of-Function Approaches.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Evaluation of the Effects of CCN4 on Pancreatic Beta Cell Proliferation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- A morphological study of adipose-derived stem cell sheets created with temperature-responsive culture dishes using scanning electron microscopy.Medical molecular morphology · 2022Article
- Fibroblast Growth Factors and Cellular Communication Network Factors: Intimate Interplay by the Founding Members in Cartilage.International journal of molecular sciences · 2022Review
- Contribution to the 3R Principle: Description of a Specimen-Specific Finite Element Model Simulating 3-Point-Bending Tests in Mouse Tibiae.Bioengineering (Basel, Switzerland) · 2022Article
- The Roles of Long-Term Hyperhomocysteinemia and Micronutrient Supplementation in theFrontiers in aging neuroscience · 2022Article
- Intermittent Hypoxic Therapy Inhibits Allogenic Bone-Graft Resorption by Inhibition of Osteoclastogenesis in a Mouse Model.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
WISP1/CCN4 (hereafter referred to as WISP1), a member of the CCN family, is found in mineralized tissues and is produced by osteoblasts and their precursors. In this study, Wisp1-deficient (Wisp1(-/-)) mice were generated. Using dual-energy x-ray absorptiometry, we showed that by 3 months, the total bone mineral density of Wisp1(-/-) mice was significantly lower than that of WT mice. Further investigation by micro-computed tomography showed that female Wisp1(-/-) mice had decreased trabecular bone volume/total volume and that both male and female Wisp1(-/-) mice had decreased cortical bone thickness accompanied by diminished biomechanical strength. The molecular basis for decreased bone mass in Wisp1(-/-) mice arises from reduced bone formation likely caused by osteogenic progenitors that differentiate poorly compared with WT cells. Osteoclast precursors from Wisp1(-/-) mice developed more tartrate-resistant acid phosphatase-positive cells in vitro and in transplants, suggesting that WISP1 is also a negative regulator of osteoclast differentiation. When bone turnover (formation and resorption) was induced by ovariectomy, Wisp1(-/-) mice had lower bone mineral density compared WT mice, confirming the potential for multiple roles for WISP1 in controlling bone homeostasis. Wisp1(-/-) bone marrow stromal cells had reduced expression of β-catenin and its target genes, potentially caused by WISP1 inhibition of SOST binding to LRP6. Taken together, our data suggest that the decreased bone mass found in Wisp1(-/-) mice could potentially be caused by an insufficiency in the osteodifferentiation capacity of bone marrow stromal cells arising from diminished Wnt signaling, ultimately leading to altered bone turnover and weaker biomechanically compromised 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.