ArticleNature communications2021
SLPI is a critical mediator that controls PTH-induced bone formation.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Secretory Leukocyte Protease Inhibitor: A Pleiotropic Molecule for the Potential Diagnosis of and Therapy for Acute Kidney Injury.International journal of molecular sciences · 2025Review
- The RANK/RANKL axis controls vascular dynamics in the bone marrow.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Role ofBiomolecules · 2025Review
- Secretory leucocyte protease inhibitor regulates bone metabolism and inflammation in experimental mouse periodontitis.Communications biology · 2025Article
- Optical histopathology based on the nonlabeling analysis with multiphoton excitation imaging.Pathology international · 2025Review
- METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.Cell death discovery · 2024Article
- Review
- Secretory leukocyte protease inhibitor protects against severe urinary tract infection in mice.mBio · 2024Article
- Review
- Recombinant human secretory leukocyte protease inhibitor (rhSLPI) coated titanium enhanced human osteoblast adhesion and differentiation.Scientific reports · 2023Article
- Secretory Leukocyte Protease Inhibitor Protects Against Severe Urinary Tract Infection in Mice.bioRxiv : the preprint server for biology · 2023Article
- Screening of immune-related secretory proteins linking chronic kidney disease with calcific aortic valve disease based on comprehensive bioinformatics analysis and machine learning.Journal of translational medicine · 2023Article
- Distinct fibroblast progenitor subpopulation expedites regenerative mucosal healing by immunomodulation.The Journal of experimental medicine · 2023Article
- Connection between Osteoarthritis and Nitric Oxide: From Pathophysiology to Therapeutic Target.Molecules (Basel, Switzerland) · 2023Review
- Identification of the key immune-related genes and immune cell infiltration changes in renal interstitial fibrosis.Frontiers in endocrinology · 2023Article
- Bone Strength of the Calcaneus Is Associated with Dietary Calcium Intake in Older Japanese Men, but Not Women.Nutrients · 2022Article
- Effect of secretory leucocyte protease inhibitor on early tendon-to-bone healing after anterior cruciate ligament reconstruction in a rat model.Bone & joint research · 2022Article
- Determination of the physiological range of oxygen tension in bone marrow monocytes using two-photon phosphorescence lifetime imaging microscopy.Scientific reports · 2022Article
- Multiphoton intravital microscopy of rodents.Nature reviews. Methods primers · 2022Article
- Osteoclasts adapt to physioxia perturbation through DNA demethylation.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclastic bone resorption and osteoblastic bone formation/replenishment are closely coupled in bone metabolism. Anabolic parathyroid hormone (PTH), which is commonly used for treating osteoporosis, shifts the balance from osteoclastic to osteoblastic, although it is unclear how these cells are coordinately regulated by PTH. Here, we identify a serine protease inhibitor, secretory leukocyte protease inhibitor (SLPI), as a critical mediator that is involved in the PTH-mediated shift to the osteoblastic phase. Slpi is highly upregulated in osteoblasts by PTH, while genetic ablation of Slpi severely impairs PTH-induced bone formation. Slpi induction in osteoblasts enhances its differentiation, and increases osteoblast-osteoclast contact, thereby suppressing osteoclastic function. Intravital bone imaging reveals that the PTH-mediated association between osteoblasts and osteoclasts is disrupted in the absence of SLPI. Collectively, these results demonstrate that SLPI regulates the communication between osteoblasts and osteoclasts to promote PTH-induced bone anabolism.
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