ArticleScientific reports2022
Hyaluronidase 1 deficiency decreases bone mineral density in mice.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Genomic dissection of hoof and leg conformation in Swiss dairy cattle populations reveals polygenic architecture and a recessive HYAL1 nonsense variant affecting longevity in Holstein cattle.Genetics, selection, evolution : GSE · 2026Article
- Thiolated Hyaluronic Acid: A Gateway for Targeted Killing of Staphylococcus aureus on the Race for Surface Colonization.Advanced healthcare materials · 2026Article
- Genetic Deficiencies of Hyaluronan Degradation.Cells · 2024Review
- Mechanobiology of Hyaluronan: Connecting Biomechanics and Bioactivity in Musculoskeletal Tissues.Annual review of biomedical engineering · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mucopolysaccharidosis IX is a lysosomal storage disorder caused by a deficiency in HYAL1, an enzyme that degrades hyaluronic acid at acidic pH. This disease causes juvenile arthritis in humans and osteoarthritis in the Hyal1 knockout mouse model. Our past research revealed that HYAL1 is strikingly upregulated (~ 25x) upon differentiation of bone marrow monocytes into osteoclasts. To investigate whether HYAL1 is involved in the differentiation and/or resorption activity of osteoclasts, and in bone remodeling in general, we analyzed several bone parameters in Hyal1 -/- mice and studied the differentiation and activity of their osteoclasts and osteoblasts when differentiated in vitro. These experiments revealed that, upon aging, HYAL1 deficient mice exhibit reduced femur length and a ~ 15% decrease in bone mineral density compared to wild-type mice. We found elevated osteoclast numbers in the femurs of these mice as well as an increase of the bone resorbing activity of Hyal1 -/- osteoclasts. Moreover, we detected decreased mineralization by Hyal1 -/- osteoblasts. Taken together with the observed accumulation of hyaluronic acid in Hyal1 -/- bones, these results support the premise that the catabolism of hyaluronic acid by osteoclasts and osteoblasts is an intrinsic part of bone remodeling.
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