Genetic Rescue of Chondrodysplasia and the Perinatal Lethal Effect of Cartilage Link Protein Deficiency
Open accessAbstract
The targeted disruption of cartilage link protein gene (Crtl1) in homozygous mice resulted in a severe chondrodysplasia and perinatal lethality. This raised the question of whether the abnormalities seen in Crtl1 null mice are all caused by the absence of link protein in cartilage or whether the deficiency of the protein in other tissues and organs contributed to the phenotype. To address this question we have generated transgenic mice overexpressing cartilage link protein under the control of a cartilage-specific promoter, and then these transgenic mice were used for a genetic rescue of abnormalities in Crtl1 null mice. While the overexpression of cartilage link protein resulted in no abnormal phenotype, the cartilage-specific transgene expression of link protein could completely prevent the perinatal mortality of link protein-deficient mice and, depending on the level of the link protein expression, rescue skeletal abnormalities. Although link protein was originally isolated from cartilage, we found and determined Crtl1 transcripts and corresponding proteins in every organ tested from mouse embryos to aging animals. We also identified three additional members of the link protein family, all co-localized with hyaluronic acid-binding proteoglycans in the mouse genome. The ubiquitous presence of link protein suggests a general and systemic function of link protein in the organization of extracellular matrix in a number of tissues, possibly interacting with other proteoglycans, such as versican, brevican, and neurocan.
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HAPLN1−/− mice are link protein-deficient.
“link protein-deficient (HAPLN1−/−) mice”
From Aggrecan, link protein and tenascin-R are essential components of the perineuronal net to protect neurons against iron-induced oxidative stress (2014) · cites this paper as [56]
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Self-citationSánchez-Ventura, J., Lago, N., Penas, C., Navarro, X., & Udina, E. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25084267 · Cited by 1 · see citing works
Proteoglycans of the Central Nervous System
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Regulation of proteoglycan-specific immune responses in arthritis
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The roles of Beta1 integrin in cartilage development
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Self-citationHyaluronan and hyalectans: The good, the bad, and the ugly
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- Authors
- Czipri, M., Otto, J. M., Cs-Szabó, G., Kamath, R. V., Vermes, C., Firneisz, G., Kolman, K. J., Watanabe, H., Li, Y., Roughley, P. J., Yamada, Y., Olsen, B. R., & Glant, T. T.
- Affiliations
- Rush University Medical Center (US)
- Rush University (US)
- Aichi Medical University (JP)
- Harvard University (US)
- Shriners Hospitals for Children - Canada (CA)
- National Institutes of Health (US)
- Corresponding author
- Glant, Tibor T.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-10
- Volume
- 278
- Issue
- 40
- Pages
- 39214-39223
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2147041011
- Cited by
- 46
- References
- 63
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 1 · 2022: 4 · 2020: 2 · 2019: 2 · 2018: 2 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 2
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion)
- Funders
- Bladder Cancer Advocacy Network
- National Institutes of Health (1r21ar047135-01)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-47135, R01AR040310, AR 40310)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Connective tissue disorders research
- Keywords
- chondrodysplasia, perinatal lethality, genetic rescue, transgenic overexpression, extracellular matrix, versican, brevican, neurocan, skeletal abnormalities
- MeSH terms
- Proteoglycan Link Protein, Animals, Base Sequence, Cartilage, Cloning, Molecular, Exostoses, Multiple Hereditary, Genotype, Homozygote, Hyaluronic Acid, Mice, Inbred BALB C, Mice, Transgenic, Microscopy, Fluorescence, Models, Genetic, Molecular Sequence Data, Nerve Tissue Proteins, Phenotype, Promoter Regions, Genetic, Protein Binding, Proteins, Chondroitin Sulfate Proteoglycans, Proteoglycans, Tissue Distribution, Transcription, Genetic, Blotting, Northern, Blotting, Western, Extracellular Matrix Proteins, Transgenes, Reverse Transcriptase Polymerase Chain Reaction, Lectins, C-Type, Mice, Versicans, Neurocan, Brevican
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