Low-density lipoprotein receptor–related protein 5 governs Wnt-mediated osteoarthritic cartilage destruction
Introduction Wnt ligands bind to low-density lipoprotein receptor–related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice....
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| Published in | Arthritis research & therapy Vol. 16; no. 1; p. R37 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
31.01.2014
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1478-6362 1478-6354 1478-6362 |
| DOI | 10.1186/ar4466 |
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| Abstract | Introduction
Wnt ligands bind to low-density lipoprotein receptor–related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice.
Methods
The expression levels of LRP5, type II collagen, and catabolic factors were determined in mouse articular chondrocytes, human OA cartilage, and mouse experimental OA cartilage. Experimental OA in wild-type,
Lrp5
total knockout (
Lrp5
-/-
) and chondrocyte-specific knockout (
Lrp5
fl/fl
;
Col2a1-cre
) mice was caused by aging, destabilization of the medial meniscus (DMM), or intra-articular injection of collagenase. The role of LRP5 was confirmed
in vitro
by small interfering RNA–mediated knockdown of
Lrp5
or in
Lrp5
-/-
cells treated with IL-1β or Wnt proteins.
Results
IL-1β treatment increased the expression of LRP5 (but not LRP6) via JNK and NF-κB signaling. LRP5 was upregulated in human and mouse OA cartilage, and
Lrp5
deficiency in mice inhibited cartilage destruction. Treatment with IL-1β or Wnt decreased the level of
Col2a1
and increased those of
Mmp3
or
Mmp13
, whereas
Lrp5
knockdown ameliorated these effects. In addition, we found that the functions of LRP5 in arthritic cartilage were subject to transcriptional activation by β-catenin. Moreover,
Lrp5
-/-
and
Lrp5
fl/fl
;
Col2a1-cre
mice exhibited decreased cartilage destruction (and related changes in gene expression) in response to experimental OA.
Conclusions
Our findings indicate that LRP5 (but not LRP6) plays an essential role in Wnt/β-catenin-signaling-mediated OA cartilage destruction in part by regulating the expression levels of type II collagen, MMP3, and MMP13. |
|---|---|
| AbstractList | Introduction
Wnt ligands bind to low-density lipoprotein receptor–related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice.
Methods
The expression levels of LRP5, type II collagen, and catabolic factors were determined in mouse articular chondrocytes, human OA cartilage, and mouse experimental OA cartilage. Experimental OA in wild-type,
Lrp5
total knockout (
Lrp5
-/-
) and chondrocyte-specific knockout (
Lrp5
fl/fl
;
Col2a1-cre
) mice was caused by aging, destabilization of the medial meniscus (DMM), or intra-articular injection of collagenase. The role of LRP5 was confirmed
in vitro
by small interfering RNA–mediated knockdown of
Lrp5
or in
Lrp5
-/-
cells treated with IL-1β or Wnt proteins.
Results
IL-1β treatment increased the expression of LRP5 (but not LRP6) via JNK and NF-κB signaling. LRP5 was upregulated in human and mouse OA cartilage, and
Lrp5
deficiency in mice inhibited cartilage destruction. Treatment with IL-1β or Wnt decreased the level of
Col2a1
and increased those of
Mmp3
or
Mmp13
, whereas
Lrp5
knockdown ameliorated these effects. In addition, we found that the functions of LRP5 in arthritic cartilage were subject to transcriptional activation by β-catenin. Moreover,
Lrp5
-/-
and
Lrp5
fl/fl
;
Col2a1-cre
mice exhibited decreased cartilage destruction (and related changes in gene expression) in response to experimental OA.
Conclusions
Our findings indicate that LRP5 (but not LRP6) plays an essential role in Wnt/β-catenin-signaling-mediated OA cartilage destruction in part by regulating the expression levels of type II collagen, MMP3, and MMP13. Wnt ligands bind to low-density lipoprotein receptor-related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice.INTRODUCTIONWnt ligands bind to low-density lipoprotein receptor-related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice.The expression levels of LRP5, type II collagen, and catabolic factors were determined in mouse articular chondrocytes, human OA cartilage, and mouse experimental OA cartilage. Experimental OA in wild-type, Lrp5 total knockout (Lrp5⁻/⁻) and chondrocyte-specific knockout (Lrp5fl/fl;Col2a1-cre) mice was caused by aging, destabilization of the medial meniscus (DMM), or intra-articular injection of collagenase. The role of LRP5 was confirmed in vitro by small interfering RNA-mediated knockdown of Lrp5 or in Lrp5⁻/⁻ cells treated with IL-1β or Wnt proteins.METHODSThe expression levels of LRP5, type II collagen, and catabolic factors were determined in mouse articular chondrocytes, human OA cartilage, and mouse experimental OA cartilage. Experimental OA in wild-type, Lrp5 total knockout (Lrp5⁻/⁻) and chondrocyte-specific knockout (Lrp5fl/fl;Col2a1-cre) mice was caused by aging, destabilization of the medial meniscus (DMM), or intra-articular injection of collagenase. The role of LRP5 was confirmed in vitro by small interfering RNA-mediated knockdown of Lrp5 or in Lrp5⁻/⁻ cells treated with IL-1β or Wnt proteins.IL-1β treatment increased the expression of LRP5 (but not LRP6) via JNK and NF-κB signaling. LRP5 was upregulated in human and mouse OA cartilage, and Lrp5 deficiency in mice inhibited cartilage destruction. Treatment with IL-1β or Wnt decreased the level of Col2a1 and increased those of Mmp3 or Mmp13, whereas Lrp5 knockdown ameliorated these effects. In addition, we found that the functions of LRP5 in arthritic cartilage were subject to transcriptional activation by β-catenin. Moreover, Lrp5⁻/⁻ and Lrp5fl/fl;Col2a1-cre mice exhibited decreased cartilage destruction (and related changes in gene expression) in response to experimental OA.RESULTSIL-1β treatment increased the expression of LRP5 (but not LRP6) via JNK and NF-κB signaling. LRP5 was upregulated in human and mouse OA cartilage, and Lrp5 deficiency in mice inhibited cartilage destruction. Treatment with IL-1β or Wnt decreased the level of Col2a1 and increased those of Mmp3 or Mmp13, whereas Lrp5 knockdown ameliorated these effects. In addition, we found that the functions of LRP5 in arthritic cartilage were subject to transcriptional activation by β-catenin. Moreover, Lrp5⁻/⁻ and Lrp5fl/fl;Col2a1-cre mice exhibited decreased cartilage destruction (and related changes in gene expression) in response to experimental OA.Our findings indicate that LRP5 (but not LRP6) plays an essential role in Wnt/β-catenin-signaling-mediated OA cartilage destruction in part by regulating the expression levels of type II collagen, MMP3, and MMP13.CONCLUSIONSOur findings indicate that LRP5 (but not LRP6) plays an essential role in Wnt/β-catenin-signaling-mediated OA cartilage destruction in part by regulating the expression levels of type II collagen, MMP3, and MMP13. Wnt ligands bind to low-density lipoprotein receptor-related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling. Here we explored the roles of LRP5 in interleukin 1β (IL-1β)- or Wnt-mediated osteoarthritic (OA) cartilage destruction in mice. The expression levels of LRP5, type II collagen, and catabolic factors were determined in mouse articular chondrocytes, human OA cartilage, and mouse experimental OA cartilage. Experimental OA in wild-type, Lrp5 total knockout (Lrp5⁻/⁻) and chondrocyte-specific knockout (Lrp5fl/fl;Col2a1-cre) mice was caused by aging, destabilization of the medial meniscus (DMM), or intra-articular injection of collagenase. The role of LRP5 was confirmed in vitro by small interfering RNA-mediated knockdown of Lrp5 or in Lrp5⁻/⁻ cells treated with IL-1β or Wnt proteins. IL-1β treatment increased the expression of LRP5 (but not LRP6) via JNK and NF-κB signaling. LRP5 was upregulated in human and mouse OA cartilage, and Lrp5 deficiency in mice inhibited cartilage destruction. Treatment with IL-1β or Wnt decreased the level of Col2a1 and increased those of Mmp3 or Mmp13, whereas Lrp5 knockdown ameliorated these effects. In addition, we found that the functions of LRP5 in arthritic cartilage were subject to transcriptional activation by β-catenin. Moreover, Lrp5⁻/⁻ and Lrp5fl/fl;Col2a1-cre mice exhibited decreased cartilage destruction (and related changes in gene expression) in response to experimental OA. Our findings indicate that LRP5 (but not LRP6) plays an essential role in Wnt/β-catenin-signaling-mediated OA cartilage destruction in part by regulating the expression levels of type II collagen, MMP3, and MMP13. |
| ArticleNumber | R37 |
| Author | Kim, Kieun Kim, Suyeon Koh, Jeong-Tae Chun, Jang-Soo Shin, Youngnim Huh, Yun Hyun Ryu, Je-Hwang Park, Ka Hyon |
| AuthorAffiliation | 2 BioImaging and Cell Dynamics Research Center, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 500-712, Republic of Korea 1 Cell Dynamics Research Center and School of Life Sciences, Gwangju Institute of Science and Technology, 123 Cheomdangwagi-ro, Buk-gu, Gwangju 500-712, Republic of Korea 4 Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University, 77 Yongbong-ro, Buk-gu, Gwangju 500-757, Republic of Korea 3 Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University, 77 Yongbong-ro, Buk-gu, Gwangju 500-757, Republic of Korea |
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| Author_xml | – sequence: 1 givenname: Youngnim surname: Shin fullname: Shin, Youngnim organization: Cell Dynamics Research Center and School of Life Sciences, Gwangju Institute of Science and Technology – sequence: 2 givenname: Yun Hyun surname: Huh fullname: Huh, Yun Hyun organization: BioImaging and Cell Dynamics Research Center, Gwangju Institute of Science and Technology – sequence: 3 givenname: Kieun surname: Kim fullname: Kim, Kieun organization: Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University – sequence: 4 givenname: Suyeon surname: Kim fullname: Kim, Suyeon organization: Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University – sequence: 5 givenname: Ka Hyon surname: Park fullname: Park, Ka Hyon organization: Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University – sequence: 6 givenname: Jeong-Tae surname: Koh fullname: Koh, Jeong-Tae organization: Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University, Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University – sequence: 7 givenname: Jang-Soo surname: Chun fullname: Chun, Jang-Soo organization: Cell Dynamics Research Center and School of Life Sciences, Gwangju Institute of Science and Technology – sequence: 8 givenname: Je-Hwang surname: Ryu fullname: Ryu, Je-Hwang email: jesryu@jnu.ac.kr organization: Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University, Research Center for Biomineralization Disorders, School of Dentistry, Chonnam National University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24479426$$D View this record in MEDLINE/PubMed |
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| Keywords | Micromass Culture Catabolic Factor Cartilage Destruction International Cartilage Repair Society Chondrocyte Apoptosis |
| Language | English |
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| PublicationTitle | Arthritis research & therapy |
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| Snippet | Introduction
Wnt ligands bind to low-density lipoprotein receptor–related protein (LRP) 5 or 6, triggering a cascade of downstream events that include... Wnt ligands bind to low-density lipoprotein receptor-related protein (LRP) 5 or 6, triggering a cascade of downstream events that include β-catenin signaling.... |
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| SubjectTerms | Animals Arthritis, Experimental - metabolism Arthritis, Experimental - pathology Blotting, Western Cartilage, Articular - metabolism Cartilage, Articular - pathology Cells, Cultured Chondrocytes - metabolism Chondrocytes - pathology Humans Immunohistochemistry In Situ Nick-End Labeling Low Density Lipoprotein Receptor-Related Protein-5 - metabolism Medicine Medicine & Public Health Mice Mice, Inbred C57BL Mice, Knockout Microscopy, Fluorescence Orthopedics Osteoarthritis - metabolism Osteoarthritis - pathology Real-Time Polymerase Chain Reaction Research Article Reverse Transcriptase Polymerase Chain Reaction Rheumatology Transfection Up-Regulation Wnt Proteins - metabolism Wnt Signaling Pathway - physiology |
| Title | Low-density lipoprotein receptor–related protein 5 governs Wnt-mediated osteoarthritic cartilage destruction |
| URI | https://link.springer.com/article/10.1186/ar4466 https://www.ncbi.nlm.nih.gov/pubmed/24479426 https://www.proquest.com/docview/1558520431 https://pubmed.ncbi.nlm.nih.gov/PMC3978879 |
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