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The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis

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The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis. / Gossan, Nicole; Zeef, Leo; Hensman, James et al.
In: Arthritis and Rheumatism, Vol. 65, No. 9, 09.2013, p. 2334-2345.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Gossan, N, Zeef, L, Hensman, J, Hughes, A, Bateman, JF, Rowley, L, Little, CB, Piggins, HD, Rattray, M, Boot-Handford, RP & Meng, QJ 2013, 'The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis', Arthritis and Rheumatism, vol. 65, no. 9, pp. 2334-2345. https://doi.org/10.1002/art.38035

APA

Gossan, N., Zeef, L., Hensman, J., Hughes, A., Bateman, J. F., Rowley, L., Little, C. B., Piggins, H. D., Rattray, M., Boot-Handford, R. P., & Meng, Q. J. (2013). The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis. Arthritis and Rheumatism, 65(9), 2334-2345. https://doi.org/10.1002/art.38035

Vancouver

Gossan N, Zeef L, Hensman J, Hughes A, Bateman JF, Rowley L et al. The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis. Arthritis and Rheumatism. 2013 Sept;65(9):2334-2345. Epub 2013 Aug 26. doi: 10.1002/art.38035

Author

Gossan, Nicole ; Zeef, Leo ; Hensman, James et al. / The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis. In: Arthritis and Rheumatism. 2013 ; Vol. 65, No. 9. pp. 2334-2345.

Bibtex

@article{95a9f67b735e4ca784b5ce1ba773d214,
title = "The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis",
abstract = "Objective To characterize the circadian clock in murine cartilage tissue and identify tissue-specific clock target genes, and to investigate whether the circadian clock changes during aging or during cartilage degeneration using an experimental mouse model of osteoarthritis (OA). Methods Cartilage explants were obtained from aged and young adult mice after transduction with the circadian clock fusion protein reporter PER2::luc, and real-time bioluminescence recordings were used to characterize the properties of the clock. Time-series microarrays were performed on mouse cartilage tissue to identify genes expressed in a circadian manner. Rhythmic genes were confirmed by quantitative reverse transcription-polymerase chain reaction using mouse tissue, primary chondrocytes, and a human chondrocyte cell line. Experimental OA was induced in mice by destabilization of the medial meniscus (DMM), and articular cartilage samples were microdissected and subjected to microarray analysis. Results Mouse cartilage tissue and a human chondrocyte cell line were found to contain intrinsic molecular circadian clocks. The cartilage clock could be reset by temperature signals, while the circadian period was temperature compensated. PER2::luc bioluminescence demonstrated that circadian oscillations were significantly lower in amplitude in cartilage from aged mice. Time-series microarray analyses of the mouse tissue identified the first circadian transcriptome in cartilage, revealing that 615 genes (∼3.9% of the expressed genes) displayed a circadian pattern of expression. This included genes involved in cartilage homeostasis and survival, as well as genes with potential importance in the pathogenesis of OA. Several clock genes were disrupted in the early stages of cartilage degeneration in the DMM mouse model of OA. Conclusion These results reveal an autonomous circadian clock in chondrocytes that can be implicated in key aspects of cartilage biology and pathology. Consequently, circadian disruption (e.g., during aging) may compromise tissue homeostasis and increase susceptibility to joint damage or disease.",
author = "Nicole Gossan and Leo Zeef and James Hensman and Alun Hughes and Bateman, {John F.} and Lynn Rowley and Little, {Christopher B.} and Piggins, {Hugh D.} and Magnus Rattray and Boot-Handford, {Raymond P.} and Meng, {Qing Jun}",
year = "2013",
month = sep,
doi = "10.1002/art.38035",
language = "English",
volume = "65",
pages = "2334--2345",
journal = "Arthritis and Rheumatism",
issn = "0004-3591",
publisher = "John Wiley and Sons Inc.",
number = "9",

}

RIS

TY - JOUR

T1 - The circadian clock in murine chondrocytes regulates genes controlling key aspects of cartilage homeostasis

AU - Gossan, Nicole

AU - Zeef, Leo

AU - Hensman, James

AU - Hughes, Alun

AU - Bateman, John F.

AU - Rowley, Lynn

AU - Little, Christopher B.

AU - Piggins, Hugh D.

AU - Rattray, Magnus

AU - Boot-Handford, Raymond P.

AU - Meng, Qing Jun

PY - 2013/9

Y1 - 2013/9

N2 - Objective To characterize the circadian clock in murine cartilage tissue and identify tissue-specific clock target genes, and to investigate whether the circadian clock changes during aging or during cartilage degeneration using an experimental mouse model of osteoarthritis (OA). Methods Cartilage explants were obtained from aged and young adult mice after transduction with the circadian clock fusion protein reporter PER2::luc, and real-time bioluminescence recordings were used to characterize the properties of the clock. Time-series microarrays were performed on mouse cartilage tissue to identify genes expressed in a circadian manner. Rhythmic genes were confirmed by quantitative reverse transcription-polymerase chain reaction using mouse tissue, primary chondrocytes, and a human chondrocyte cell line. Experimental OA was induced in mice by destabilization of the medial meniscus (DMM), and articular cartilage samples were microdissected and subjected to microarray analysis. Results Mouse cartilage tissue and a human chondrocyte cell line were found to contain intrinsic molecular circadian clocks. The cartilage clock could be reset by temperature signals, while the circadian period was temperature compensated. PER2::luc bioluminescence demonstrated that circadian oscillations were significantly lower in amplitude in cartilage from aged mice. Time-series microarray analyses of the mouse tissue identified the first circadian transcriptome in cartilage, revealing that 615 genes (∼3.9% of the expressed genes) displayed a circadian pattern of expression. This included genes involved in cartilage homeostasis and survival, as well as genes with potential importance in the pathogenesis of OA. Several clock genes were disrupted in the early stages of cartilage degeneration in the DMM mouse model of OA. Conclusion These results reveal an autonomous circadian clock in chondrocytes that can be implicated in key aspects of cartilage biology and pathology. Consequently, circadian disruption (e.g., during aging) may compromise tissue homeostasis and increase susceptibility to joint damage or disease.

AB - Objective To characterize the circadian clock in murine cartilage tissue and identify tissue-specific clock target genes, and to investigate whether the circadian clock changes during aging or during cartilage degeneration using an experimental mouse model of osteoarthritis (OA). Methods Cartilage explants were obtained from aged and young adult mice after transduction with the circadian clock fusion protein reporter PER2::luc, and real-time bioluminescence recordings were used to characterize the properties of the clock. Time-series microarrays were performed on mouse cartilage tissue to identify genes expressed in a circadian manner. Rhythmic genes were confirmed by quantitative reverse transcription-polymerase chain reaction using mouse tissue, primary chondrocytes, and a human chondrocyte cell line. Experimental OA was induced in mice by destabilization of the medial meniscus (DMM), and articular cartilage samples were microdissected and subjected to microarray analysis. Results Mouse cartilage tissue and a human chondrocyte cell line were found to contain intrinsic molecular circadian clocks. The cartilage clock could be reset by temperature signals, while the circadian period was temperature compensated. PER2::luc bioluminescence demonstrated that circadian oscillations were significantly lower in amplitude in cartilage from aged mice. Time-series microarray analyses of the mouse tissue identified the first circadian transcriptome in cartilage, revealing that 615 genes (∼3.9% of the expressed genes) displayed a circadian pattern of expression. This included genes involved in cartilage homeostasis and survival, as well as genes with potential importance in the pathogenesis of OA. Several clock genes were disrupted in the early stages of cartilage degeneration in the DMM mouse model of OA. Conclusion These results reveal an autonomous circadian clock in chondrocytes that can be implicated in key aspects of cartilage biology and pathology. Consequently, circadian disruption (e.g., during aging) may compromise tissue homeostasis and increase susceptibility to joint damage or disease.

U2 - 10.1002/art.38035

DO - 10.1002/art.38035

M3 - Journal article

C2 - 23896777

AN - SCOPUS:84883223007

VL - 65

SP - 2334

EP - 2345

JO - Arthritis and Rheumatism

JF - Arthritis and Rheumatism

SN - 0004-3591

IS - 9

ER -