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CD24 enrichment protects while its loss increases susceptibility of juvenile chondrocytes towards inflammation

Overview of attention for article published in Arthritis Research & Therapy, December 2016
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Good Attention Score compared to outputs of the same age (74th percentile)
  • Good Attention Score compared to outputs of the same age and source (65th percentile)

Mentioned by

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1 tweeter
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2 patents

Citations

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7 Dimensions

Readers on

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29 Mendeley
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Title
CD24 enrichment protects while its loss increases susceptibility of juvenile chondrocytes towards inflammation
Published in
Arthritis Research & Therapy, December 2016
DOI 10.1186/s13075-016-1183-y
Pubmed ID
Authors

Jieun Lee, Piera Smeriglio, Jason Dragoo, William J. Maloney, Nidhi Bhutani

Abstract

Diseases associated with human cartilage, including rheumatoid arthritis (RA) and osteoarthritis (OA) have manifested age, mechanical stresses and inflammation as the leading risk factors. Although inflammatory processes are known to be upregulated upon aging, we sought to gain a molecular understanding of how aging affects the tissue-specific response to inflammation. In this report, we explored the role of cluster of differentiation 24 (CD24) in regulating differential inflammatory responses in juvenile and adult human chondrocytes. Differential cell-surface CD24 expression was assessed in juvenile and adult chondrocytes along with human induced pluripotent stem cell (hiPSC)-derived neonatal chondrocytes through gene expression and fluorescence-activated cell sorting (FACS) analyses. Loss of function of CD24 was achieved through silencing in chondrocytes and the effects on the response to inflammatory cues were assessed through gene expression and NFκB activity. CD24 expression in chondrocytes caused a differential response to cytokine-induced inflammation, with the CD24(high) juvenile chondrocytes being resistant to IL-1ß treatment as compared to CD24(low) adult chondrocytes. CD24 protects from inflammatory response by reducing NFκB activation, as an acute loss of CD24 via silencing led to an increase in NFκB activation. Moreover, the loss of CD24 in chondrocytes subsequently increased inflammatory and catabolic gene expression both in the absence and presence of IL-1ß. We have identified CD24 as a novel regulator of inflammatory response in cartilage that is altered during development and aging and could potentially be therapeutic in RA and OA.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 29 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 29 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 28%
Researcher 4 14%
Student > Bachelor 4 14%
Lecturer 3 10%
Student > Master 3 10%
Other 2 7%
Unknown 5 17%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 31%
Medicine and Dentistry 3 10%
Immunology and Microbiology 3 10%
Agricultural and Biological Sciences 2 7%
Nursing and Health Professions 2 7%
Other 4 14%
Unknown 6 21%

Attention Score in Context

This research output has an Altmetric Attention Score of 7. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 25 August 2021.
All research outputs
#3,851,279
of 19,467,557 outputs
Outputs from Arthritis Research & Therapy
#960
of 2,736 outputs
Outputs of similar age
#85,043
of 331,747 outputs
Outputs of similar age from Arthritis Research & Therapy
#73
of 209 outputs
Altmetric has tracked 19,467,557 research outputs across all sources so far. Compared to these this one has done well and is in the 80th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,736 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.2. This one has gotten more attention than average, scoring higher than 64% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 331,747 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 74% of its contemporaries.
We're also able to compare this research output to 209 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 65% of its contemporaries.