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Abstract Number: 1332

Periostin Deficiency Exacerbates Joint Inflammation and Bone Destruction in Mouse Models of Rheumatoid Arthritis

Yun-Hong Cheon, Division of Rheumatology, Department of Internal Medicine, Gyeongsang National University School of Medicine, Jinju, Korea, Republic of (South)

Meeting: 2017 ACR/ARHP Annual Meeting

Date of first publication: September 18, 2017

Keywords: Rheumatoid arthritis (RA)

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Session Information

Date: Monday, November 6, 2017

Title: Rheumatoid Arthritis – Animal Models Poster II

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose:

Periostin (POSTN), a matricellular protein, is involved in many fundamental biological processes such as bone metabolism, cell proliferation, cell invasion, and angiogenesis. Also, POSTN has been shown to be involved in many aspects of inflammation, wound fibrosis and recruitment several immune cells. Although POSTN expression has been reported to promote migration and invasion of fibroblast-like synoviocyte (FLS) in vitro, there is no study to investigate the role of POSTN in mouse models of rheumatoid arthritis (RA). This study was performed to assess the function of POSTN in 3 mouse models of arthritis, K/BxN serum transfer arthritis (STA), collagen-induced arthritis (CIA) and collagen-antibody induced arthritis (CAIA).

Methods:

Periostin level in synovial fluid from RA and osteoarthritis (OA) patients were measured by ELISA. The expression of periostin FLS was stained by immunohistochemistry. STA, CIA and CAIA was induced in POSTN-/- and POSTN+/+ mice. Arthritis was monitored in 3 mouse models of arthritis using defined criteria (clinical and histologic). Osteoclastogenesis was assessed using bone marrow monocytes (BMM) cultures from POSTN-/- and POSTN+/+ mice.

Results:

POSTN level in synoviocyte tissue were increased in patient with RA compare to OA patient. In STA studies, the clinical score and hind paw thickness were significantly increased in POSTN-/- mice compared with POSTN+/+ mice. Mean histologic severity scores including synovial inflammation, bone erosion and cartilage damage were increased in diseased joints from POSTN-/- mice compared with those from POSTN+/+ mice. The IL-1β was increased in the serum, and TNF-α, IL-1β, and MMPs were increased in the ankle of POSTN-/- mice than wild type control. BMMs from POSTN-/- mice showed increased osteoclast formation compared with BMMs from POSTN+/+ mice. Similarly, in CAIA and CIA model, both mean clinical severity scores and ankle joint swelling were significantly increased in POSTN-/- mice compared with POSTN+/+ mice.

Conclusion:

This study suggests that POSTN contributes to pathogenesis of RA and might have a potential protective role in RA.


Disclosure: Y. H. Cheon, None;

To cite this abstract in AMA style:

Cheon YH. Periostin Deficiency Exacerbates Joint Inflammation and Bone Destruction in Mouse Models of Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/periostin-deficiency-exacerbates-joint-inflammation-and-bone-destruction-in-mouse-models-of-rheumatoid-arthritis/. Accessed .
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