Influence of Periostin on Synoviocytes in Knee Osteoarthritis

Tajika, Yutaro; Moue, Tatsuya; Ishikawa, Shintaro; Asano, Koichiro; Okumo, Takayuki; Takagi, Hiroshi; Hisamitsu, Tadashi

doi:10.21873/invivo.11027

Cited by 20 publications

(17 citation statements)

References 39 publications

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“…Cartilage from human and mouse OA knees has been shown to exhibit higher expression of POSTN than normal cartilage 12,23 . This higher expression of POSTN was confined mainly to chondrocytes in the periphery of erosive lesions 34 and has been associated with higher expression of MMPs in chondrocytes 12,23 and synoviocytes 26 . There are some studies that report significant up-regulation of the POSTN gene in subchondral bone during OA 37e39 .…”

Section: Discussionmentioning

confidence: 89%

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Proteomic analysis of synovial fluid identifies periostin as a biomarker for anterior cruciate ligament injury

Brophy

Cai

Duan

et al. 2019

Osteoarthritis and Cartilage

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Objective: Emerging evidence suggests that injury to the anterior cruciate ligament (ACL) typically initiates biological changes that contribute to the development of osteoarthritis (OA). The molecular biomarkers or mediators of these biological events remain unknown. The goal of this exploratory study was to identify novel synovial fluid biomarkers associated with early biological changes following ACL injury distinct from findings in end-stage OA. Methods: Synovial fluid was aspirated from patients with acute (30 days) and subacute (31e90 days) ACL tears and from patients with advanced OA and probed via tandem mass spectrometry for biomarkers to distinguish OA from ACL injury. Periostin (POSTN) was identified as a potential candidate. Further analyses of POSTN were performed in synovial fluid, OA cartilage, torn ACL remnants, and cultured cells and media by Western blot, PCR, immunostaining and ELISA. Results: Synovial fluid analysis revealed that POSTN exhibited higher expression in subacute ACL injury than OA. POSTN expression was relatively low in cartilage/chondrocytes suggesting it is also produced by other intra-articular tissues. Conversely, high and time-dependent expression of POSTN in ACL tear remnants and isolated cells was consistent with the synovial fluid results. Conclusions: Elevated POSTN may provide a synovial fluid biomarker of subacute ACL injury setting separate from OA. Increased expression of POSTN in ACL suggests that the injured ACL may play a pivotal role in POSTN production, which is sensitive to time from injury. Previous studies have shown potential catabolic effects of POSTN, raising the possibility that POSTN contributes to the initiation of joint degeneration and may offer a window of opportunity to intervene in the early stages of post-traumatic OA.

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Section: Discussionmentioning

confidence: 89%

“…In addition, higher levels of POSTN have been shown to correlate with severity of OA 24,25 . Certain studies have shown that POSTN is involved in cartilage matrix degradation via MMP-13 12,23 and MMP-9 26 . However, the levels of POSTN in knees after ACL injury has not been compared to levels in knees with OA.…”

Section: Introductionmentioning

confidence: 99%

Proteomic analysis of synovial fluid identifies periostin as a biomarker for anterior cruciate ligament injury

Brophy

Cai

Duan

et al. 2019

Osteoarthritis and Cartilage

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“…As a ligand of α V β 3 and α V β 5 integrins, periostin fostered adhesion and migration of epithelial cells 37 . Moreover, periostin is upregulated in OA cartilage and intensifies inflammation and metalloproteinases production 38,39 . We also showed that CEMIP regulated SERPINE1 gene coding for PAI-1.…”

Section: Discussionmentioning

confidence: 99%

CEMIP (KIAA1199) induces a fibrosis-like process in osteoarthritic chondrocytes

et al. 2019

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CEMIP (for “Cell migration-inducing protein” also called KIAA1199 and Hybid for “Hyaluronan-binding protein”) expression is increased in cancers and described as a regulator of cell survival, growth and invasion. In rheumatoid arthritis, CEMIP is referred to as an angiogenic marker and participates in hyaluronic acid degradation. In this study, CEMIP expression is investigated in healthy and osteoarthritis (OA) cartilage from human and mouse. Its role in OA physiopathology is deciphered, specifically in chondrocytes proliferation and dedifferentiation and in the extracellular matrix remodeling. To this end, CEMIP, αSMA and types I and III collagen expressions were assessed in human OA and non-OA cartilage. CEMIP expression was also investigated in a mouse OA model. CEMIP expression was studied in vitro using a chondrocyte dedifferentiation model. High-throughput RNA sequencing was performed on chondrocytes after CEMIP silencing. Results showed that CEMIP was overexpressed in human and murine OA cartilage and along chondrocytes dedifferentiation. Most of genes deregulated in CEMIP-depleted cells were involved in cartilage turnover (e.g., collagens), mesenchymal transition and fibrosis. CEMIP regulated β-catenin protein level. Moreover, CEMIP was essential for chondrocytes proliferation and promoted αSMA expression, a fibrosis marker, and TGFβ signaling towards the p-Smad2/3 (Alk5/PAI-1) pathway. Interestingly, CEMIP was induced by the pSmad1/5 (Alk1) pathway. αSMA and type III collagen expressions were overexpressed in human OA cartilage and along chondrocytes dedifferentiation. Finally, CEMIP was co-expressed in situ with αSMA in all OA cartilage layers. In conclusion, CEMIP was sharply overexpressed in human and mouse OA cartilage and along chondrocytes dedifferentiation. CEMIP-regulated transdifferentiation of chondrocytes into “chondro-myo-fibroblasts” expressing α-SMA and type III collagen, two fibrosis markers. Moreover, these “chondro-myo-fibroblasts” were found in OA cartilage but not in healthy cartilage.

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“…Among proteins up-regulated in both conditions, we identified some extracellular matrix proteins that have been previously implicated in osteoarthritis pathogenesis. Among these, elevated expression levels Follistatin-related protein 1 (FSTL1) [48] and Periostin (POSTN) [49] were previously correlated to OA progression and severity. In addition, increased expression levels of Fibrillin-1 (FBN1), the major constituent of tissue elastic microfibers and previously identified also in human osteoarthritis synovial fluids [40], were identified by MS secretome analysis and confirmed by Western blot.…”

Section: Discussionmentioning

confidence: 99%

Differential Secretome Profiling of Human Osteoarthritic Synoviocytes Treated with Biotechnological Unsulfated and Marine Sulfated Chondroitins

Russo

Vassallo

Stellavato

et al. 2020

IJMS

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Symptomatic slow-acting drugs (SYSADOA) are increasingly used as effective therapies for osteoarthritis, representing an attractive alternative to analgesics or non-steroidal anti-inflammatory drugs to relieve disease symptoms. Pharmaceutical preparations of chondroitin sulfate, derived from animal sources, alone or in combination with glucosamine sulfate, are widely recognized for their beneficial effect on osteoarthritis treatment. A growing interest has also been devoted to understanding the molecular mechanisms modulated by SYSADOA using -omic strategies, most of which rely on chondrocytes as a model system. In this work, by using an integrated strategy based on unbiased proteomics and targeted cytokine profiling by a multiplexed protein array, we identified differences in the secretomes of human osteoarthritic synoviocytes in response to biotechnological unsulfated, and marine sulfated chondroitins treatments. The combined strategy allowed the identification of candidate proteins showing both common and distinct regulation responses to the two treatments of chondroitins. These molecules, mainly belonging to ECM proteins, enzymes, enzymatic inhibitors and cytokines, are potentially correlated to treatment outcomes. Overall, the present results provide an integrated overview of protein changes in human osteoarthritic synoviocytes secretome associated to different chondroitin treatments, thus improving current knowledge of the biochemical effects driven by these drugs potentially involved in pathways associated to osteoarthritis pathogenesis.

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Influence of Periostin on Synoviocytes in Knee Osteoarthritis

Cited by 20 publications

References 39 publications

Proteomic analysis of synovial fluid identifies periostin as a biomarker for anterior cruciate ligament injury

Proteomic analysis of synovial fluid identifies periostin as a biomarker for anterior cruciate ligament injury

CEMIP (KIAA1199) induces a fibrosis-like process in osteoarthritic chondrocytes

Differential Secretome Profiling of Human Osteoarthritic Synoviocytes Treated with Biotechnological Unsulfated and Marine Sulfated Chondroitins

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