Cartilage tissue engineering: From proinflammatory and anti‑inflammatory cytokines to osteoarthritis treatments (Review)

Liu, Shuyu; Deng, Zhenhan; Chen, Kang; Jian, Shengsheng; Zhou, Feifei; Yang, Yuan; Fu, Zicai; Xie, Huanyu; Xiong, Jianyi; Zhu, Weimin

doi:10.3892/mmr.2022.12615

Cited by 106 publications

(60 citation statements)

References 184 publications

(194 reference statements)

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“…Furthermore, TNF-α blocks the chondrocyte synthesis of proteoglycans and type II collagen. IL-1β activates transcription factors via the MAPK and NF-κB signalling pathways to regulate inflammatory responses, resulting in the production of inflammatory mediators such as NO, PGE2, COX-2, and other catabolic factors that may accelerate cartilage degeneration [ 30 , 31 , 32 ]. Moreover, cytokines upregulate the gene expression of MMPs, which promotes the degradation of articular cartilage by breaking down proteoglycan, the main component of the ECM [ 33 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory and Analgesic Effects of Schisandra chinensis Leaf Extracts and Monosodium Iodoacetate-Induced Osteoarthritis in Rats and Acetic Acid-Induced Writhing in Mice

et al. 2022

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In this study, we aimed to determine the anti-inflammatory and antinociceptive activities of Schisandra chinensis leaf extracts (SCLE) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages, an acetic acid-induced mouse model of writhing, and a monosodium iodoacetate (MIA)-induced rat model of osteoarthritis (OA). In LPS-stimulated RAW264.7 cells, a 100 µg/mL dose of SCLE significantly reduced the production of nitric oxide (NO), interleukin-1β (IL-1β), tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and prostaglandin E2 (PGE2). Acetic acid-induced writhing responses in mice that quantitatively determine pain were significantly inhibited by SCLE treatment. In addition, SCLE significantly decreased the MIA-induced elevation in OA symptoms, the expression levels of pro-inflammatory mediators/cytokines and matrix metalloproteinases, and cartilage damage in the serum and joint tissues. Our data demonstrated that SCLE exerts anti-osteoarthritic effects by regulating inflammation and pain and can be a useful therapeutic candidate against OA.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory and Analgesic Effects of Schisandra chinensis Leaf Extracts and Monosodium Iodoacetate-Induced Osteoarthritis in Rats and Acetic Acid-Induced Writhing in Mice

et al. 2022

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“…IL‐1β, TNF‐α and IL‐6) involved in OA pathogenesis are released by chondrocytes, macrophages, and fibroblasts. These cytokines induced catabolic events such as promoting the production of MMPs, ADAMTS and pro‐inflammatory mediators (NO, PGE‐2) 42,43 . However, IL‐1β or TNF‐α inhibition did not produce the desired effects of preventing OA progression 44,45 .…”

Section: Discussionmentioning

confidence: 99%

“…These cytokines induced catabolic events such as promoting the production of MMPs, ADAMTS and pro‐inflammatory mediators (NO, PGE‐2). 42 , 43 However, IL‐1β or TNF‐α inhibition did not produce the desired effects of preventing OA progression. 44 , 45 Therefore, future studies should consider that the development of OA does not depend on a single cytokine; rather, the same signalling pathway can be activated by different cytokines, and the interaction of multiple factors plays a key role in the occurrence and development of diseases.…”

Section: Discussionmentioning

confidence: 99%

Activation of adenosine A3 receptor attenuates progression of osteoarthritis through inhibiting the NLRP3/caspase‐1/GSDMD induced signalling

Bai

Zhang

Liu

et al. 2022

J Cellular Molecular Medi

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The specific adenosine A3 receptor (A3AR) agonist (CF101) has potential for inflammation and pain in various disease, such as arthritis, cancer and neuropathic pain, while the role of A3AR in post‐traumatic OA and the underlying mechanism is largely unknown. CF101 was orally administrated in OA rats induced by anterior cruciate ligament transection (ACLT) surgery, and the rat primary chondrocytes were stimulated by hydrogen peroxide (H2O2, 300 μM). Histologic grading system was performed for detecting cartilage degeneration and immunohistochemistry for determining pyroptosis. The moleculars associated with cartilage homeostasis and inflammatory cytokines were analysed; moreover, the activation of NLRP3 inflammasome was determined. CF101 treatment significantly attenuated OA cartilage damage, OA‐related pain and cartilage pyroptosis. Chondrocytes stimulated by H2O2 evoked ROS release, thereby promoting the activation of NLRP3 inflammasome and facilitating the cleavage of GSDMD, which ultimately resulted in the mass release of pro‐inflammatory cytokines including IL‐1β and IL‐18, and production of matrix hydrolase. The pre‐treatment with CF101 powerfully inhibited the above process both in vivo and in vitro. Our findings demonstrated that activation of A3AR attenuates OA progression and relieves pain perception through suppression of cartilage degradation and inhibition of ROS/NLRP3/GSDMD signalling, indicating pyroptosis is a potential candidate for OA treatment.

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“…In this study, we first reported a significant increase in TGF-β1 and VEGF in ACS of the OA dogs compared to the sham plasma control, similar to the previous report in human OA [ 16 ]. These growth factors are believed to play a role in joint homeostasis [ 25 ] and vascular regeneration [ 8 , 38 ], which are essential for joint and tendon repairs [ 36 , 39 ]. However, previous reports investigating ACS in normal dogs did not find the differences in these cytokines when compared to the normal serum [ 15 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

In Vitro Anti-Inflammatory and Regenerative Effects of Autologous Conditioned Serum from Dogs with Osteoarthritis

Soontararak

Ardaum

Senarat

et al. 2022

Animals

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Osteoarthritis (OA) is mostly incurable and non-regenerative with long-term complications. Autologous conditioned serum (ACS), which is enriched in Interleukin 1 receptor antagonists (IL-1RA) and growth factors, could be an alternative treatment to accelerate the positive therapeutic effects. ACS is proposed to alleviate inflammation by blocking IL-1 receptors. However, to date, there is no report focusing on the cell-mediated anti-inflammation and regenerative effect caused by ACS, especially the ACS from patients. Therefore, this study aims to investigate the therapeutic potential of ACS generated from dogs with spontaneous OA, focusing on its promising anti-inflammatory and regenerative properties in vitro compared to the matched plasma. We found that ACS prepared from ten OA dogs contained significant concentrations of IL-1RA, vascular endothelial growth factor, and transforming growth factor beta, which are key cytokines in anti-inflammation and angiogenesis. Furthermore, we found that ACS suppressed T cell activity by reducing proliferation of effector T cells and simultaneously expanding numbers of immune suppressive FOXP3+ T cells. Lastly, we showed that ACS enhanced the proliferation of osteocytes and fibroblasts and promoted extracellular matrix gene expression in primary chondrocyte culture. Therefore, these studies indicate that ACS prepared from dogs with OA is active as an immunomodulatory and regenerative strategy for use in OA management.

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Cartilage tissue engineering: From proinflammatory and anti‑inflammatory cytokines to osteoarthritis treatments (Review)

Cited by 106 publications

References 184 publications

Anti-Inflammatory and Analgesic Effects of Schisandra chinensis Leaf Extracts and Monosodium Iodoacetate-Induced Osteoarthritis in Rats and Acetic Acid-Induced Writhing in Mice

Anti-Inflammatory and Analgesic Effects of Schisandra chinensis Leaf Extracts and Monosodium Iodoacetate-Induced Osteoarthritis in Rats and Acetic Acid-Induced Writhing in Mice

Activation of adenosine A3 receptor attenuates progression of osteoarthritis through inhibiting the NLRP3/caspase‐1/GSDMD induced signalling

In Vitro Anti-Inflammatory and Regenerative Effects of Autologous Conditioned Serum from Dogs with Osteoarthritis

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