Attenuation of subchondral bone abnormal changes in osteoarthritis by inhibition of SDF-1 signaling

Chen, Y.; Lin, Sien; Sun, Yuxin; Guo, Jiaxin; Lu, Yuan-Qiang; Suen, Chun-wai; Zhang, J.; Zha, Zhengang; Ho, Kwok W.; Xiao-ting, Pan; Li, G.

doi:10.1016/j.joca.2017.01.008

Cited by 36 publications

(38 citation statements)

References 41 publications

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“…Although the subchondral bone‐cartilage interplay is believed to contribute strongly to OA progression (Chen et al, ; Hayami et al, ; Zhen et al, ), the potential molecular signaling for the subchondral bone—cartilage interaction has been rarely investigated. Previously, it was shown that the subchondral bone‐derived TGF‐β could be released and therefore accelerate cartilage degradation in anterior cruciate ligament transection (ACLT) mice (Zhen et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Various signaling pathways have been found involved in the OA progression, and the modulatory role of the phosphoinositide 3‐kinase (PI3K)/protein kinase B (PKB), or AKT signaling in the pathogenesis process of OA has received substantial attentions (Chen, Wu, Sun, Dong, & Zhao, ; Chen et al, ; Dong et al, ). An upregulation of PI3K/AKT signaling in synovial fibroblasts of OA patients was recently reported (Chen, Hou, Hou, & Liu, ).…”

Section: Introductionmentioning

confidence: 99%

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Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post‐traumatic osteoarthritis

Lin

Shao

Zeng

et al. 2018

Journal Cellular Physiology

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PI3K/AKT signaling is essential in regulating pathophysiology of osteoarthritis (OA). However, its potential modulatory role in early OA progression has not been investigated yet. Here, a mouse destabilization OA model in the tibia was used to investigate roles of PI3K/AKT signaling in the early subchondral bone changes and OA pathological process. We revealed a significant increase in PI3K/AKT signaling activation which was associated with aberrant bone formation in tibial subchondral bone following destabilizing the medial meniscus (DMM), which was effectively prevented by treatment with PI3K/AKT signaling inhibitor LY294002. PI3K/AKT signaling inhibition attenuated articular cartilage degeneration. Serum and bone biochemical analyses revealed increased levels of MMP-13, which was found expressed mainly by osteoblastic cells in subchondral bone. However, this MMP-13 induction was attenuated by LY294002 treatment. Furthermore, PI3K/AKT signaling was found to enhance preosteoblast proliferation, differentiation, and expression of MMP-13 by activating NF-κB pathway. In conclusion, inhibition of PI3K/AKT/NF-κB axis was able to prevent aberrant bone formation and attenuate cartilage degeneration in OA mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post‐traumatic osteoarthritis

Lin

Shao

Zeng

et al. 2018

Journal Cellular Physiology

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“…Subchondral bone is a mechanical support of overlying cartilage and plays a critical role in bone modeling and remodeling. Lesions of subchondral bone re ect serious cartilage damage [2]. At 12 weeks, subchondral bone of pigs in two experimental groups was visibly destroyed, especially in the chemical group, which means that late OA appeared at this time; papain injection brought about more severe changes.…”

Section: Discussionmentioning

confidence: 97%

“…Osteoarthritis (OA) is a multifactorial disease characterized by synovial in ammation, extracellular matrix (ECM) degradation, and chondrocyte hypocellularity [1]. Stromal cell-derived factor-1 (SDF-1) was identi ed as a strong in ammatory cytokine existing in the synovium, and its speci c receptor C-X-C chemokine receptor type 4 (CXCR4) locates on the surface of chondrocytes [2]. The binding of SDF-1 and CXCR4 can lead to a cascade of matrix metalloproteinase (MMP) release and collagen (mostly collagen type II, Col II) and proteoglycan (mostly aggrecan, ACAN) degradation, hence exacerbating and accelerating the OA process [3].…”

Section: Introductionmentioning

confidence: 99%

Comparative effectiveness of two methods for inducing osteoarthritis in a novel animal model, the Diannan small-ear pig1

Jia

Cai

et al. 2020

Preprint

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Abstract Background: Varieties of animals were used to study osteoarthritis pathogenesis. The Diannan small-ear pig, which is native to Yunnan, China, is thought to have an articular anatomy similar to that of humans and is more likely to be a source of pathological tissues than other animals. The aim of this study was determine whether this animal can serve as a more effective osteoarthritis model.[A1] Methods: Twenty-seven adult pigs were randomly divided into three groups and underwent the Hulth procedure, papain articular injection [A2] , and conventional breeding. After 4, 8, and 12 weeks, cartilage tissues from knee joint were extracted for general and histological observation, immunofluorescence, and biochemical analysis. [A3] Synovium was taken out for stromal cell-derived factor-1 analysis. Results: Histopathological observation showed obvious cartilage loss in two experimental groups, this cartilage loss was more severe in the chemical groups. Synovial stromal cell-derived factor1 levels increased over time in all groups. mRNA and protein levels of matrix metalloproteinase-3 were much higher in the chemical groups than in the other groups, whereas levels of collagen type II[A4] and aggrecan were significantly lower in the chemical groups than in the other groups. Immunofluorescence assays of collagen type II[A5] revealed an apparent reduction in this marker in the chemical groups compared with the other groups. Conclusions: These results indicated that the Diannan small-ear pig can be used as an effective osteoarthritis model. In addition, it is much more convenient and much faster to induce osteoarthritis by intra-articular injection of papain, which is a method worthy of being promoted.

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“…In brief, each rat was anesthetized by administrating 0.2% (v/v) xylazine and 1% (v/v) ketamine; after being shaved and disinfected, the right knee joint was exposed through a medial parapatellar arthrotomy approach. The patella was dislocated laterally, and the knee was placed in full flexion followed by ACL and medial collateral ligament (MCL) transection with microscissors and resection of the medial meniscus . Rats were allocated randomly into four groups and received intra‐articular injections at the right knees.…”

Section: Methodsmentioning

confidence: 99%

Bioadhesive Polymersome for Localized and Sustained Drug Delivery at Pathological Sites with Harsh Enzymatic and Fluidic Environment via Supramolecular Host–Guest Complexation

Zhu

Wei

Lin

et al. 2017

Small

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Targeted and sustained delivery of drugs to diseased tissues/organs, where body fluid exchange and catabolic activity are substantial, is challenging due to the fast cleansing and degradation of the drugs by these harsh environmental factors. Herein, a multifunctional and bioadhesive polycaprolactone-β-cyclodextrin (PCL-CD) polymersome is developed for localized and sustained co-delivery of hydrophilic and hydrophobic drug molecules. This PCL-CD polymersome affords multivalent crosslinking action via surface CD-mediated host-guest interactions to generate a supramolecular hydrogel that exhibits evident shear thinning and efficient self-healing behavior. The co-delivery of small molecule and proteinaceous agents by the encapsulated PCL-CD polymersomes enhances the differentiation of stem cells seeded in the hydrogel. Furthermore, the PCL-CD polymersomes are capable of in situ grafting to biological tissues via host-guest complexation between surface CD and native guest groups in the tissue matrix both in vitro and in vivo, thereby effectively extending the retention of loaded cargo in the grafted tissue. It is further demonstrated that the co-delivery of small molecule and proteinaceous drugs via PCL-CD polymersomes averts cartilage degeneration in animal osteoarthritic (OA) knee joints, which are known for their biochemically harsh and fluidically dynamic environment.

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Attenuation of subchondral bone abnormal changes in osteoarthritis by inhibition of SDF-1 signaling

Abstract: Higher level of SDF-1 may induce the subchondral bone abnormal changes in OA and inhibition of SDF-1 signaling could be a potential therapeutic approach for OA.

Cited by 36 publications

References 41 publications

Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post‐traumatic osteoarthritis

Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post‐traumatic osteoarthritis

Comparative effectiveness of two methods for inducing osteoarthritis in a novel animal model, the Diannan small-ear pig1

Bioadhesive Polymersome for Localized and Sustained Drug Delivery at Pathological Sites with Harsh Enzymatic and Fluidic Environment via Supramolecular Host–Guest Complexation

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