Salinomycin causes dedifferentiation via the extracellular signal-regulated kinase (ERK) pathway in rabbit articular chondrocytes

Yu, Seon‐Mi; Kim, Song Ja

doi:10.1016/j.jphs.2014.12.009

Cited by 14 publications

(7 citation statements)

References 27 publications

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“…TQ-induced inflammation is mediated by the phosphoinositide 3-kinase (PI3K) and p38 pathways, while PEP-1-SIRT2-induced inflammation is mediated by the p38 and ERK pathways. The authors also reported that salinomycin (SAL) causes the dedifferentiation of rabbit articular chondrocytes via the ERK pathway, as determined by increased ERK activity without alterations in JNK and p38 activity following treatment with SAL 79 . Recently, the authors revealed that PEP-1-glutaredoxin-1 increased endoplasmic reticulum-stress and then stimulated the dedifferentiation of rabbit chondrocytes via the ERK-1/2 pathway 75 .…”

Section: Introductionmentioning

confidence: 97%

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Yao

Wang

2020

npj Regen Med

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Cell dedifferentiation is the process by which cells grow reversely from a partially or terminally differentiated stage to a less differentiated stage within their own lineage. This extraordinary phenomenon, observed in many physiological processes, inspires the possibility of developing new therapeutic approaches to regenerate damaged tissue and organs. Meanwhile, studies also indicate that dedifferentiation can cause pathological changes. In this review, we compile the literature describing recent advances in research on dedifferentiation, with an emphasis on tissue-specific findings, cellular mechanisms, and potential therapeutic applications from an engineering perspective. A critical understanding of such knowledge may provide fresh insights for designing new therapeutic strategies for regenerative medicine based on the principle of cell dedifferentiation.

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Section: Introductionmentioning

confidence: 97%

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Yao

Wang

2020

npj Regen Med

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“…The observation of aggrecan fluorescent staining in cells isolated from rabbit knee cartilage indicates isolated chondrocyte activity ( Figure 5 E). Furthermore, Sox-9 played a crucial role in the specific activation of collagen type II, and was a key transcriptional regulator of chondrocyte differentiation, demonstrating it to be an important protein for chondrocyte expression [ 38 , 41 , 42 ]. Sox9 was observed by fluorescent staining, indicating chondrocyte expression, as shown in Figure 5 F.…”

Section: Resultsmentioning

confidence: 99%

Highly Organized Porous Gelatin-Based Scaffold by Microfluidic 3D-Foaming Technology and Dynamic Culture for Cartilage Tissue Engineering

Liu

et al. 2022

IJMS

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A gelatin-based hydrogel scaffold with highly uniform pore size and biocompatibility was fabricated for cartilage tissue engineering using microfluidic 3D-foaming technology. Mainly, bubbles with different diameters, such as 100 μm and 160 μm, were produced by introducing an optimized nitrogen gas and gelatin solution at an optimized flow rate, and N2/gelatin bubbles were formed. Furthermore, a cross-linking agent (1-ethyl-3-(3-dimethyl aminopropyl)-carbodiimide, EDC) was employed for the cross-linking reaction of the gelatin-based hydrogel scaffold with uniform bubbles, and then the interface between the close cells were broken by degassing. The pore uniformity of the gelatin-based hydrogel scaffolds was confirmed by use of a bright field microscope, conjugate focus microscope and scanning electron microscope. The in vitro degradation rate, mechanical properties, and swelling rate of gelatin-based hydrogel scaffolds with highly uniform pore size were studied. Rabbit knee cartilage was cultured, and its extracellular matrix content was analyzed. Histological analysis and immunofluorescence staining were employed to confirm the activity of the rabbit knee chondrocytes. The chondrocytes were seeded into the resulting 3D porous gelatin-based hydrogel scaffolds. The growth conditions of the chondrocyte culture on the resulting 3D porous gelatin-based hydrogel scaffolds were evaluated by MTT analysis, live/dead cell activity analysis, and extracellular matrix content analysis. Additionally, a dynamic culture of cartilage tissue was performed, and the expression of cartilage-specific proteins within the culture time was studied by immunofluorescence staining analysis. The gelatin-based hydrogel scaffold encouraged chondrocyte proliferation, promoting the expression of collagen type II, aggrecan, and sox9 while retaining the structural stability and durability of the cartilage after dynamic compression and promoting cartilage repair.

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“…The knee joint was a common sight of OA [6] , cartilage degeneration will affect the physiological function of chondrocytes [21] . The classical Wnt/β-catenin pathway regulates the bone metabolism and bone formation and the development and remodeling of cartilage tissue, which was related to OA [8,22] .…”

Section: Protein and Mrna Expression Of Wnt-1 β-Catenin And Gsk-3β In Chondrocytesmentioning

confidence: 99%

“…PRP can treat skeletal muscle injury [24] and release the growth factors involved in cartilage repair to promote cartilage regeneration [28] . Intra-articular injection of PRP can improve the International Knee Documentation Committee (IKDC) score of patients with knee cartilage degeneration [20] , while PRP can promote the proliferation of rabbit auricle chondrocytes in vitro [21] .…”

Section: Protein and Mrna Expression Of Wnt-1 β-Catenin And Gsk-3β In Chondrocytesmentioning

confidence: 99%

Platelet Rich Plasma Regulates Wnt/Beta-Catenin Signal Pathway in Rabbit Chondrocytes by Mediating Interleukin 1 Beta

Zuo¹,

Sun²,

Xie³

et al. 2021

ijps

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It was reported that platelet rich plasma can reduce the degeneration of articular cartilage. The purpose of this study was to investigate the effect of platelet rich plasma on Wnt/beta-catenin signal transduction in rabbit chondrocytes. Platelet rich plasma was prepared from the ear vein blood of 3-mo old New Zealand white rabbits. Chondrocytes were isolated from knee cartilage and cultured. The cell identification and the effect of platelet rich plasma on the viability of chondrocytes were measured by the C-terminal telopeptide II and proteoglycan staining. Chondrocytes were divided into 5 groups, control group, interleukin-1 beta group, platelet rich plasma (100 x dilutions) group, Dickkopf WNT signaling pathway inhibitor 1 (100 ng/mL) group and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group. After being treated with interleukin-1 beta (50 μL, 10 μg/mL) for 24 h, the morphology of chondrocytes was observed by an electron microscope. The levels of C-terminal telopeptide II and cartilage oligomeric matrix protein in the culture medium were determined by enzyme linked immunosorbent assay. The messenger RNA and protein expression levels of Wnt-1, beta-catenin and glycogen synthase kinase 3 beta were detected by Real-time polymerase chain reaction and Western blot respectively. Platelet rich plasma promotes the proliferation of chondrocytes. The chondrocytes in the interleukin-1 beta group showed an ultrastructural abnormality, which was not obvious in platelet rich plasma group, Dickkopf WNT signaling pathway inhibitor 1group, and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group. The concentrations of C-terminal telopeptide II and cartilage oligomeric matrix protein in the interleukin-1 beta group were higher than those in the control group, platelet rich plasma group, Dickkopf WNT signaling pathway inhibitor 1group and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group. Compared with the control group, platelet rich plasma group, Dickkopf WNT signaling pathway inhibitor 1group and Dickkopf WNT signaling pathway inhibitor 1+platelet rich plasma group, the expression of Wnt1 and beta-catenin was higher and the level of glycogen synthase kinase 3 beta was lower in the interleukin-1 beta group. Platelet rich plasma may protect interleukin-1 beta activated chondrocytes by inhibiting Wnt/beta-catenin signal.

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Salinomycin causes dedifferentiation via the extracellular signal-regulated kinase (ERK) pathway in rabbit articular chondrocytes

Cited by 14 publications

References 27 publications

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Dedifferentiation: inspiration for devising engineering strategies for regenerative medicine

Highly Organized Porous Gelatin-Based Scaffold by Microfluidic 3D-Foaming Technology and Dynamic Culture for Cartilage Tissue Engineering

Platelet Rich Plasma Regulates Wnt/Beta-Catenin Signal Pathway in Rabbit Chondrocytes by Mediating Interleukin 1 Beta

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