The role of stromal cell-derived factor 1 on cartilage development and disease

Li, Jiazhou; Chen, Hao; Zhang, Demao; Xie, Jing; Zhou, Xuedong

doi:10.1016/j.joca.2020.10.010

Cited by 48 publications

(41 citation statements)

References 97 publications

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“…Furthermore, as determined using the TIMER algorithm, various mutation types in the four hub genes, especially deletions, were signi cantly associated with immune cells in bladder cancer, and the deletion of hub genes can reduce the level of immune in ltration in multiple immune cell types (supplemental online Table 1 and Table 2). Additionally, we found that levels of both PLP1 and RELN were signi cantly associated with levels of CXCL12, which plays an important role in numerous physiological and pathological processes, including tumour metastasis 25 .…”

Section: Discussionmentioning

confidence: 82%

WITHDRAWN: Identification of Hub Genes related to the Progression of Bladder Cancer by an Integrated Bioinformatics Analysis

Wang

Chen

Liao

et al. 2021

Preprint

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BACKGROUND and OBJECTIVE: A better understanding of the molecular mechanisms underlying bladder cancer is necessary to identify candidate therapeutic targets. METHODS: We screened for genes associated with bladder cancer progression and prognosis. Publicly available expression data were obtained from TCGA and GEO to identify differentially expressed genes (DEGs) between bladder cancer and normal bladder tissues. Weighted co-expression networks were constructed, and Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Associations between hub genes and immune infiltration and immune therapy were evaluated. RESULTS: 3461 DEGs in TCGA-BC and 1069 DEGs in the GSE dataset were identified, with 87 overlapping differentially expressed genes between the bladder cancer and normal bladder groups. Hub genes in the tumour group were mainly enriched for cell proliferation-related GO terms and KEGG pathways, while hub genes in the normal group were related to the synthesis and secretion of neurotransmitters. PPI networks for the genes identified in the normal and tumour groups were constructed. Based on a survival analysis, CDH19, RELN, PLP1, and TRIB3 were significantly associated with prognosis (P < 0.05). Four hub genes were significantly enriched in the MAPK signalling pathway, VEGF signalling pathway, WNT signalling pathway, cell cycle, and P53 signalling pathway based on a gene set enrichment analysis; these genes were associated with immune infiltration levels in bladder cancer. CONCLUSIONS: CDH19, RELN, PLP1, and TRIB3 may play important roles in the development of bladder cancer and are potential therapeutic and prognostic targets.

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Section: Discussionmentioning

confidence: 82%

WITHDRAWN: Identification of Hub Genes related to the Progression of Bladder Cancer by an Integrated Bioinformatics Analysis

Wang

Chen

Liao

et al. 2021

Preprint

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“…1 C). Binding to CXCR4 on BMSCs, SDF-1 can drive cell migration in tissue repair after injury [ 38 , 39 ] or cartilage repair after osteoarthritis [ 40 , 41 ]. It has also been shown to induce the migration of BMSCs to other locations, such as the brain [ 42 ] and heart [ 43 ].…”

Section: Resultsmentioning

confidence: 99%

Exosomes derived from platelet-rich plasma administration in site mediate cartilage protection in subtalar osteoarthritis

et al. 2022

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Subtalar osteoarthritis (STOA) is often secondary to chronic ankle sprains, which seriously affects the quality of life of patients. Due to its etiology and pathogenesis was not studied equivocally yet, there is currently a lack of effective conservative treatments. Although they have been used for tissue repair, platelet-rich plasma-derived exosomes (PRP-Exo) have the disadvantage of low retention and short-lived therapeutic effects. This study aimed to determine whether incorporation of PRP-Exo in thermosensitive hydrogel (Gel) increased their retention in the joint and thereby playing a therapeutic role on STOA due to chronic mechanical instability established by transecting lateral ligaments (anterior talofibular ligament (ATFL)/calcaneal fibular ligament (CFL)). PRP-Exo incorporated Gel (Exo-Gel) system, composed of Poloxamer-407 and 188 mixture-based thermoresponsive hydrogel matrix in an optimal ratio, was determined by its release ability of Exo and rheology of Gel response to different temperature. The biological activity of Exo-Gel was evaluated in vitro, and the therapeutic effect of Exo-Gel on STOA was evaluated in vivo. Exo released from Exo-Gel continuously for 28 days could promote the proliferation and migration of mouse bone mesenchymal stem cells (mBMSCs) and chondrocytes, at the same time enhance the chondrogenic differentiation of mBMSCs, and inhibit inflammation-induced chondrocyte degeneration. In vivo experiments confirmed that Exo-Gel increased the local retention of Exo, inhibited the apoptosis and hypertrophy of chondrocytes, enhanced their proliferation, and potentially played the role in stem cell recruitment to delay the development of STOA. Thus, Delivery of PRP-Exo incorporated in thermosensitive Gel provides a novel approach of cell-free therapy and has therapeutic effect on STOA. Graphical Abstract

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“…For instance, various proinflammatory factors such as IL-1, MMP-13, and TNF-α are highly expressed in articular cartilage of OA. 147 - 149 In the deeper zone, chondrocytes undergo terminal differentiation, which can synthesize collagen type X (ColX), and this accelerates the progression of OA. 94 The calcified zone exhibited several pathological changes, manifested by vascularization, innervation from subchondral bone, and duplication of tidemark.…”

Section: Effect Of Tgf-β2 On Cartilage Diseasesmentioning

confidence: 99%

“… 157 Interestingly, studies indicated that TGF-β2 could effectively inhibit the progression of OA. 147 - 149 TGF-β2 not only inhibits the cleavage of Col2 but also suppresses the expression of hypertrophic markers such as Runx2, Col10a1, and MMP-13. 20 , 158 SnoN, which is induced by the TGF-β2/TAK1/p38 signalling pathway, can inhibit the expression of MMP13 by BMP/Smad1/5/8 signalling pathway in OA.…”

Section: Effect Of Tgf-β2 On Cartilage Diseasesmentioning

confidence: 99%

The role of TGF-β2 in cartilage development and diseases

Duan

Wang

Liu

et al. 2021

Bone & Joint Research

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Transforming growth factor-beta2 (TGF-β2) is recognized as a versatile cytokine that plays a vital role in regulation of joint development, homeostasis, and diseases, but its role as a biological mechanism is understood far less than that of its counterpart, TGF-β1. Cartilage as a load-resisting structure in vertebrates however displays a fragile performance when any tissue disturbance occurs, due to its lack of blood vessels, nerves, and lymphatics. Recent reports have indicated that TGF-β2 is involved in the physiological processes of chondrocytes such as proliferation, differentiation, migration, and apoptosis, and the pathological progress of cartilage such as osteoarthritis (OA) and rheumatoid arthritis (RA). TGF-β2 also shows its potent capacity in the repair of cartilage defects by recruiting autologous mesenchymal stem cells and promoting secretion of other growth factor clusters. In addition, some pioneering studies have already considered it as a potential target in the treatment of OA and RA. This article aims to summarize the current progress of TGF-β2 in cartilage development and diseases, which might provide new cues for remodelling of cartilage defect and intervention of cartilage diseases.

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The role of stromal cell-derived factor 1 on cartilage development and disease

Cited by 48 publications

References 97 publications

WITHDRAWN: Identification of Hub Genes related to the Progression of Bladder Cancer by an Integrated Bioinformatics Analysis

WITHDRAWN: Identification of Hub Genes related to the Progression of Bladder Cancer by an Integrated Bioinformatics Analysis

Exosomes derived from platelet-rich plasma administration in site mediate cartilage protection in subtalar osteoarthritis

The role of TGF-β2 in cartilage development and diseases

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