Comparison of microRNA expression profiles of Kashin-Beck disease, osteoarthritis and rheumatoid arthritis

Wu, Wenhong; He, Awen; Wen, Yan; Xiao, Xiao; Hao, Jingcan; Zhang, Feng; Guo, Xiong

doi:10.1038/s41598-017-00522-z

Cited by 20 publications

(16 citation statements)

References 31 publications

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“…In human studies, Wu and colleagues examined the miRNA expression profiles of cartilage samples from OA, RA, and Kashin-Beck disease 28 . They found 18 differentially expressed miRNAs which were shared between KBD and OA vs. RA patients, including several with previous links to OA.…”

Section: Epigenetics: Noncoding Rnasmentioning

confidence: 99%

Osteoarthritis year in review 2017: genetics and epigenetics

Peffers¹,

Balaskas²,

Smagul³

2018

Osteoarthritis and Cartilage

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Section: Epigenetics: Noncoding Rnasmentioning

confidence: 99%

Osteoarthritis year in review 2017: genetics and epigenetics

Peffers¹,

Balaskas²,

Smagul³

2018

Osteoarthritis and Cartilage

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“…Meanwhile, adult KBD patients typically have advanced KBD, often accompanied by OA 4,6 . Recent studies have found differences in various cellular pathways between KBD and OA chondrocytes 5,7,8 , suggesting differences in multiple processes, such as metabolism, apoptosis, adaptive immune defence, cytoskeleton, cell movement and extracellular matrix turnover 4,[9][10][11][12] . However, these studies do not take into consideration the heterogeneity of articular cartilage cell types and therefore may be missing important information on cartilage degeneration processes specific to KBD or OA.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the major cell populations among osteoarthritis, Kashin–Beck disease and healthy chondrocytes by single-cell RNA-seq analysis

Ning

Zhang

et al. 2021

Cell Death Dis

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Chondrocytes are the key target cells of the cartilage degeneration that occurs in Kashin–Beck disease (KBD) and osteoarthritis (OA). However, the heterogeneity of articular cartilage cell types present in KBD and OA patients and healthy controls is still unknown, which has prevented the study of the pathophysiology of the mechanisms underlying the roles of different populations of chondrocytes in the processes leading to KBD and OA. Here, we aimed to identify the transcriptional programmes and all major cell populations in patients with KBD, patients with OA and healthy controls to identify the markers that discriminate among chondrocytes in these three groups. Single-cell RNA sequencing was performed to identify chondrocyte populations and their gene signatures in KBD, OA and healthy cells to investigate their differences as related to the pathogenetic mechanisms of these two osteochondral diseases. We performed immunohistochemistry and quantitative reverse-transcription PCR (qRT-PCR) assays to validate the markers for chondrocyte population. Ten clusters were labelled by cell type according to the expression of previously described markers, and one novel population was identified according to the expression of a new set of markers. The homeostatic and mitochondrial chondrocyte populations, which were identified by the expression of the unknown markers MT1X and MT2A and MT-ND1 and MT-ATP6, were markedly expanded in KBD. The regulatory chondrocyte population, identified by the expression of CHI3L1, was markedly expanded in OA. Our study allows us to better understand the heterogeneity of chondrocytes in KBD and OA and provides new evidence of differences in the pathogenetic mechanisms between these two diseases.

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“…Epigenetics enables tight control of gene expression at the transcriptional level, resulting in changes in chromatin 3D structure, and at the translational level (microRNAs (miRNAs), long noncoding RNAs (lncRNAs), mRNA editing and mRNA stability) affecting protein expression [18]. The deregulation and dysfunction of mRNAs [19][20][21][22], lncRNAs [23,24] and miRNAs [25][26][27][28] in OA have been reported. Previously, Fu et al [23] revealed that a total of 710 mRNAs were differentially expressed in OA tissues.…”

Section: Introductionmentioning

confidence: 99%

LINC00623/miR-101/HRAS axis modulates IL-1β-mediated ECM degradation, apoptosis and senescence of osteoarthritis chondrocytes

Wang

et al. 2020

Aging

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Chondrocyte apoptosis and extracellular matrix (ECM) degeneration have been implicated in the pathogenesis of osteoarthritis (OA). Based on previously reported microarray analysis, HRAS (Harvey rat sarcoma viral oncogene homolog), a member of the RAS protein family, was chosen as a potential regulator of OA chondrocyte apoptosis and ECM degradation. HRAS expression was downregulated in OA tissues, particularly in mild-OA tissues. HRAS overexpression partially attenuated IL-1β-induced OA chondrocyte apoptosis and ECM degradation. Similar to HRAS, the long non-coding RNA LINC00623 was downregulated in OA tissues. LINC00623 knockdown enhanced IL-1β-induced OA chondrocyte apoptosis and ECM degradation, which could be partially reversed by HRAS overexpression. It has been reported that lncRNAs act as ceRNAs of miRNAs to exert their function. Herein, miR-101 was predicted to bind to both LINC00623 and HRAS, which was further confirmed by luciferase reporter and RIP assays. LINC00623 competed with HRAS for miR-101 binding, therefore reducing the inhibitory effect of miR-101 on HRAS expression. More importantly, the effect of LINC00623 was partially eliminated by miR-101 inhibition. Overall, the LINC00623/miR-101/HRAS axis modulates OA chondrocyte apoptosis, senescence and ECM degradation through MAPK signaling, which might play a critical role in OA development.

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Comparison of microRNA expression profiles of Kashin-Beck disease, osteoarthritis and rheumatoid arthritis

Cited by 20 publications

References 31 publications

Osteoarthritis year in review 2017: genetics and epigenetics

Osteoarthritis year in review 2017: genetics and epigenetics

Comparison of the major cell populations among osteoarthritis, Kashin–Beck disease and healthy chondrocytes by single-cell RNA-seq analysis

LINC00623/miR-101/HRAS axis modulates IL-1β-mediated ECM degradation, apoptosis and senescence of osteoarthritis chondrocytes

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