Two non-coding RNAs, MicroRNA-101 and HOTTIP contribute cartilage integrity by epigenetic and homeotic regulation of integrin-α1

Kim, Dongkyun; Song, Jinping; Han, Jiyeon; Kim, Yunha; Chun, Churl Hong; Jin, Eun‐Jung

doi:10.1016/j.cellsig.2013.08.034

Cited by 67 publications

(56 citation statements)

References 74 publications

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“…HOTTIP expression has been observed to elevate in developing hind limbs, and it is implicated in bat wing development [25]. HOTTIP has also been shown to be significantly upregulated in the chondrocytes of osteoarthritis, and it has been demonstrated to regulate cartilage integrity [26]. The present study is the first to evaluate the role of HOTTIP in liver fibrosis and confirmed that HOTTIP dysregulation is associates with in vivo HSC activation.…”

Section: Discussionsupporting

confidence: 50%

Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a

Li¹,

Wang²,

Zeng³

et al. 2018

Cell Physiol Biochem

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Background/Aims: HOTTIP is a critical modulator in human diseases including liver cancer, but its role and molecular biological mechanisms in liver fibrosis are still unclear. Methods: The expression profile of HOTTIP during the progression of liver fibrosis was detected in human liver samples and in CCl₄-treated mice using qRT-PCR. The expressing sh-HOTTIP adenoviral vector was used to reduce HOTTIP levels in vivo. Dual-Luciferase Reporter Assay was performed to validate the interaction between miR-148a and HOTTIP, TGFBR1, or TGFBR2. Results: HOTTIP expressions in fibrotic liver samples and cirrhotic liver samples were significantly upregulated compared with healthy liver controls, and cirrhotic samples exhibited the highest levels of HOTTIP. Moreover, HOTTIP expressions were substantially induced in the liver tissues and hepatic stellate cells (HSC) of CCl₄-treated mice. Ad-shHOTTIP delivery could alleviate CCl₄- induced liver fibrosis in mice. Down-regulation of HOTTIP inhibited the viability and activation of HSCs in vitro, and HOTTIP negatively regulated miR-148a expression in HSCs. miR-148a had a negative effect on HSC activation by targeting TGFBR1 and TGFBR2. Conclusion: HOTTIP is involved in the progression of liver fibrosis by promoting HSC activation. The high level of HOTTIP downregulates miR-148a, thus to increase the level of TGFBR1 and TGFBR2 and contribute to liver fibrosis.

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Section: Discussionsupporting

confidence: 50%

Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a

Li¹,

Wang²,

Zeng³

et al. 2018

Cell Physiol Biochem

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“…Subsequently, H19 was found to be significantly elevated in osteoarthritic cartilage (Steck et al 2012). Several well-known lncRNAs (PTENP1, HOTAIR, TUG1, HOTTIP, GAS5) were found to have increased expression in osteoarthritic chondrocytes compared to normal tissue, while others were downregulated (SNHG4, Emx2os, DISC2) when lncRNA profiles were investigated by qPCR array (Kim et al 2013). Interestingly in this study, it was noted that HOTTIP expression was changed 10-fold between in the cartilage of arthritic patients.…”

Section: Chondrogenesis and Osteoarthritismentioning

confidence: 99%

Could lncRNAs be the Missing Links in Control of Mesenchymal Stem Cell Differentiation?

Tye

Gordon

Martin-Buley

et al. 2014

Journal Cellular Physiology

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Long suspected, recently recognized, and increasingly studied, non protein-coding RNAs (ncRNAs) are emerging as key drivers of biological control and pathology. Since their discovery in 1993, microRNAs (miRNAs) have been the subject of intense research focus and investigations have revealed striking findings, establishing that these molecules can exert multiples levels of biological control in numerous tissues. More recently, long ncRNAs (lncRNAs), the lesser-studied siblings of miRNA, have been suggested to have a similar robust role in developmental and adult tissue regulation. Mesenchymal stem cells (MSCs) are an important source of multipotent cells for normal and therapeutic tissue repair. Much is known about the critical role of miRNAs in biogenesis and differentiation of MSCs however; recent studies have suggested lncRNAs may play an equally important role in the regulation of these cells. Here we highlight the role of lncRNAs in the regulation of mesenchymal stem cell lineages including adipocytes, chondrocytes, myoblasts and osteoblasts. In addition, the potential for these noncoding RNAs to be used as biomarkers for disease or therapeutic targets is also discussed.

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“…Several studies have indicated that altered levels of miRNAs and lncRNAs could result in aberrant expressions of a gene that contributes to a variety of disease states and biological functions [6-8]. Literature has reported that alterations in non-coding genes can contribute to OA pathogenesis [9]. Synovial fluid microRNA signature is correlated with knee osteoarthritis stage, and microRNA-181a-5p and microRNA-4454 are known mediators of facet cartilage degeneration [10, 11].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA CIR Promotes Chondrocyte Extracellular Matrix Degradation in Osteoarthritis by Acting as a Sponge For Mir-27b

Li¹,

Li²,

Liu³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation. The degradation of the extracellular matrix (ECM) of chondrocyte is closely associated with the destruction of joints in OA patients. lncRNAs are non-coding segments of RNA that possess important regulatory functions at the cellular level and in a variety of pathophysiological processes. The present study was conducted to investigate whether lncRNA-CIR regulated the expression of MMP13 as a sponge of miR-27 in OA. Methods: Primary cultured chondrocytes were challenged by IL-1β and TNF-α to simulate OA conditions. qRT-PCR was performed to detect the miR-27, lncRNA-CIR, MMP13 mRNA expression levels. Western blot was applied to detect MMP13 protein expression. Soluble sGAG secretion/ formation was analysed by the dimethylmethylene blue (DMMB) assay. lncRNA-CIR overexpression or inhibition was performed using overexpression plasmid and small interfering RNAs (siRNAs), respectively. Results: lncRNA-CIR significantly up-regulated in OA patients, concomitantly down-regulated miR-27 and up-regulated MMP13. Bioinformatics analysis predicted miR-27 was the target of both lncRNA-CIR and MMP13. Overexpression of lncRNA-CIR significantly increased the expression of MMP13, while miR-27 remarkably suppressed the expression of MMP13, Accompanying with the increases of mRNA level, protein level and relative luciferase activity. Conclusion: The present findings indicated that lncRNA-CIR/miR-27/MMP13 axis involved in the degradation of the ECM of chondrocyte in OA.

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Two non-coding RNAs, MicroRNA-101 and HOTTIP contribute cartilage integrity by epigenetic and homeotic regulation of integrin-α1

Cited by 67 publications

References 74 publications

Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a

Long Noncoding RNA HOTTIP Promotes Mouse Hepatic Stellate Cell Activation via Downregulating miR-148a

Could lncRNAs be the Missing Links in Control of Mesenchymal Stem Cell Differentiation?

Long Noncoding RNA CIR Promotes Chondrocyte Extracellular Matrix Degradation in Osteoarthritis by Acting as a Sponge For Mir-27b

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