Research progress of long non-coding RNA H19 in osteoarthritis cartilage and subchondral boner

doi:10.3877/cma.j.issn.1674-134X.2021.06.007

Abstract

Abstract:

Long non-coding RNAs (lncRNAs) are a class of long non-coding RNAs about 200 bp in length that generally cannot be protein-encoded and have various biological functions. It is involved in the regulation of gene expression through transcriptional, translational and DNA epigenetic modifications. As a relatively nascent field, current research on lnc-RNA has focused on regulatory roles in the regulation of embryonic growth and stem cell differentiation as well as the development and progression of tumors. However, an increasing number of lncRNAs have been implicated as candidate regulators of inflammatory pathways associated with osteoarthritis pathology. In addition, more and more studies have found that lncRNAs are differentially expressed in osteoarthritic joint tissues. However, there are few reports on the correlation between lncRNAH19 and osteoarthritis (OA). Based on the latest research at home and abroad, this review focued on the regulatory mechanism of lncRNAH19 in osteoarthritis, including Notch signaling, wingless(Wnt)signaling, endogenous competitive RNAs (ceRNA), lnc-RNA/microRNA/messenger RNA(mRNA), etc. Determining the expression and functional roles of lncRNAs in osteoarthritis can not only advance the understanding of epigenetics underlying osteoarthritis pathology, but may ultimately help identify novel targets for therapeutic intervention.

Key words: RNA, long non-coding, Osteoarthritis

Hui Zheng, Yongyou Luo, Denghui Xie, Jianli Fang, Hang Fang, Rongkai Zhang. Research progress of long non-coding RNA H19 in osteoarthritis cartilage and subchondral boner[J]. Chinese Journal of Joint Surgery(Electronic Edition), 2021, 15(06): 693-699.

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References 57

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癌症	lncRNA H19表达水平	机制
乳腺癌	上调	lncRNA H19/miR-675
肝癌	上调	H19 /miR-193a-3p/PSEN1
胃肠道癌	上调	H19作为ceRNA通过抑制let-7c调节HER2表达
胰腺癌	上调	H19/miR-675/E2F-1
胶质瘤	上调	lncRNA H19/ miR-29a/ vasohibin 2 (VASH2)
膀胱癌	上调	H19增加miR-675表达，抑制p53的活化，减少Bax/Bcl-2和cyclin D1的表达，进而导致膀胱癌

癌症	lncRNA H19表达水平	机制
乳腺癌	上调	lncRNA H19/miR-675
肝癌	上调	H19 /miR-193a-3p/PSEN1
胃肠道癌	上调	H19作为ceRNA通过抑制let-7c调节HER2表达
胰腺癌	上调	H19/miR-675/E2F-1
胶质瘤	上调	lncRNA H19/ miR-29a/ vasohibin 2 (VASH2)
膀胱癌	上调	H19增加miR-675表达，抑制p53的活化，减少Bax/Bcl-2和cyclin D1的表达，进而导致膀胱癌

lncRNA种类	组织/细胞	表达水平	功能
H19	软骨细胞	上调	合成代谢功能^[42]
CIR	软骨细胞	上调	促进MMP-13和ADAMTS5的表达^[13]，同时抑制胶原和ACAN的生成
GAS5	软骨	下调	增加MMPs和ADAMTS4的表达，诱导凋亡^[39]
FOXD2- AS1	软骨细胞	上调	促进软骨细胞的增殖^[50]
HOTAIR	软骨细胞	上调	通过增强ADAMTS- 5 ^[51]在OA关节软骨细胞中其mRNA的稳定性来促进它的表达
ROR	软骨细胞	上调	调节细胞凋亡和软骨细胞自噬^[52]
ZFAS1	软骨细胞	下调	促进软骨细胞增殖^[53]
DANCR	软骨	上调	DANCR表达的抑制能够诱导OA细胞的凋亡^[54]
BLACAT1	骨髓间充质干细胞	上调	抑制BMSCs增殖，Caspase 3活性增加，ALP活性降低
MIR4435-2HG	软骨细胞	下调	抑制软骨细胞凋亡^[55]
TNFSF10	软骨细胞	上调	刺激软骨细胞的细胞增殖、抗凋亡和炎症^[56]
ANCR	软骨细胞	上调	ANCR过表达促进软骨细胞的增殖，抑制TGF-β1表达^[57]

lncRNA种类	组织/细胞	表达水平	功能
H19	软骨细胞	上调	合成代谢功能^[42]
CIR	软骨细胞	上调	促进MMP-13和ADAMTS5的表达^[13]，同时抑制胶原和ACAN的生成
GAS5	软骨	下调	增加MMPs和ADAMTS4的表达，诱导凋亡^[39]
FOXD2- AS1	软骨细胞	上调	促进软骨细胞的增殖^[50]
HOTAIR	软骨细胞	上调	通过增强ADAMTS- 5 ^[51]在OA关节软骨细胞中其mRNA的稳定性来促进它的表达
ROR	软骨细胞	上调	调节细胞凋亡和软骨细胞自噬^[52]
ZFAS1	软骨细胞	下调	促进软骨细胞增殖^[53]
DANCR	软骨	上调	DANCR表达的抑制能够诱导OA细胞的凋亡^[54]
BLACAT1	骨髓间充质干细胞	上调	抑制BMSCs增殖，Caspase 3活性增加，ALP活性降低
MIR4435-2HG	软骨细胞	下调	抑制软骨细胞凋亡^[55]
TNFSF10	软骨细胞	上调	刺激软骨细胞的细胞增殖、抗凋亡和炎症^[56]
ANCR	软骨细胞	上调	ANCR过表达促进软骨细胞的增殖，抑制TGF-β1表达^[57]

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