MiR-193b regulates early chondrogenesis by inhibiting the TGF-beta2 signaling pathway.
Cartilage generation and degradation are regulated by miRNAs. Our previous study has shown altered expression of miR-193b in chondrogenic human adipose-derived mesenchymal stem cells (hADSCs). In the current study, we investigated the role of miR-193b in chondrogenesis and cartilage degradation. Luciferase reporter assays showed that miR-193b targeted seed sequences of the TGFB2 and TGFBR3 3'-UTRs. MiR-193b suppressed the expression of early chondrogenic markers in chondrogenic ATDC5 cells, and TNF-alpha expression in IL-1b-induced PMCs. In conclusion, MiR-193b may inhibit early chondrogenesis by targeting TGFB2 and TGFBR3, and may regulate inflammation by repressing TNF-alpha expression in inflamed chondrocytes.
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Changhe
C
Hou
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Zibo
Z
Yang
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Yan
Y
Kang
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Ziji
Z
Zhang
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Ming
M
Fu
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China.
Aishan
A
He
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China. Electronic address: zhzhiqi@163.com.
Zhiqi
Z
Zhang
Joint Department, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China. Electronic address: lwmjoint@163.com.
Weiming
W
Liao
D020413:3' Untranslated Regions / Q000235:genetics; D000273:Adipose Tissue / Q000166:cytology; D000818:Animals; D015153:Blotting, Western; D002454:Cell Differentiation / Q000187:drug effects / Q000235:genetics; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology / Q000378:metabolism; D020219:Chondrogenesis / Q000235:genetics*; D050659:Core Binding Factor Alpha 1 Subunit / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D035683:MicroRNAs / Q000235:genetics*; D010766:Phosphorylation; D011509:Proteoglycans / Q000235:genetics* / Q000378:metabolism; D034622:RNA Interference; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D055758:SOX9 Transcription Factor / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics*; D051900:Smad3 Protein / Q000235:genetics / Q000378:metabolism; D053781:Transforming Growth Factor beta2 / Q000235:genetics* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D020413:3' Untranslated Regions; D050659:Core Binding Factor Alpha 1 Subunit; D053583:Interleukin-1beta; C546818:MIRN193 microRNA, human; D035683:MicroRNAs; D011509:Proteoglycans; D018125:Receptors, Transforming Growth Factor beta; D055758:SOX9 Transcription Factor; D051900:Smad3 Protein; D053781:Transforming Growth Factor beta2; D014409:Tumor Necrosis Factor-alpha; C071736:betaglycan
Chondrogenesis; MiR-193b; Osteoarthritis; TGF-beta; TNF-alpha