Stomatology ›› 2022, Vol. 42 ›› Issue (11): 966-973.doi: 10.13591/j.cnki.kqyx.2022.11.002

• Basic Research • Previous Articles     Next Articles

Impacts of LncRNA MALAT1 on human periodontal ligament stem cells by regulating miR-383-5p/SOCS3 axis

GU Tingli, LIU Yahua, QIAN Liang, ZHANG Qian   

  1. Department of Oral and Maxillofacial Surgery, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing 210008, China
  • Received:2022-05-29 Online:2022-11-28 Published:2022-11-25

Abstract: Objective To investigate the impacts of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the proliferation, apoptosis and osteogenic differentiation of lipopolysaccharide (LPS)-stimulated human periodontal ligament stem cells (hPDLSCs) by regulating the microRNA-383-5p (miR-383-5p)/suppressor of cytokine signaling 3 (SOCS3) axis. Methods hPDLSCs were treated with LPS and transfected with small interfering RNA targeting MALAT1 (si-MALAT1) or miR-383-5p inhibitor (in-miR-383-5p) or SOCS3 overexpression plasmid (SOCS3). ELISA was implemented to detect inflammatory factor levels; RT-qPCR and Western blot were used to check transfection efficiency; CCK-8 and TUNEL were implemented to detect cell proliferation and apoptosis;alkaline phosphatase (ALP) staining and alizarin red S (ARS) staining were performed to analyze osteogenic differentiation; Western blot was implemented to measure the proliferation, apoptosis and osteogenic differentiation-related proteins. Bioinformatics and dual-luciferase experiments were performed to analyze the relationship between miR-383-5p and MALAT1/SOCS3. Results LPS induced the inflammation and apoptosis of hPDLSCs, and down-regulated cell proliferation and osteogenic differentiation. In the meantime, the expressions of MALAT1 and SOCS3 were up-regulated, and the expression of miR-383-5p was down-regulated (P<0.05).Knockdown of MALAT1 could greatly reduce LPS-induced inflammatory response and apoptosis of hPDLSCs, and increase cell proliferation and osteogenic differentiation. Meanwhile, it also up-regulated the expression of miR-383-5p and down-regulated the expression of SOCS3 (P<0.05). In addition, reverse experiments showed that inhibiting miR-383-5p expression or up-regulating SOCS3 expression could partially reverse the effects of MALAT1 knockdown on LPS-induced hPDLSCs (P<0.05). Further analysis confirmed that MALAT1 targeted the regulation of SOCS3 expression by sponging miR-383-5p (P<0.05). Conclusion Knockdown of MALAT1 can modulate the miR-383-5p/SOCS3 axis to improve the proliferation, apoptosis and osteogenic differentiation of inflammatory hPDLSCs.

Key words: long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, microRNA-383-5p, suppressor of cytokine signaling 3, human periodontal ligament stem cells

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