Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs.
Necroptosis is a programmed necrosis, regulated by receptor interacting protein kinase 1(RIP1) and receptor interacting protein kinase 3(RIP3), and could be inhibited by necrostatin-1(Nec-1) specifically. This study aims to evaluate the effect of Nec-1 on LPS-treated periodontal ligament stem cells...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2018-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC6248998?pdf=render |
| _version_ | 1828451739999666176 |
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| author | Bingbing Yan Hongmei Zhang Taiqiang Dai Yongchun Gu Xinyu Qiu Cheng Hu Yan Liu Kewen Wei Dehua Li |
| author_facet | Bingbing Yan Hongmei Zhang Taiqiang Dai Yongchun Gu Xinyu Qiu Cheng Hu Yan Liu Kewen Wei Dehua Li |
| author_sort | Bingbing Yan |
| collection | DOAJ |
| description | Necroptosis is a programmed necrosis, regulated by receptor interacting protein kinase 1(RIP1) and receptor interacting protein kinase 3(RIP3), and could be inhibited by necrostatin-1(Nec-1) specifically. This study aims to evaluate the effect of Nec-1 on LPS-treated periodontal ligament stem cells (PDLSCs). In the research, three groups were established: normal cultured PDLSCs, Porphyromonas gingivalis (Pg)-LPS stimulated PDLSCs and Pg-LPS+Nec-1 treated PDLSCs. The expression of RIP1 and RIP3 and osteogenic differentiation of PDLSCs in three groups were analyzed. Then, we constructed cell aggregates (CA) using PDLSCs, then PDLSCs-CA were combined with Bio-Oss in three groups were transplanted subcutaneously in nude mice to assess their potentials of periodontal tissue regeneration. The results showed that RIP1 and RIP3 were fully expressed in Pg-LPS stimulated PDLSCs and the level increased significantly. Nec-1 inhibited RIP1-RIP3 interaction, and further inhibited necroptosis of PDLSCs in inflammatory state. Moreover, Nec-1 pretreatment ameliorates the osteogenic differentiation of LPS-treated PDLSCs and can effectively promote the cementum like structure ectopic regenerative ability of PDLSCs in nude mice. These findings show RIP1/RIP3-mediated necroptosis is an important mechanism of cell death in PDLSCs. Nec-1 has a protective effect in reducing cell death and promotes ectopic periodontal tissue like structure regeneration by inhibiting necroptosis. Nec-1 is a hopeful therapeutic agent which protects cells from necroptosis and ameliorates functional outcome. |
| first_indexed | 2024-12-10T23:41:43Z |
| format | Article |
| id | doaj.art-282849d3f9c1427b9cf0ce41024b4418 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-10T23:41:43Z |
| publishDate | 2018-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-282849d3f9c1427b9cf0ce41024b44182022-12-22T01:29:01ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-011311e020776010.1371/journal.pone.0207760Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs.Bingbing YanHongmei ZhangTaiqiang DaiYongchun GuXinyu QiuCheng HuYan LiuKewen WeiDehua LiNecroptosis is a programmed necrosis, regulated by receptor interacting protein kinase 1(RIP1) and receptor interacting protein kinase 3(RIP3), and could be inhibited by necrostatin-1(Nec-1) specifically. This study aims to evaluate the effect of Nec-1 on LPS-treated periodontal ligament stem cells (PDLSCs). In the research, three groups were established: normal cultured PDLSCs, Porphyromonas gingivalis (Pg)-LPS stimulated PDLSCs and Pg-LPS+Nec-1 treated PDLSCs. The expression of RIP1 and RIP3 and osteogenic differentiation of PDLSCs in three groups were analyzed. Then, we constructed cell aggregates (CA) using PDLSCs, then PDLSCs-CA were combined with Bio-Oss in three groups were transplanted subcutaneously in nude mice to assess their potentials of periodontal tissue regeneration. The results showed that RIP1 and RIP3 were fully expressed in Pg-LPS stimulated PDLSCs and the level increased significantly. Nec-1 inhibited RIP1-RIP3 interaction, and further inhibited necroptosis of PDLSCs in inflammatory state. Moreover, Nec-1 pretreatment ameliorates the osteogenic differentiation of LPS-treated PDLSCs and can effectively promote the cementum like structure ectopic regenerative ability of PDLSCs in nude mice. These findings show RIP1/RIP3-mediated necroptosis is an important mechanism of cell death in PDLSCs. Nec-1 has a protective effect in reducing cell death and promotes ectopic periodontal tissue like structure regeneration by inhibiting necroptosis. Nec-1 is a hopeful therapeutic agent which protects cells from necroptosis and ameliorates functional outcome.http://europepmc.org/articles/PMC6248998?pdf=render |
| spellingShingle | Bingbing Yan Hongmei Zhang Taiqiang Dai Yongchun Gu Xinyu Qiu Cheng Hu Yan Liu Kewen Wei Dehua Li Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs. PLoS ONE |
| title | Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs. |
| title_full | Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs. |
| title_fullStr | Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs. |
| title_full_unstemmed | Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs. |
| title_short | Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs. |
| title_sort | necrostatin 1 promotes ectopic periodontal tissue like structure regeneration in lps treated pdlscs |
| url | http://europepmc.org/articles/PMC6248998?pdf=render |
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