MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts
Background Methionine adenosyl transferase II alpha (MAT2A) is the key enzyme to transform methionine into S-adenosylmethionine (SAM), the main methylgroup donor involved in the methylation. The purpose of our study wasto explore whether MAT2A-mediated methionine metabolism affected theexpression of...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | Journal of Oral Microbiology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/20002297.2023.2292375 |
| _version_ | 1826963082540220416 |
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| author | Lishan Jiang Jingwen Li Kun Ji Lang Lei Houxuan Li |
| author_facet | Lishan Jiang Jingwen Li Kun Ji Lang Lei Houxuan Li |
| author_sort | Lishan Jiang |
| collection | DOAJ |
| description | Background Methionine adenosyl transferase II alpha (MAT2A) is the key enzyme to transform methionine into S-adenosylmethionine (SAM), the main methylgroup donor involved in the methylation. The purpose of our study wasto explore whether MAT2A-mediated methionine metabolism affected theexpression of inflammatory cytokines in human gingival fibroblasts(hGFs).Methods Both healthy and inflamed human gingiva were collected. HGFs werecultured and treated with P. gingivalis, with or without MAT2Ainhibitor (PF9366), small interference RNA (siRNA), or extrinsic SAMpretreatment. The levels of inflammatory cytokines were detected byreal-time PCR, western blotting, and ELISA. SAM levels were detectedby ELISA. The nuclear factor-kappa B (NF-κB) and mitogen-activatedprotein kinase (MAPK) pathway was explored by western blotting.Results The expression of MAT2A was increased in the inflamed tissues. P.gingivalis infection promoted the expression of MAT2A and SAM inhGFs. Meanwhile, PF9366 and MAT2A-knockdown significantly decreasedexpression of inflammatory cytokines and SAM production. PF9366inhibited activation of NF-κB/MAPK pathway in P. gingivalis-treatedhGFs.Conclusions MAT2A-mediated methionine metabolism promoted P. gingivalis-inducedinflammation in hGFs. Targeting MAT2A may provide a novel therapeuticmethod for modulating periodontitis. |
| first_indexed | 2024-03-08T23:01:05Z |
| format | Article |
| id | doaj.art-06a7f1793a2d499d89f100135d638a66 |
| institution | Directory Open Access Journal |
| issn | 2000-2297 |
| language | English |
| last_indexed | 2025-02-18T02:34:37Z |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Journal of Oral Microbiology |
| spelling | doaj.art-06a7f1793a2d499d89f100135d638a662024-11-26T06:52:11ZengTaylor & Francis GroupJournal of Oral Microbiology2000-22972024-12-0116110.1080/20002297.2023.2292375MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblastsLishan Jiang0Jingwen Li1Kun Ji2Lang Lei3Houxuan Li4Nanjing Stomatological Hospital, Affiliated Hospital of medical School, Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Affiliated Hospital of medical School, Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Affiliated Hospital of medical School, Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Affiliated Hospital of medical School, Nanjing University, Nanjing, ChinaNanjing Stomatological Hospital, Affiliated Hospital of medical School, Nanjing University, Nanjing, ChinaBackground Methionine adenosyl transferase II alpha (MAT2A) is the key enzyme to transform methionine into S-adenosylmethionine (SAM), the main methylgroup donor involved in the methylation. The purpose of our study wasto explore whether MAT2A-mediated methionine metabolism affected theexpression of inflammatory cytokines in human gingival fibroblasts(hGFs).Methods Both healthy and inflamed human gingiva were collected. HGFs werecultured and treated with P. gingivalis, with or without MAT2Ainhibitor (PF9366), small interference RNA (siRNA), or extrinsic SAMpretreatment. The levels of inflammatory cytokines were detected byreal-time PCR, western blotting, and ELISA. SAM levels were detectedby ELISA. The nuclear factor-kappa B (NF-κB) and mitogen-activatedprotein kinase (MAPK) pathway was explored by western blotting.Results The expression of MAT2A was increased in the inflamed tissues. P.gingivalis infection promoted the expression of MAT2A and SAM inhGFs. Meanwhile, PF9366 and MAT2A-knockdown significantly decreasedexpression of inflammatory cytokines and SAM production. PF9366inhibited activation of NF-κB/MAPK pathway in P. gingivalis-treatedhGFs.Conclusions MAT2A-mediated methionine metabolism promoted P. gingivalis-inducedinflammation in hGFs. Targeting MAT2A may provide a novel therapeuticmethod for modulating periodontitis.https://www.tandfonline.com/doi/10.1080/20002297.2023.2292375S-adenosylmethionineMAT2Ainflammationgingival fibroblastsPorphyromonas gingivalis |
| spellingShingle | Lishan Jiang Jingwen Li Kun Ji Lang Lei Houxuan Li MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts Journal of Oral Microbiology S-adenosylmethionine MAT2A inflammation gingival fibroblasts Porphyromonas gingivalis |
| title | MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts |
| title_full | MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts |
| title_fullStr | MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts |
| title_full_unstemmed | MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts |
| title_short | MAT2A inhibition suppresses inflammation in Porphyromonas gingivalis-infected human gingival fibroblasts |
| title_sort | mat2a inhibition suppresses inflammation in porphyromonas gingivalis infected human gingival fibroblasts |
| topic | S-adenosylmethionine MAT2A inflammation gingival fibroblasts Porphyromonas gingivalis |
| url | https://www.tandfonline.com/doi/10.1080/20002297.2023.2292375 |
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