Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts
<p>Abstract</p> <p>p38 MAP kinase is known to be activated by cellular stress finally leading to cell cycle arrest or apoptosis. Furthermore, a tumour suppressor role of p38 MAPK has been proposed. In contrast, a requirement of p38 for proliferation has also been described. To clar...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2012-03-01
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| Series: | Cell Communication and Signaling |
| Subjects: | |
| Online Access: | http://www.biosignaling.com/content/10/1/6 |
| _version_ | 1818084673882947584 |
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| author | Faust Dagmar Schmitt Christina Oesch Franz Oesch-Bartlomowicz Barbara Schreck Ilona Weiss Carsten Dietrich Cornelia |
| author_facet | Faust Dagmar Schmitt Christina Oesch Franz Oesch-Bartlomowicz Barbara Schreck Ilona Weiss Carsten Dietrich Cornelia |
| author_sort | Faust Dagmar |
| collection | DOAJ |
| description | <p>Abstract</p> <p>p38 MAP kinase is known to be activated by cellular stress finally leading to cell cycle arrest or apoptosis. Furthermore, a tumour suppressor role of p38 MAPK has been proposed. In contrast, a requirement of p38 for proliferation has also been described. To clarify this paradox, we investigated <it>stress</it>- and <it>mitogen</it>-induced p38 signalling in the same cell type using fibroblasts. We demonstrate that - in the same cell line - p38 is activated by mitogens or cellular stress, but p38-dependent signalling is different. Exposure to cellular stress, such as anisomycin, leads to a strong and persistent p38 activation independent of GTPases. As a result, MK2 and downstream the transcription factor CREB are phosphorylated. In contrast, mitogenic stimulation results in a weaker and transient p38 activation, which upstream involves small GTPases and is required for cyclin D1 induction. Consequently, the retinoblastoma protein is phosphorylated and allows G1/S transition. Our data suggest a dual role of p38 and indicate that the level and/or duration of p38 activation determines the cellular response, i.e either proliferation or cell cycle arrest.</p> |
| first_indexed | 2024-12-10T19:57:38Z |
| format | Article |
| id | doaj.art-4c3ddcd4a0d34c8a9bb8c959a1c23b4f |
| institution | Directory Open Access Journal |
| issn | 1478-811X |
| language | English |
| last_indexed | 2024-12-10T19:57:38Z |
| publishDate | 2012-03-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell Communication and Signaling |
| spelling | doaj.art-4c3ddcd4a0d34c8a9bb8c959a1c23b4f2022-12-22T01:35:37ZengBMCCell Communication and Signaling1478-811X2012-03-01101610.1186/1478-811X-10-6Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblastsFaust DagmarSchmitt ChristinaOesch FranzOesch-Bartlomowicz BarbaraSchreck IlonaWeiss CarstenDietrich Cornelia<p>Abstract</p> <p>p38 MAP kinase is known to be activated by cellular stress finally leading to cell cycle arrest or apoptosis. Furthermore, a tumour suppressor role of p38 MAPK has been proposed. In contrast, a requirement of p38 for proliferation has also been described. To clarify this paradox, we investigated <it>stress</it>- and <it>mitogen</it>-induced p38 signalling in the same cell type using fibroblasts. We demonstrate that - in the same cell line - p38 is activated by mitogens or cellular stress, but p38-dependent signalling is different. Exposure to cellular stress, such as anisomycin, leads to a strong and persistent p38 activation independent of GTPases. As a result, MK2 and downstream the transcription factor CREB are phosphorylated. In contrast, mitogenic stimulation results in a weaker and transient p38 activation, which upstream involves small GTPases and is required for cyclin D1 induction. Consequently, the retinoblastoma protein is phosphorylated and allows G1/S transition. Our data suggest a dual role of p38 and indicate that the level and/or duration of p38 activation determines the cellular response, i.e either proliferation or cell cycle arrest.</p>http://www.biosignaling.com/content/10/1/6p38 MAPKSignallingCellular stressMitogensFibroblasts |
| spellingShingle | Faust Dagmar Schmitt Christina Oesch Franz Oesch-Bartlomowicz Barbara Schreck Ilona Weiss Carsten Dietrich Cornelia Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts Cell Communication and Signaling p38 MAPK Signalling Cellular stress Mitogens Fibroblasts |
| title | Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts |
| title_full | Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts |
| title_fullStr | Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts |
| title_full_unstemmed | Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts |
| title_short | Differential p38-dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts |
| title_sort | differential p38 dependent signalling in response to cellular stress and mitogenic stimulation in fibroblasts |
| topic | p38 MAPK Signalling Cellular stress Mitogens Fibroblasts |
| url | http://www.biosignaling.com/content/10/1/6 |
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