Suppression of phosphorylated MAPK and caspase 3 by carbon dioxide
| Autor: | Vijayan Elimban, Yan-Jun Xu, Naranjan S. Dhalla |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine MAPK/ERK pathway p38 mitogen-activated protein kinases Clinical Biochemistry Caspase 3 030204 cardiovascular system & hematology Biology Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Phosphorylation Extracellular Signal-Regulated MAP Kinases Muscle Skeletal Molecular Biology Protein kinase B Gasotransmitters Skeletal muscle Cell Biology General Medicine Carbon Dioxide Rats Cell biology Vascular endothelial growth factor 030104 developmental biology medicine.anatomical_structure chemistry Biochemistry Signal transduction |
| Zdroj: | Molecular and Cellular Biochemistry. 436:23-28 |
| ISSN: | 1573-4919 0300-8177 |
| Popis: | Although CO2 is produced during the oxidation of different substrates in all types of cells, the role of this gas in the regulation of cellular function is not clearly understood. Since changes in several signal transduction as well as apoptotic, anti-apoptotic, and other proteins are known to modify cellular function, we investigated if some of these proteins are altered upon incubating the rat hind leg skeletal muscle in a medium enriched with CO2 (1000–1200 ppm) for 30 min. CO2 was observed to depress phosphorylated levels of ERK1 (P44) and ERK2 (P42) without affecting the unphosphorylated content of these MAPK proteins. On the other hand, no change in p38 MAPK protein was found but the content of its degradation product 30 kDa proteins (both phosphorylated and unphosphorylated) was decreased. No alterations in the content of other signaling proteins (PKA and Akt), inflammatory molecule (TNF-α), and vascular endothelial growth factor (VEGF) were seen upon exposure of the muscle to CO2. The content for apoptotic and anti-apoptotic proteins (Bad and Bcl2), except for a decrease in caspase 3, were also not affected by CO2. These results indicate that CO2 may serve as a gasotransmitter to regulate cellular function by depressing MAPK and caspase 3 activities. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink