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Phosphatidic acid-induced elevation of intracellular Ca2+ is mediated by RhoA and H2O2 in Rat-2 fibroblasts
- Source :
- The Journal of biological chemistry. 273(21)
- Publication Year :
- 1998
-
Abstract
- We have investigated possible roles of RhoA and H2O2 in the elevation of intracellular Ca2+ ([Ca2+]i) by phosphatidic acid (PA) in Rat-2 fibroblasts. PA induced a transient elevation of [Ca2+]i in the presence or absence of EGTA. Lysophosphatidic acid (LPA) also increased [Ca2+]i, but the sustained Ca2+response was inhibited by EGTA. LPA stimulated the production of inositol phosphates, but PA did not. In the presence of EGTA, preincubation with LPA completely blocked the subsequent elevation of [Ca2+]i by PA, but not vice versa. PA stimulated the translocation of RhoA to the particulate fraction as did LPA. Scrape loading of C3 transferase inhibited the transient Ca2+ response to PA, but not to LPA, suggesting an essential role of RhoA in the elevation of [Ca2+]i by PA. H2O2 also induced a transient increase of [Ca2+]i as did PA. H2O2 scavengers, catalase andN-acetyl-l-cysteine, completely blocked the rise of [Ca2+]i stimulated by PA, but not by LPA. Furthermore, preincubation with PA blocked the subsequent Ca2+ response to H2O2, and the incubation with H2O2 also blocked the PA-induced rise of [Ca2+]i. Thus, it was suggested that PA stimulated Ca2+ release from PA-sensitive, but not inositol 1,4,5-trisphosphate-sensitive, Ca2+ stores by the activation of RhoA and intracellular H2O2.
- Subjects :
- RHOA
Phosphatidic Acids
Biology
Biochemistry
Cell Line
chemistry.chemical_compound
GTP-Binding Proteins
Lysophosphatidic acid
Animals
Inositol
Molecular Biology
Incubation
Cell Biology
Phosphatidic acid
Hydrogen Peroxide
Molecular biology
Rats
EGTA
chemistry
Catalase
biology.protein
lipids (amino acids, peptides, and proteins)
Calcium
rhoA GTP-Binding Protein
Intracellular
Subjects
Details
- ISSN :
- 00219258
- Volume :
- 273
- Issue :
- 21
- Database :
- OpenAIRE
- Journal :
- The Journal of biological chemistry
- Accession number :
- edsair.doi.dedup.....6356b2889a635f15cb77c31c34af10c6