ArticleWorld journal of gastroenterology2005
Differential phosphorylation of p38 induced by apoptotic and anti-apoptotic stimuli in murine hepatocytes.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Novel therapeutic strategies and perspectives for pancreatic cancer: Autophagy and apoptosis are key mechanisms to fight pancreatic cancer.Medical oncology (Northwood, London, England) · 2021Review
- The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress-Driven Mucus Depletion and Exacerbates Intestinal Inflammation.Cellular and molecular gastroenterology and hepatology · 2019Article
- A triterpenoid saponin from Adenophora triphylla var. japonica suppresses the growth of human gastric cancer cells via regulation of apoptosis and autophagy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the differential phosphorylation and activation of p38 in hepatocytes by pro-apoptotic Transforming Growth Factor-beta1 (TGF-beta1), pro-survival factors Epidermal Growth Factor (EGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA) and the potential mechanisms.
methodsThe phosphorylation and activation of p38 were determined by immunoblotting. Apoptosis was analyzed by morphological staining and observation, FACS analysis of sub-G1 content and DNA fragmentation assay. To quantitatively determine caspase activation, caspase activity assay was performed in vitro.
resultsTGF-beta1-induced apoptosis was associated with the phosphorylation of p38, and SB202190, a specific inhibitor of p38, which was able to inhibit TGF-beta1-induced caspase activation and apoptosis. TPA and EGF also blocked apoptosis induced by TGF-beta1. Both of them induced the phosphorylation of p38. The results showed SB202190 had no effect on TGF-beta1-induced phosphorylation of p38, but effectively inhibited both EGF and TPA-induced phosphorylation of p38.
conclusionPro-apoptotic TGF-beta1, anti-apoptotic TPA and EGF induce the phosphorylation of p38 through different mechanisms that can be distinguished by SB202190. The data suggest that TPA and EGF-induced p38 phosphorylation is through an autophosphorylation-dependent mechanism. Since p38 phosphorylation induced by TGF-beta1 plays an important role in caspase activation and apoptosis, TPA and EGF-induced p38 phosphorylation may not be requisite for their anti-apoptotic function.
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