Gap junction blockage promotes cadmium-induced apoptosis in BRL 3A derived from Buffalo rat liver cells
| Autor: | Zongping Liu, Yan Yuan, Di Hu, Tao Han, Jianchun Bian, Nannan Dai, Xuezhong Liu, Hui Zou, Junze Xie, Liling Zhuo, Jianhong Gu |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Cell signaling cadmium p38 mitogen-activated protein kinases BRL 3A cells Connexin Cell Communication Biology gap junction blockage 03 medical and health sciences Animals General Veterinary Kinase Gap junction apoptosis Gap Junctions Molecular biology Cell biology Rats Enzyme Activation 030104 developmental biology Gene Expression Regulation Apoptosis Connexin 43 Hepatocytes Original Article Calcium Signal transduction Signal Transduction |
| Zdroj: | Journal of Veterinary Science |
| ISSN: | 1976-555X 1229-845X |
| Popis: | Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca(2+) concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18β-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δψm). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells. |
| Databáze: | OpenAIRE |
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