egf receptor-dependent mechanism may be involved in the tamm–horsfall glycoprotein-enhanced pmn phagocytosis via activating rho family and mapk signaling pathway
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2014
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Abstract
Our previous studies showed that urinary Tamm–Horsfall glycoprotein (THP) potently enhanced polymorphonuclear neutrophil (PMN) phagocytosis. However, the domain structure(s), signaling pathway and the intracellular events responsible for THP-enhanced PMN phagocytosis remain to be elucidated. THP was purified from normal human urine. The human promyelocytic leukemia cell line HL-60 was induced to differentiate into PMNs by all-trans retinoid acid. Pretreatment with different MAPK and PI3K inhibitors was used to delineate signaling pathways in THP-enhanced PMN phagocytosis. Phosphorylation of molecules responsible for PMN phagocytosis induced by bacterial lipopolysaccharide (LPS), THP, or human recombinant epidermal growth factor (EGF) was evaluated by western blot. A p38 MAPK inhibitor, SB203580, effectively inhibited both spontaneous and LPS- and THP-induced PMN phagocytosis. Both THP and LPS enhanced the expression of the Rho family proteins Cdc42 and Rac that may lead to F-actin re-arrangement. Further studies suggested that THP and EGF enhance PMN and differentiated HL-60 cell phagocytosis in a similar pattern. Furthermore, the EGF receptor inhibitor GW2974 significantly suppressed THP- and EGF-enhanced PMN phagocytosis and p38 and ERK1/2 phosphorylation in differentiated HL-60 cells. We conclude that EGF receptor-dependent signaling may be involved in THP-enhanced PMN phagocytosis by activating Rho family and MAP kinase.
| Reference Key |
li2014moleculesegf
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|---|---|
| Authors | ;Ko-Jen Li;Sue-Cien Siao;Cheng-Han Wu;Chieh-Yu Shen;Tsai-Hung Wu;Chang-Youh Tsai;Song-Chou Hsieh;Chia-Li Yu |
| Journal | Journal of ethnopharmacology |
| Year | 2014 |
| DOI |
10.3390/molecules19011328
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| URL | |
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