Effects of calcium, calmodulin, protein kinase C and protein tyrosine kinases on volume-activated taurine efflux in human erythroleukemia cells

✍ Scribed by Chiun-Chien Huang; Chirn-Bin Chang; Jer-Yuh Liu; Srisaila Basavappa; Poh-Hong Lim

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 159 KB
• Volume: 189
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.10027

✦ Synopsis

Abstract

The effects of calcium, calmodulin, protein kinase C (PKC) and protein tyrosine kinase (PTK) modulators were examined on the volume‐activated taurine efflux in the erythroleukemia cell line K562. Exposure to hypoosmotic solution significantly increased taurine efflux and intracellular calcium concentration ([Ca^2+^]~i~). The Ca^2+^ channel blockers La^3+^ (1 mM), verapamil (200 μM) and nifedipine (100 μM) inhibited the hypoosmotically‐induced [Ca^2+^]~i~ increase by more than 90%, while the volume‐activated taurine efflux was inhibited by 61.3 ± 9.5, 74.1 ± 9.3 and 38.0 ± 1.5%, respectively. Furthermore, the calmodulin inhibitors W7 (50 μM) and trifluoperazine (10 μM) and the Ca^2+^/calmodulin‐dependent protein kinase II inhibitor KN‐62 (2 μM) significantly blocked the volume‐activated taurine efflux by 93.4 ± 2.7, 77.9 ± 3.5 and 61.3 ± 15.8%, respectively. In contrast, the PKC inhibitor staurosporine (200 nM) or the PKC activator phorbol 12‐myristate 13‐acetate (100 nM) did not have significant effects on the volume‐activated taurine efflux. However, pretreatment with PTK inhibitors genistein, tyrphostin A25, and tyrphostin A47 blocked the volume‐activated taurine efflux. These results suggest that the volume‐activated taurine efflux in K562 cells may not directly involve Ca^2+^, but may require the presence of calmodulin and/or PTK. © 2001 Wiley‐Liss, Inc.