Korean J Physiol Pharmacol.  2006 Aug;10(4):199-205.

Involvement of ERK1/2 and JNK Pathways in 17beta-estradiol Induced Kir6.2 and SK2 Upregulation in Rat Osteoblast-like Cells

Affiliations
  • 1Department of Physiology, School of Medicine, Kyungpook National University, Daegu 700-422, Korea. ekyang@mail.knu.ac.kr

Abstract

The functional expression of potassium (K+) channels has electrophysiologically been studied in bone cells from several species, however, their identity and regulation of gene expressions in bone cells are not well known. In the present study, to investigate how K+ channel expressions are regulated by estrogen, we measured changes of transcript levels of various Ca2+-activated (K(Ca)) and ATP-sensitive K+ channels in rat osteoblastic ROS 17/2.8 cells after treatment with estrogen. Application of 17beta-estradiol (E2) for 24 h and 48 h increased mRNA and protein expressions of inwardly rectifying K+ channel (Kir) 6.2 and type 2 small conductance K(Ca) channel (SK2), respectively. Combined treatment of cells with 17beta-E2 and ICI 182,780, a pure antiestrogen, suppressed 17beta-E2-induced alterations of SK2 and Kir6.2 mRNA levels. In addition, treatment of cells with U0126, a specific inhibitor of extracellular receptor kinases (ERK)1/2, and SP600125, a specific inhibitor of c-jun N-terminal kinase (JNK) blocked the enhancing effects of 17beta-E2 on SK2 and Kir6.2 protein expressions. On the other hand, blocking of p38 mitogen-activated protein kinase had no effect. Taken together, these results indicate that 17beta-E2 modulates SK2 and Kir6.2 expressions through the estrogen receptor, involving ERK1/2 and JNK activations.

Keyword

Estrogen; Osteoblastic cell; Kir6.2; SK2; ERK1/2; JNK
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