Endothelin-1- and isoproterenol-induced differential protein expression and signaling pathway in HL-1 cardiomyocytes
- Endothelin-1- and isoproterenol-induced differential protein expression and signaling pathway in HL-1 cardiomyocytes
- 홍혜민; 송은주; 오을식; 카비르; 이철주; 유영숙
- 2-DE; Cardiac hypertrophy; Cell biology; Endothelin-1; HL-1 cardiomyocytes; Isoproterenol
- Issue Date
- VOL 11, NO 2, 283-297
- It is well known that the two chemical compounds endothelin-1 (ET-1) and isoproterenol
(ISO) can individually induce cardiac hypertrophy through G protein-coupled receptors in
cardiomyocytes. However, the cardiac hypertrophy signaling pathway activated by ET-1 and
ISO is not well defined. Therefore, we investigated the protein expression profile and
signaling transduction in HL-l cardiomyocyte cells treated with ET-1 and ISO. Following
separation of the cell lysates by using 2-DE and silver staining, we identified 16 protein spots
that were differentially expressed as compared to the controls. Of these 16 spots, three
changed only after treatment with ET-1, whereas four changed only after treatment with ISO,
suggesting that these two stimuli could induce different signaling pathways. In order to
reveal the differences between ET-1- and ISO-induced signaling, we studied the different
events that occur at each step of the signaling pathways, when selected biocomponents were
blocked by inhibitors. Our results indicated that ET-1 and ISO used different pathways for
phosphorylation of glycogen synthase kinase-3β (GSK3β). ET-1 mainly used the mitogenactivated
protein kinase and phosphatidylinositol-3-kinase/AKT pathways to activate GSK3β,
whereas under ISO stimulation, only the phosphatidylinositol-3-kinase/AKT pathway was
required to trigger the GSK3β pathway. Furthermore, the strength of the GSK3β signal in
ISO-induced cardiac hypertrophy was stronger than that in ET-1-induced cardiac hypertrophy.
We found that these two agonists brought about different changes in the protein
expression of HL-1 cardiomyocytes through distinct signaling pathways even though the
destination of the two signaling pathways was the same.
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