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KMID : 0811720070110000084
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Korean Journal of Physiology & Pharmacology
2007 Volume.11 No. 0 p.84 ~ p.0
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ER Proteins during HSCs’ Activation
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Park Kyu-Sang
Lee Dong-Hyun
Cha Seung-Kyu
Kim Min-Jeong
Kim Dae-Ran
Lee Joong-Woo
Kong In-Deok
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Abstract
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Hepatic stellate cells (HSCs) are known to initiate cellular components of hepatic fibrosis by trans-differentiating into myofibroblast-like cells. During this process, HSCs change into actively protein synthesizing cells. Until now, however, it has not been clearly elucidated whether there is an alteration in the expression of endoplasmic reticulum (ER) proteins involved in ER Ca2+ homeostasis and/or chaperone function, which are important for protein folding and differentiation signaling. Using quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis, we investigated the changes in the transcriptional level of Ca2+ transporting and binding proteins in the ER during the activation process of rat HSCs. Purified HSCs (＞95%) increased the expression of a-smooth muscle actin and a subunit (a1c) of the L-type voltage sensitive Ca2+ channel following the activation. The expression of type 2 sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA-2), the dominant subtype in HSCs, increased during the activation process. Among the three isoforms of inositol triphosphate (IP3) receptors, type 1 was the main subtype in HSCs, which also markedly increased its expression level during activation. Calreticulin, calnexin and calsequestrin, Ca2+ binding chaperone proteins of the ER, were up-regulated following the activation to keep up with collagen synthesis. We propose that up-regulation of Ca2+ transporting and binding proteins in the ER might be compensatory changes to prevent disruption of ER Ca2+ homeostasis and ER stress caused by increasing the ER work load.
Source: Korean Journal of Physiology & Pharmacology.2007 Oct;11(Suppl II):S80-S80
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KEYWORD
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Hepatic stellate cells, Hepatic fibrosis, Endoplasmic reticulum
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