Characterization of myogenic differentiation under endoplasmic reticulum stress and taurine treatment

Hasuk Song, Hyemin Kim, Taesun Park, Dong Hee Lee

Research output: Chapter in Book/Report/Conference proceedingConference contribution

5 Citations (Scopus)

Abstract

Cells undergo apoptosis when they are subjected to prolonged ER stress (ERS). Excessive lipid deposition causes ERS in adipocytes; however, it rarely serves as a stress factor that triggers apoptosis. This strongly implies that an anti-ERS mechanism may exist in differentiating adipocytes. We used 3T3L1 (adipocytes) and C2C12 (myocytes) to probe for a potential anti-ERS mechanism. After cells were induced to adipogenesis or myogenesis, they were treated with the ERS inducer, tunicamycin. After tunicamycin-mediated ERS, the expression of the key molecular chaperone, Bip, increased in both cell lines. The chaperone, GRP94, responded differently to extended tunicamycin treatment, with protein levels remaining largely unchanged in 3T3L1 cells but falling in C2C12 cells. In terms of CHOP expression, C2C12 cells contained higher levels than 3T3-L1 cells. When GRP94 expression was reduced by siRNAs, CHOP expression increased. Considering the high levels of GRP94 in 3T3L1 cells under ERS, the small rate of apoptosis in 3T3L1 cells might result from the downregulation of CHOP mediated by GRP94. When C2C12 cells were pretreated with taurine, GRP94 levels appeared to increase and CHOP expression decreased. These results strongly imply that taurine may play an important role in promoting GRP94 expression and blocking the progression to apoptosis under ERS through the inhibition of CHOP upregulation.

Original languageEnglish
Title of host publicationTaurine 7
EditorsJunichi Azuma, Ito Takashi, Stephen Schaffer
Pages253-261
Number of pages9
DOIs
Publication statusPublished - 2009 Apr 22

Publication series

NameAdvances in Experimental Medicine and Biology
Volume643
ISSN (Print)0065-2598

Fingerprint

Endoplasmic Reticulum Stress
Taurine
Tunicamycin
Apoptosis
Adipocytes
Molecular Chaperones
3T3-L1 Cells
Adipogenesis
glucose-regulated proteins
Muscle Development
Cells
Muscle Cells
Lipids
Up-Regulation
Down-Regulation
Cell Line
Proteins

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Song, H., Kim, H., Park, T., & Lee, D. H. (2009). Characterization of myogenic differentiation under endoplasmic reticulum stress and taurine treatment. In J. Azuma, I. Takashi, & S. Schaffer (Eds.), Taurine 7 (pp. 253-261). (Advances in Experimental Medicine and Biology; Vol. 643). https://doi.org/10.1007/978-0-387-75681-3_26
Song, Hasuk ; Kim, Hyemin ; Park, Taesun ; Lee, Dong Hee. / Characterization of myogenic differentiation under endoplasmic reticulum stress and taurine treatment. Taurine 7. editor / Junichi Azuma ; Ito Takashi ; Stephen Schaffer. 2009. pp. 253-261 (Advances in Experimental Medicine and Biology).
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abstract = "Cells undergo apoptosis when they are subjected to prolonged ER stress (ERS). Excessive lipid deposition causes ERS in adipocytes; however, it rarely serves as a stress factor that triggers apoptosis. This strongly implies that an anti-ERS mechanism may exist in differentiating adipocytes. We used 3T3L1 (adipocytes) and C2C12 (myocytes) to probe for a potential anti-ERS mechanism. After cells were induced to adipogenesis or myogenesis, they were treated with the ERS inducer, tunicamycin. After tunicamycin-mediated ERS, the expression of the key molecular chaperone, Bip, increased in both cell lines. The chaperone, GRP94, responded differently to extended tunicamycin treatment, with protein levels remaining largely unchanged in 3T3L1 cells but falling in C2C12 cells. In terms of CHOP expression, C2C12 cells contained higher levels than 3T3-L1 cells. When GRP94 expression was reduced by siRNAs, CHOP expression increased. Considering the high levels of GRP94 in 3T3L1 cells under ERS, the small rate of apoptosis in 3T3L1 cells might result from the downregulation of CHOP mediated by GRP94. When C2C12 cells were pretreated with taurine, GRP94 levels appeared to increase and CHOP expression decreased. These results strongly imply that taurine may play an important role in promoting GRP94 expression and blocking the progression to apoptosis under ERS through the inhibition of CHOP upregulation.",
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Song, H, Kim, H, Park, T & Lee, DH 2009, Characterization of myogenic differentiation under endoplasmic reticulum stress and taurine treatment. in J Azuma, I Takashi & S Schaffer (eds), Taurine 7. Advances in Experimental Medicine and Biology, vol. 643, pp. 253-261. https://doi.org/10.1007/978-0-387-75681-3_26

Characterization of myogenic differentiation under endoplasmic reticulum stress and taurine treatment. / Song, Hasuk; Kim, Hyemin; Park, Taesun; Lee, Dong Hee.

Taurine 7. ed. / Junichi Azuma; Ito Takashi; Stephen Schaffer. 2009. p. 253-261 (Advances in Experimental Medicine and Biology; Vol. 643).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

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N2 - Cells undergo apoptosis when they are subjected to prolonged ER stress (ERS). Excessive lipid deposition causes ERS in adipocytes; however, it rarely serves as a stress factor that triggers apoptosis. This strongly implies that an anti-ERS mechanism may exist in differentiating adipocytes. We used 3T3L1 (adipocytes) and C2C12 (myocytes) to probe for a potential anti-ERS mechanism. After cells were induced to adipogenesis or myogenesis, they were treated with the ERS inducer, tunicamycin. After tunicamycin-mediated ERS, the expression of the key molecular chaperone, Bip, increased in both cell lines. The chaperone, GRP94, responded differently to extended tunicamycin treatment, with protein levels remaining largely unchanged in 3T3L1 cells but falling in C2C12 cells. In terms of CHOP expression, C2C12 cells contained higher levels than 3T3-L1 cells. When GRP94 expression was reduced by siRNAs, CHOP expression increased. Considering the high levels of GRP94 in 3T3L1 cells under ERS, the small rate of apoptosis in 3T3L1 cells might result from the downregulation of CHOP mediated by GRP94. When C2C12 cells were pretreated with taurine, GRP94 levels appeared to increase and CHOP expression decreased. These results strongly imply that taurine may play an important role in promoting GRP94 expression and blocking the progression to apoptosis under ERS through the inhibition of CHOP upregulation.

AB - Cells undergo apoptosis when they are subjected to prolonged ER stress (ERS). Excessive lipid deposition causes ERS in adipocytes; however, it rarely serves as a stress factor that triggers apoptosis. This strongly implies that an anti-ERS mechanism may exist in differentiating adipocytes. We used 3T3L1 (adipocytes) and C2C12 (myocytes) to probe for a potential anti-ERS mechanism. After cells were induced to adipogenesis or myogenesis, they were treated with the ERS inducer, tunicamycin. After tunicamycin-mediated ERS, the expression of the key molecular chaperone, Bip, increased in both cell lines. The chaperone, GRP94, responded differently to extended tunicamycin treatment, with protein levels remaining largely unchanged in 3T3L1 cells but falling in C2C12 cells. In terms of CHOP expression, C2C12 cells contained higher levels than 3T3-L1 cells. When GRP94 expression was reduced by siRNAs, CHOP expression increased. Considering the high levels of GRP94 in 3T3L1 cells under ERS, the small rate of apoptosis in 3T3L1 cells might result from the downregulation of CHOP mediated by GRP94. When C2C12 cells were pretreated with taurine, GRP94 levels appeared to increase and CHOP expression decreased. These results strongly imply that taurine may play an important role in promoting GRP94 expression and blocking the progression to apoptosis under ERS through the inhibition of CHOP upregulation.

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Song H, Kim H, Park T, Lee DH. Characterization of myogenic differentiation under endoplasmic reticulum stress and taurine treatment. In Azuma J, Takashi I, Schaffer S, editors, Taurine 7. 2009. p. 253-261. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-0-387-75681-3_26