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Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction.
Hepatology 1998; 27(4):959-66Hep

Abstract

The authors previously reported that transforming growth factor beta1 (TGF-beta1) induces apoptosis in McA-RH7777 (7777) and McA-RH8994 (8994) rat hepatoma cell lines. Although these cell lines exhibit different responses to glucocorticoid treatment in various cellular functions and gene expression, dexamethasone (DEX) inhibited spontaneous and TGF-beta1-induced apoptosis in both. Analysis of analogous hormones in TGF-beta1-induced apoptosis in 8994 cells suggested the inhibitory effect to be glucocorticoid-specific. By cell-cycle analysis and DNA fragmentation assay using sodium butyrate, a G1-arrest-inducing reagent, regulation of apoptosis by TGF-beta1 and DEX was shown independent of the cell cycle. For elucidation of the mechanisms of anti-apoptotic action of DEX, the effects of various chemical probes on this apoptosis model were examined, and various reagents known to exhibit anti-apoptotic activity in other experimental systems were found to be ineffective. The effect of TGF-beta1 and DEX on cellular amounts of several apoptosis-related proteins, members of the Bcl-2 family, Bcl-2, Bcl-xL, Bcl-xS, Bad, and Bax was also examined. DEX drastically increased Bcl-xL in both cell lines irrespective of the presence of TGF-beta1. Bcl-2 and Bcl-xS proteins were not detected, and Bax and Bad content did not change by treatment with TGF-beta1 or DEX. Progesterone (Prog), a partial antagonist for glucocorticoid receptor, inhibited the effects of DEX on apoptosis and Bcl-xL expression in 8994 cells. Thus, Bcl-xL induction by DEX would appear closely associated with its inhibitory effect on spontaneous and TGF-beta1-induced apoptosis in the hepatoma cell lines.

Authors+Show Affiliations

Kampo Pharmacology Department, Tsumura and Co., Ami, Ibaraki, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9537434

Citation

Yamamoto, M, et al. "Inhibition By Dexamethasone of Transforming Growth Factor Beta1-induced Apoptosis in Rat Hepatoma Cells: a Possible Association With Bcl-xL Induction." Hepatology (Baltimore, Md.), vol. 27, no. 4, 1998, pp. 959-66.
Yamamoto M, Fukuda K, Miura N, et al. Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction. Hepatology. 1998;27(4):959-66.
Yamamoto, M., Fukuda, K., Miura, N., Suzuki, R., Kido, T., & Komatsu, Y. (1998). Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction. Hepatology (Baltimore, Md.), 27(4), pp. 959-66.
Yamamoto M, et al. Inhibition By Dexamethasone of Transforming Growth Factor Beta1-induced Apoptosis in Rat Hepatoma Cells: a Possible Association With Bcl-xL Induction. Hepatology. 1998;27(4):959-66. PubMed PMID: 9537434.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition by dexamethasone of transforming growth factor beta1-induced apoptosis in rat hepatoma cells: a possible association with Bcl-xL induction. AU - Yamamoto,M, AU - Fukuda,K, AU - Miura,N, AU - Suzuki,R, AU - Kido,T, AU - Komatsu,Y, PY - 1998/4/16/pubmed PY - 1998/4/16/medline PY - 1998/4/16/entrez SP - 959 EP - 66 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 27 IS - 4 N2 - The authors previously reported that transforming growth factor beta1 (TGF-beta1) induces apoptosis in McA-RH7777 (7777) and McA-RH8994 (8994) rat hepatoma cell lines. Although these cell lines exhibit different responses to glucocorticoid treatment in various cellular functions and gene expression, dexamethasone (DEX) inhibited spontaneous and TGF-beta1-induced apoptosis in both. Analysis of analogous hormones in TGF-beta1-induced apoptosis in 8994 cells suggested the inhibitory effect to be glucocorticoid-specific. By cell-cycle analysis and DNA fragmentation assay using sodium butyrate, a G1-arrest-inducing reagent, regulation of apoptosis by TGF-beta1 and DEX was shown independent of the cell cycle. For elucidation of the mechanisms of anti-apoptotic action of DEX, the effects of various chemical probes on this apoptosis model were examined, and various reagents known to exhibit anti-apoptotic activity in other experimental systems were found to be ineffective. The effect of TGF-beta1 and DEX on cellular amounts of several apoptosis-related proteins, members of the Bcl-2 family, Bcl-2, Bcl-xL, Bcl-xS, Bad, and Bax was also examined. DEX drastically increased Bcl-xL in both cell lines irrespective of the presence of TGF-beta1. Bcl-2 and Bcl-xS proteins were not detected, and Bax and Bad content did not change by treatment with TGF-beta1 or DEX. Progesterone (Prog), a partial antagonist for glucocorticoid receptor, inhibited the effects of DEX on apoptosis and Bcl-xL expression in 8994 cells. Thus, Bcl-xL induction by DEX would appear closely associated with its inhibitory effect on spontaneous and TGF-beta1-induced apoptosis in the hepatoma cell lines. SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/9537434/Inhibition_by_dexamethasone_of_transforming_growth_factor_beta1_induced_apoptosis_in_rat_hepatoma_cells:_a_possible_association_with_Bcl_xL_induction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0270913998001438 DB - PRIME DP - Unbound Medicine ER -