Induction of apoptosis in murine lymphoma cells by cyclosporin A.

C. Mongini, C. Waldner, E. C. Lopes, M. J. Gravisaco, A. Escalada, Mariano Sanchez-Lockhart, E. Alvarez, S. Hajos

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The aim of this study was to investigate if CsA could induce apoptosis in the murine T-lymphoma cell line LBC, whose growth is inhibited by this immunosuppressive drug. CsA induced programmed cell death in LBC cells with typical features of apoptosis demonstrated by exposure of phosphatidyl serine residues on the cell membrane, the decrease of cell DNA content, chromatin condensation, and nuclear fragmentation. Apoptosis was evident within 12 h after CsA incubation, with a maximal effect at 48 h, in a time and dose-dependent fashion. In addition, the role of apoptosis inhibitors (Bcl-2 and Bcl-x) and the apoptosis inducer (Bax) in CsA induced-apoptosis was evaluated. The expression of Bcl-2 and Bax proteins were high in LBC cells and following CsA treatment the expression of these proteins as well as Bcl-XL decreased. In this work we demonstrated that cell growth inhibition following CsA treatment in LBC was paralleled by the induction of apoptosis thus providing an interesting animal model to identify the mechanism participating in the regulation of apoptotic genes by CsA in T-cell neoplasms and to assess preclinical in vivo trials of T-cell lymphoma-related disorders.

Original languageEnglish (US)
Pages (from-to)431-437
Number of pages7
JournalInternational journal of molecular medicine
Volume7
Issue number4
StatePublished - Jan 1 2001

Fingerprint

Cyclosporine
Lymphoma
Apoptosis
bcl-2-Associated X Protein
T-Cell Lymphoma
Phosphatidylserines
Immunosuppressive Agents
Growth
Chromatin
Cell Death
Animal Models
Cell Membrane
T-Lymphocytes
Cell Line
DNA
Pharmaceutical Preparations
Genes
Neoplasms
Proteins

ASJC Scopus subject areas

  • Genetics

Cite this

Mongini, C., Waldner, C., Lopes, E. C., Gravisaco, M. J., Escalada, A., Sanchez-Lockhart, M., ... Hajos, S. (2001). Induction of apoptosis in murine lymphoma cells by cyclosporin A. International journal of molecular medicine, 7(4), 431-437.

Induction of apoptosis in murine lymphoma cells by cyclosporin A. / Mongini, C.; Waldner, C.; Lopes, E. C.; Gravisaco, M. J.; Escalada, A.; Sanchez-Lockhart, Mariano; Alvarez, E.; Hajos, S.

In: International journal of molecular medicine, Vol. 7, No. 4, 01.01.2001, p. 431-437.

Research output: Contribution to journalArticle

Mongini, C, Waldner, C, Lopes, EC, Gravisaco, MJ, Escalada, A, Sanchez-Lockhart, M, Alvarez, E & Hajos, S 2001, 'Induction of apoptosis in murine lymphoma cells by cyclosporin A.', International journal of molecular medicine, vol. 7, no. 4, pp. 431-437.
Mongini C, Waldner C, Lopes EC, Gravisaco MJ, Escalada A, Sanchez-Lockhart M et al. Induction of apoptosis in murine lymphoma cells by cyclosporin A. International journal of molecular medicine. 2001 Jan 1;7(4):431-437.
Mongini, C. ; Waldner, C. ; Lopes, E. C. ; Gravisaco, M. J. ; Escalada, A. ; Sanchez-Lockhart, Mariano ; Alvarez, E. ; Hajos, S. / Induction of apoptosis in murine lymphoma cells by cyclosporin A. In: International journal of molecular medicine. 2001 ; Vol. 7, No. 4. pp. 431-437.
@article{c24bbedd5fa84eb894b90d487b237add,
title = "Induction of apoptosis in murine lymphoma cells by cyclosporin A.",
abstract = "The aim of this study was to investigate if CsA could induce apoptosis in the murine T-lymphoma cell line LBC, whose growth is inhibited by this immunosuppressive drug. CsA induced programmed cell death in LBC cells with typical features of apoptosis demonstrated by exposure of phosphatidyl serine residues on the cell membrane, the decrease of cell DNA content, chromatin condensation, and nuclear fragmentation. Apoptosis was evident within 12 h after CsA incubation, with a maximal effect at 48 h, in a time and dose-dependent fashion. In addition, the role of apoptosis inhibitors (Bcl-2 and Bcl-x) and the apoptosis inducer (Bax) in CsA induced-apoptosis was evaluated. The expression of Bcl-2 and Bax proteins were high in LBC cells and following CsA treatment the expression of these proteins as well as Bcl-XL decreased. In this work we demonstrated that cell growth inhibition following CsA treatment in LBC was paralleled by the induction of apoptosis thus providing an interesting animal model to identify the mechanism participating in the regulation of apoptotic genes by CsA in T-cell neoplasms and to assess preclinical in vivo trials of T-cell lymphoma-related disorders.",
author = "C. Mongini and C. Waldner and Lopes, {E. C.} and Gravisaco, {M. J.} and A. Escalada and Mariano Sanchez-Lockhart and E. Alvarez and S. Hajos",
year = "2001",
month = "1",
day = "1",
language = "English (US)",
volume = "7",
pages = "431--437",
journal = "International Journal of Molecular Medicine",
issn = "1107-3756",
publisher = "Spandidos Publications",
number = "4",

}

TY - JOUR

T1 - Induction of apoptosis in murine lymphoma cells by cyclosporin A.

AU - Mongini, C.

AU - Waldner, C.

AU - Lopes, E. C.

AU - Gravisaco, M. J.

AU - Escalada, A.

AU - Sanchez-Lockhart, Mariano

AU - Alvarez, E.

AU - Hajos, S.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - The aim of this study was to investigate if CsA could induce apoptosis in the murine T-lymphoma cell line LBC, whose growth is inhibited by this immunosuppressive drug. CsA induced programmed cell death in LBC cells with typical features of apoptosis demonstrated by exposure of phosphatidyl serine residues on the cell membrane, the decrease of cell DNA content, chromatin condensation, and nuclear fragmentation. Apoptosis was evident within 12 h after CsA incubation, with a maximal effect at 48 h, in a time and dose-dependent fashion. In addition, the role of apoptosis inhibitors (Bcl-2 and Bcl-x) and the apoptosis inducer (Bax) in CsA induced-apoptosis was evaluated. The expression of Bcl-2 and Bax proteins were high in LBC cells and following CsA treatment the expression of these proteins as well as Bcl-XL decreased. In this work we demonstrated that cell growth inhibition following CsA treatment in LBC was paralleled by the induction of apoptosis thus providing an interesting animal model to identify the mechanism participating in the regulation of apoptotic genes by CsA in T-cell neoplasms and to assess preclinical in vivo trials of T-cell lymphoma-related disorders.

AB - The aim of this study was to investigate if CsA could induce apoptosis in the murine T-lymphoma cell line LBC, whose growth is inhibited by this immunosuppressive drug. CsA induced programmed cell death in LBC cells with typical features of apoptosis demonstrated by exposure of phosphatidyl serine residues on the cell membrane, the decrease of cell DNA content, chromatin condensation, and nuclear fragmentation. Apoptosis was evident within 12 h after CsA incubation, with a maximal effect at 48 h, in a time and dose-dependent fashion. In addition, the role of apoptosis inhibitors (Bcl-2 and Bcl-x) and the apoptosis inducer (Bax) in CsA induced-apoptosis was evaluated. The expression of Bcl-2 and Bax proteins were high in LBC cells and following CsA treatment the expression of these proteins as well as Bcl-XL decreased. In this work we demonstrated that cell growth inhibition following CsA treatment in LBC was paralleled by the induction of apoptosis thus providing an interesting animal model to identify the mechanism participating in the regulation of apoptotic genes by CsA in T-cell neoplasms and to assess preclinical in vivo trials of T-cell lymphoma-related disorders.

UR - http://www.scopus.com/inward/record.url?scp=0035315797&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035315797&partnerID=8YFLogxK

M3 - Article

VL - 7

SP - 431

EP - 437

JO - International Journal of Molecular Medicine

JF - International Journal of Molecular Medicine

SN - 1107-3756

IS - 4

ER -