Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection

Boumediene Bouzahzah; Fnu Nagajyothi; Mahalia S. Desruisseaux; Mohan Krishnamachary; Stephen M. Factor; Alex W. Cohen; Michael P. Lisanti; Stefka B. Petkova; Richard G. Pestell; Murray Wittner; Shankar Mukherjee; Louis M. Weiss; Linda A. Jelicks; Chris Albanese; Herbert B. Tanowitz

doi:10.4161/cc.5.20.3380

Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection

Boumediene Bouzahzah, Fnu Nagajyothi, Mahalia S. Desruisseaux, Mohan Krishnamachary, Stephen M. Factor, Alex W. Cohen, Michael P. Lisanti, Stefka B. Petkova, Richard G. Pestell, Murray Wittner, Shankar Mukherjee, Louis M. Weiss, Linda A. Jelicks, Chris Albanese, Herbert B. Tanowitz

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

The liver is an important target of Trypanosoma cruzi infection. Infection of CD-1 mice with T. cruzi (Brazil strain) resulted in parasitism of the liver, primarily in sinusoidal and Kupffer cells. Immunoblot analysis revealed activation of extra cellular signal-regulated kinase (ERK) during the acute and subacute period of infection, but p38 mitogen activated kinase (MAPK) and JNK were not activated. The activity of important cell cycle regulatory genes was also examined in the liver following infection. There was increased expression of cyclin D1, cyclin E and cyclin A as well as proliferating cell nuclear antigen (PCNA) at 45, 60 and 215 days post infection. In addition, the levels of the cyclin-dependent kinase inhibitors p27^KIP1, p21^WAF1 and the tumor suppressor p53 were increased in the livers obtained from infected mice. Quantitative PCR revealed increased abundance of mRNA for cyclins A, D1 and E. Interestingly, cyclin A and E are ordinarily not found in the adult liver. Thus infection caused a reversion to a fetal/neonatal phenotype. These data provide a molecular basis for cell proliferation in the liver following T. cruzi infection.

Original language	English (US)
Pages (from-to)	2396-2400
Number of pages	5
Journal	Cell Cycle
Volume	5
Issue number	20
DOIs	https://doi.org/10.4161/cc.5.20.3380
State	Published - Oct 15 2006

Keywords

Cell cycle regulatory proteins
Chagas' disease
Cyclin A
Cyclin D1
Cylin E
Liver
Mitogen-activated protein kinase
Trypanosoma cruzi

ASJC Scopus subject areas

Molecular Biology
Developmental Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.4161/cc.5.20.3380

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Bouzahzah, B., Nagajyothi, F., Desruisseaux, M. S., Krishnamachary, M., Factor, S. M., Cohen, A. W., Lisanti, M. P., Petkova, S. B., Pestell, R. G., Wittner, M., Mukherjee, S., Weiss, L. M., Jelicks, L. A., Albanese, C., & Tanowitz, H. B. (2006). Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection. Cell Cycle, 5(20), 2396-2400. https://doi.org/10.4161/cc.5.20.3380

Bouzahzah, B, Nagajyothi, F, Desruisseaux, MS, Krishnamachary, M, Factor, SM, Cohen, AW, Lisanti, MP, Petkova, SB, Pestell, RG, Wittner, M, Mukherjee, S, Weiss, LM, Jelicks, LA, Albanese, C & Tanowitz, HB 2006, 'Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection', Cell Cycle, vol. 5, no. 20, pp. 2396-2400. https://doi.org/10.4161/cc.5.20.3380

@article{4242790663924d9e8daad027f6b6649b,

title = "Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection",

abstract = "The liver is an important target of Trypanosoma cruzi infection. Infection of CD-1 mice with T. cruzi (Brazil strain) resulted in parasitism of the liver, primarily in sinusoidal and Kupffer cells. Immunoblot analysis revealed activation of extra cellular signal-regulated kinase (ERK) during the acute and subacute period of infection, but p38 mitogen activated kinase (MAPK) and JNK were not activated. The activity of important cell cycle regulatory genes was also examined in the liver following infection. There was increased expression of cyclin D1, cyclin E and cyclin A as well as proliferating cell nuclear antigen (PCNA) at 45, 60 and 215 days post infection. In addition, the levels of the cyclin-dependent kinase inhibitors p27KIP1, p21WAF1 and the tumor suppressor p53 were increased in the livers obtained from infected mice. Quantitative PCR revealed increased abundance of mRNA for cyclins A, D1 and E. Interestingly, cyclin A and E are ordinarily not found in the adult liver. Thus infection caused a reversion to a fetal/neonatal phenotype. These data provide a molecular basis for cell proliferation in the liver following T. cruzi infection.",

keywords = "Cell cycle regulatory proteins, Chagas' disease, Cyclin A, Cyclin D1, Cylin E, Liver, Mitogen-activated protein kinase, Trypanosoma cruzi",

author = "Boumediene Bouzahzah and Fnu Nagajyothi and Desruisseaux, {Mahalia S.} and Mohan Krishnamachary and Factor, {Stephen M.} and Cohen, {Alex W.} and Lisanti, {Michael P.} and Petkova, {Stefka B.} and Pestell, {Richard G.} and Murray Wittner and Shankar Mukherjee and Weiss, {Louis M.} and Jelicks, {Linda A.} and Chris Albanese and Tanowitz, {Herbert B.}",

note = "Funding Information: This work was supported by NIH grants AI-052739 and AI-12770 (HBT). MPL was supported by grants from the NIH and the American Heart Association and by the Hirschl/Weil-Caulier Career Scientist Award. MSD is the recipient of the IDSA ERF/ NFID Colin L. Powell Minority Postdoctoral Fellowship in Tropical Disease Research sponsored by GlaxoSmithKline, and was supported by the NIH Training Grant in Mechanisms of Cardiovascular Diseases (T32 HL-07675).",

year = "2006",

month = oct,

day = "15",

doi = "10.4161/cc.5.20.3380",

language = "English (US)",

volume = "5",

pages = "2396--2400",

journal = "Cell Cycle",

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T1 - Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection

AU - Bouzahzah, Boumediene

AU - Nagajyothi, Fnu

AU - Desruisseaux, Mahalia S.

AU - Krishnamachary, Mohan

AU - Factor, Stephen M.

AU - Cohen, Alex W.

AU - Lisanti, Michael P.

AU - Petkova, Stefka B.

AU - Pestell, Richard G.

AU - Wittner, Murray

AU - Mukherjee, Shankar

AU - Weiss, Louis M.

AU - Jelicks, Linda A.

AU - Albanese, Chris

AU - Tanowitz, Herbert B.

N1 - Funding Information: This work was supported by NIH grants AI-052739 and AI-12770 (HBT). MPL was supported by grants from the NIH and the American Heart Association and by the Hirschl/Weil-Caulier Career Scientist Award. MSD is the recipient of the IDSA ERF/ NFID Colin L. Powell Minority Postdoctoral Fellowship in Tropical Disease Research sponsored by GlaxoSmithKline, and was supported by the NIH Training Grant in Mechanisms of Cardiovascular Diseases (T32 HL-07675).

PY - 2006/10/15

Y1 - 2006/10/15

N2 - The liver is an important target of Trypanosoma cruzi infection. Infection of CD-1 mice with T. cruzi (Brazil strain) resulted in parasitism of the liver, primarily in sinusoidal and Kupffer cells. Immunoblot analysis revealed activation of extra cellular signal-regulated kinase (ERK) during the acute and subacute period of infection, but p38 mitogen activated kinase (MAPK) and JNK were not activated. The activity of important cell cycle regulatory genes was also examined in the liver following infection. There was increased expression of cyclin D1, cyclin E and cyclin A as well as proliferating cell nuclear antigen (PCNA) at 45, 60 and 215 days post infection. In addition, the levels of the cyclin-dependent kinase inhibitors p27KIP1, p21WAF1 and the tumor suppressor p53 were increased in the livers obtained from infected mice. Quantitative PCR revealed increased abundance of mRNA for cyclins A, D1 and E. Interestingly, cyclin A and E are ordinarily not found in the adult liver. Thus infection caused a reversion to a fetal/neonatal phenotype. These data provide a molecular basis for cell proliferation in the liver following T. cruzi infection.

AB - The liver is an important target of Trypanosoma cruzi infection. Infection of CD-1 mice with T. cruzi (Brazil strain) resulted in parasitism of the liver, primarily in sinusoidal and Kupffer cells. Immunoblot analysis revealed activation of extra cellular signal-regulated kinase (ERK) during the acute and subacute period of infection, but p38 mitogen activated kinase (MAPK) and JNK were not activated. The activity of important cell cycle regulatory genes was also examined in the liver following infection. There was increased expression of cyclin D1, cyclin E and cyclin A as well as proliferating cell nuclear antigen (PCNA) at 45, 60 and 215 days post infection. In addition, the levels of the cyclin-dependent kinase inhibitors p27KIP1, p21WAF1 and the tumor suppressor p53 were increased in the livers obtained from infected mice. Quantitative PCR revealed increased abundance of mRNA for cyclins A, D1 and E. Interestingly, cyclin A and E are ordinarily not found in the adult liver. Thus infection caused a reversion to a fetal/neonatal phenotype. These data provide a molecular basis for cell proliferation in the liver following T. cruzi infection.

KW - Cell cycle regulatory proteins

KW - Chagas' disease

KW - Cyclin A

KW - Cyclin D1

KW - Cylin E

KW - Liver

KW - Mitogen-activated protein kinase

KW - Trypanosoma cruzi

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DO - 10.4161/cc.5.20.3380

M3 - Article

C2 - 17102609

AN - SCOPUS:33751206509

SN - 1538-4101

VL - 5

SP - 2396

EP - 2400

JO - Cell Cycle

JF - Cell Cycle

IS - 20

ER -

Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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