|
|
 Previous Article | Table of Contents | Next Article 
The Tetrapeptide Acetyl-N-Ser-Asp-Lys-Pro (Goralatide) Protects
From Doxorubicin-Induced Toxicity: Improvement in Mice Survival and
Protection of Bone Marrow Stem Cells and Progenitors
A. Massé,
L.H. Ramirez,
G. Bindoula,
C. Grillon,
J. Wdzieczak-Bakala,
K. Raddassi,
E. Deschamps de Paillette,
J.M. Mencia-Huerta,
S. Koscielny,
P. Potier,
F. Sainteny, and
P. Carde
From Institut Gustave Roussy, Villejuif, IPSEN-Biotech, Paris; and
Institut de Chimie des Substances Naturelles, CNRS, Gif-sur-Yvette,
France.
The tetrapeptide Acetyl-N-Ser-Asp-Lys-Pro (AcSDKP or Goralatide), a
physiological regulator of hematopoiesis, inhibits the entry into the
S-phase of murine and human hematopoietic stem cells. It has been shown
to reduce the damage to specific compartments in the bone marrow
resulting from treatment with chemotherapeutic agents, ionizing
radiations, hyperthermy, or phototherapy. The present study was
performed to assess the therapeutic potential of AcSDKP in vivo in
reducing both the toxicity and the hematopoietic damage induced by
fractionated administration of doxorubicin (DOX), a widely used
anticancer drug. Here we showed that AcSDKP could reduce DOX-induced
mortality in mice and could protect particularly the long-term
reconstituting cells (LTRCs) in addition to colony forming
units-spleen, high proliferative potential colony-forming cells, and
colony-forming units-granulocyte-macrophage (CFU-GM) from DOX
toxicity. The protection against DOX-induced mortality in mice was
improved when AcSDKP was administered for 3 days, at a dose of 2.4 µg/d, by continuous subcutaneous (SC) infusion or fractionated SC
injections starting 48 hours before DOX treatment. Moreover, the
recovery of the CFU-GM population in the AcSDKP-DOX-treated mice was
optimized by the subsequent administration of granulocyte colony-stimulating factor (G-CSF). The coadministration of AcSDKP with
DOX may improve its therapeutic index by reducing both acute hematotoxicity on late stem cells and progenitors and long-term toxicity on LTRCs. Optimization of these treatments combined with G-CSF
may provide an additional approach to facilitate hematopoietic recovery
after cancer chemotherapy.
Blood, Vol. 91 No. 2 (January 15), 1998:
pp. 441-449
© 1998 by The American Society of Hematology.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
U. Sharma, N.-E. Rhaleb, S. Pokharel, P. Harding, S. Rasoul, H. Peng, and O. A. Carretero
Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage
Am J Physiol Heart Circ Physiol,
March 1, 2008;
294(3):
H1226 - H1232.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Wang, O. A. Carretero, X.-Y. Yang, N.-E. Rhaleb, Y.-H. Liu, T.-D. Liao, and X.-P. Yang
N-acetyl-seryl-aspartyl-lysyl-proline stimulates angiogenesis in vitro and in vivo
Am J Physiol Heart Circ Physiol,
November 1, 2004;
287(5):
H2099 - H2105.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Charrier, A. Michaud, S. Badaoui, S. Giroux, E. Ezan, F. Sainteny, P. Corvol, and W. Vainchenker
Inhibition of angiotensin I-converting enzyme induces radioprotection by preserving murine hematopoietic short-term reconstituting cells
Blood,
August 15, 2004;
104(4):
978 - 985.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J.-M. Liu, F. Lawrence, M. Kovacevic, J. Bignon, E. Papadimitriou, J.-Y. Lallemand, P. Katsoris, P. Potier, Y. Fromes, and J. Wdzieczak-Bakala
The tetrapeptide AcSDKP, an inhibitor of primitive hematopoietic cell proliferation, induces angiogenesis in vitro and in vivo
Blood,
April 15, 2003;
101(8):
3014 - 3020.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Junot, M.-F. Gonzales, E. Ezan, J. Cotton, G. Vazeux, A. Michaud, M. Azizi, S. Vassiliou, A. Yiotakis, P. Corvol, et al.
RXP 407, a Selective Inhibitor of the N-Domain of Angiotensin I-Converting Enzyme, Blocks in Vivo the Degradation of Hemoregulatory Peptide Acetyl-Ser-Asp-Lys-Pro with No Effect on Angiotensin I Hydrolysis
J. Pharmacol. Exp. Ther.,
April 12, 2001;
297(2):
606 - 611.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
Y. Shiotsu, K. Yamashita, F. Kanai, Y. Ikuina, C. Murakata, M. Teramura, H. Mizoguchi, T. Tamaoki, and S. Akinaga
Chemoprotective effects of KF41399, a derivative of carbazole compounds, on nimustine-induced thrombocytopenia
Blood,
June 15, 2000;
95(12):
3771 - 3780.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J Stephan, N Melaine, E Ezan, H Hakovirta, S Maddocks, J Toppari, D Garnier, J Wdzieczak-Bakala, and B Jegou
Source, catabolism and role of the tetrapeptide N-acetyl-ser-asp-lys-Pro within the testis
J. Cell Sci.,
January 1, 2000;
113(1):
113 - 121.
[Abstract]
[PDF]
|
|
|
|
|
|
|
C. Junot, L. Nicolet, E. Ezan, M.-F. Gonzales, J. Menard, and M. Azizi
Effect of Angiotensin-Converting Enzyme Inhibition on Plasma, Urine, and Tissue Concentrations of Hemoregulatory Peptide Acetyl-Ser-Asp-Lys-Pro in Rats
J. Pharmacol. Exp. Ther.,
December 1, 1999;
291(3):
982 - 987.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
V. Dive, J. Cotton, A. Yiotakis, A. Michaud, S. Vassiliou, J. Jiracek, G. Vazeux, M.-T. Chauvet, P. Cuniasse, and P. Corvol
RXP 407, a phosphinic peptide, is a potent inhibitor of angiotensin I converting enzyme able to differentiate between its two active sites
PNAS,
April 13, 1999;
96(8):
4330 - 4335.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
