|
|
Blood, 1 September 2006, Vol. 108, No. 5, pp. 1551-1554.
Prepublished online as a Blood First Edition Paper on May 9, 2006; DOI 10.1182/blood-2005-10-009514.
 Previous Article | Table of Contents | Next Article 
HEMATOPOIESIS
Brief report
Constitutive activation of STAT5 and Bcl-xL overexpression can induce endogenous erythroid colony formation in human primary cells
Loïc Garçon,
Christine Rivat,
Chloé James,
Catherine Lacout,
Valérie Camara-Clayette,
Valérie Ugo,
Yann Lecluse,
Annelise Bennaceur-Griscelli, and
William Vainchenker
From the Unité (U) 790 Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Gustave Roussy, Villejuif, France; Laboratoire d'Hématologie, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France; and Laboratoire d'Hématologie, Centre Hospitalo-Universitaire (CHU) de Brest-Hôpital Morvan, Institut Gustave Roussy, Villejuif, France.
The biologic hallmark of polycythemia vera (PV) is the formation of endogenous erythroid colonies (EECs) with an erythropoietin-independent differentiation. Recently, it has been shown that an activating mutation of JAK2 (V617F) was at the origin of PV. In this work, we studied whether the STAT5/Bcl-xL pathway could be responsible for EEC formation. A constitutively active form of STAT5 was transduced into human erythroid progenitors and induced an erythropoietin-independent terminal differentiation and EEC formation. Furthermore, Bcl-xL overexpression in erythroid progenitors was also able to induce erythroid colonies despite the absence of erythropoietin. Conversely, siRNA-mediated STAT5 and Bcl-xL knock-down in human erythroid progenitors inhibited colony-forming unit-erythroid (CFU-E) formation in the presence of Epo. Altogether, these results demonstrate that a sustained level of the sole Bcl-xL is capable of giving rise to Epo-independent erythroid colony formation and suggest that, in PV patients, JAK2V617F may induce EEC via the STAT5/Bcl-xL pathway.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
Related Article in Blood Online:
-
Erythropoietin-independent erythroid colonies: is the molecular basis clarified?
- Josef Prchal
Blood 2006 108: 1431-1432.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
A. M. Vannucchi, P. Guglielmelli, and A. Tefferi
Advances in Understanding and Management of Myeloproliferative Neoplasms
CA Cancer J Clin,
May 1, 2009;
59(3):
171 - 191.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
X Han, X Ren, I Jurickova, K Groschwitz, B A Pasternak, H Xu, T A Wilson, S P Hogan, and L A Denson
Regulation of intestinal barrier function by signal transducer and activator of transcription 5b
Gut,
January 1, 2009;
58(1):
49 - 58.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Zhao, G. A. Follows, P. A. Beer, L. M. Scott, B. J.P. Huntly, A. R. Green, and D. R. Alexander
Inhibition of the Bcl-xL Deamidation Pathway in Myeloproliferative Disorders
N. Engl. J. Med.,
December 25, 2008;
359(26):
2778 - 2789.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. O. Hexner, C. Serdikoff, M. Jan, C. R. Swider, C. Robinson, S. Yang, T. Angeles, S. G. Emerson, M. Carroll, B. Ruggeri, et al.
Lestaurtinib (CEP701) is a JAK2 inhibitor that suppresses JAK2/STAT5 signaling and the proliferation of primary erythroid cells from patients with myeloproliferative disorders
Blood,
June 15, 2008;
111(12):
5663 - 5671.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Grebien, M. A. Kerenyi, B. Kovacic, T. Kolbe, V. Becker, H. Dolznig, K. Pfeffer, U. Klingmuller, M. Muller, H. Beug, et al.
Stat5 activation enables erythropoiesis in the absence of EpoR and Jak2
Blood,
May 1, 2008;
111(9):
4511 - 4522.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. O. Ciurea, D. Merchant, N. Mahmud, T. Ishii, Y. Zhao, W. Hu, E. Bruno, G. Barosi, M. Xu, and R. Hoffman
Pivotal contributions of megakaryocytes to the biology of idiopathic myelofibrosis
Blood,
August 1, 2007;
110(3):
986 - 993.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Teofili, M. Martini, T. Cenci, G. Petrucci, L. Torti, S. Storti, F. Guidi, G. Leone, and L. M. Larocca
Different STAT-3 and STAT-5 phosphorylation discriminates among Ph-negative chronic myeloproliferative diseases and is independent of the V617F JAK-2 mutation
Blood,
July 1, 2007;
110(1):
354 - 359.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. A. Kennedy, F. Barabe, B. J. Patterson, J. Bayani, J. A. Squire, D. L. Barber, and J. E. Dick
Expression of TEL-JAK2 in primary human hematopoietic cells drives erythropoietin-independent erythropoiesis and induces myelofibrosis in vivo
PNAS,
November 7, 2006;
103(45):
16930 - 16935.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
