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Clinical Chemistry 51: 2411-2414, 2005; 10.1373/clinchem.2005.057802
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(Clinical Chemistry. 2005;51:2411-2414.)
© 2005 American Association for Clinical Chemistry, Inc.

Technical Briefs

SDF1-3'A Gene Polymorphism Is Associated with Chronic Myeloproliferative Disease and Thrombotic Events

GianCarla Gerli1,a, Chiara Vanelli1, Olivia Turri2, Maddalena Erario2, Angelo Gardellini1, Mariateresa Pugliano1 and Maria Luisa Biondi2

1 Dipartimento di Medicina, Chirurgia, Odontoiatria–San Paolo–Università degli Studi di Milano, Milan, Italy;2 Laboratorio Analisi Chimica Clinica e Microbiologia, Ospedale San Paolo, Milan, Italy

aaddress correspondence to this author at: Dipartimento di Medicina, Chirurgia, Odontoiatria–San Paolo–Università degli Studi di Milano, Milan, Italy; fax 39-0250-323089, e-mail giancarla.gerli@unimi.it

The first 300 words of the full text of this article appear below.

Stromal cell-derived factor-1 (SDF-1), a member of the CXC chemokine family, is constitutively produced by bone marrow stromal cells, and it induces chemotaxis on a variety of cell types that contain the G-protein–linked receptor CXCR4. SDF-1 plays a key role in hematopoiesis, and its involvement in migration, homing, and survival of hematopoietic progenitors has been well established. It is the first chemoattractant agent reported for human CD34+ progenitor cells (1), and it promotes CD34+ cell survival by counteracting apoptosis (2).

SDF-1 may also have a role in neoangiogenesis. It increases production of vascular endothelial growth factor (VEGF), the main angiogenic factor, which in turn enhances the expression of CXCR4 receptor in endothelial cells, in an autocrine loop (3).

SDF-1 may participate in atherothrombosis. It is a potent chemoattractant of monocytes and lymphocytes (4) and has a direct effect on platelet activation (5). SDF-1 is also involved in the neovascularization and angiogenesis response that occurs during formation of unstable atherosclerotic plaques (6), in which increased expression of this chemokine has been found (5).

The 2 isoforms, SDF-1{alpha} and SDF-1ß, arise from a single gene by alternative splicing (7). Sequence analysis reveals a common polymorphism in the 3'-untranslated region (3'-UTR), implicated in mRNA turnover regulation, of the SDF-1ß gene transcript, which contains a G->A transition at position 801, designated SDF1-3'UTR-801G-A, abbreviated as SDF1-3'A (8). It has been reported that SDF1-3'A genotype action involves up-regulation of the quantity of SDF-1 protein available to bind CXCR4 (7). In addition, the SDF1-3'A polymorphism has been associated with high mobilization of CD34+ progenitor cells into peripheral blood (9).

Philadelphia-negative chronic myeloproliferative disorders (CMDs) are characterized by clonal proliferation of hematopoietic progenitor cells . . . [Full Text of this Article]






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