Perinatal Plasma Monocyte Chemotactic Protein-1 Concentrations in Intrauterine Growth Restriction

Briana, Despina D.; Boutsikou, Maria; Baka, Stavroula; Papadopoulos, George; Gourgiotis, Dimitrios; Puchner, Karl Philipp; Hassiakos, Dimitrios; Malamitsi-Puchner, Ariadne

doi:https://doi.org/10.1155/2007/65032

Mediators of Inflammation

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Research Article | Open Access

Volume 2007 | Article ID 065032 | https://doi.org/10.1155/2007/65032

Perinatal Plasma Monocyte Chemotactic Protein-1 Concentrations in Intrauterine Growth Restriction

Despina D. Briana,¹Maria Boutsikou,¹Stavroula Baka,¹George Papadopoulos,¹Dimitrios Gourgiotis,²Karl Philipp Puchner,¹Dimitrios Hassiakos,¹and Ariadne Malamitsi-Puchner¹

Received23 Jul 2007

Accepted11 Oct 2007

Published15 Nov 2007

Abstract

Monocyte chemotactic protein-1 (MCP-1) plays vital roles in immune response, angiogenesis, and pregnancy outcome. We investigated plasma MCP-1 concentrations in 40 mothers and their 20 intrauterine-growth-restricted (IUGR) and 20 appropriate-for-gestational-age (AGA) fetuses and neonates on postnatal days 1 (N1) and 4 (N4). Maternal and fetal MCP-1 concentrations were decreased (P<001 and P = .018, resp.), whereas N1 MCP-1 concentrations were elevated in IUGR group (P = .012). In both groups, fetal MCP-1 concentrations were lower compared to N1 and N4 ones (P = .045, P = .012, resp., for AGA, P< .001 in each case for IUGR). Reduced maternal and fetal MCP-1 concentrations in IUGR may reflect failure of trophoblast invasion, suggesting that down-regulation of MCP-1 may be involved in the pathogenesis of IUGR. Increased MCP-1 concentrations in IUGR neonates and higher postnatal ones in all infants may be attributed to gradual initiation of ex utero angiogenesis, which is possibly enhanced in IUGR.

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Copyright © 2007 Despina D. Briana et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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