Background: Chemokines induce cell motility during embryogenesis by activating specific receptors. While the orchestration of organogenesis is complex and requires the interaction of many morphoregulatory molecules that lead to coordinated organ development, limited knowledge exists regarding the human developmental biology of chemokines and their receptors. Such information on chemokine receptor expression could potentially enhance our understanding of organogenesis in the normal human fetus.
Aim: To determine the distribution of the CXC receptors (CXCR-1, CXCR-2, CXCR-3, and CXCR-4) and SDF-1 in human fetuses.
Subjects: Tissues from human fetuses 12-15 weeks (n = 5) and 16-19 weeks (n = 5) gestation were studied.
Outcome Measures: Reverse transcription-PCR was performed to simultaneously determine the gene expression of CXCR-1-4 and SDF-1, and immunohistochemical staining of non-hematopoietic tissues was used to determine the specific cellular proteins.
Results: CXCR-1-4 and SDF-1 mRNA were present in every tissue examined. The expression of CXCR-3 in kidney, liver, and brain was dependent upon gestational age. CXCR-1-4 protein was expressed in non-hematopoietic cells in the brain, heart, intestine, and kidney.
Conclusions: CXCR-1-4 and SDF-1 genes are widely expressed in the normal human fetus. This suggests that these gene products could influence fetal development.
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http://dx.doi.org/10.1016/j.earlhumdev.2004.10.022 | DOI Listing |
Early Hum Dev
June 2005
Department of Pediatrics, Division of Neonatology, University of Florida, Gainesville, FL 32610, USA.
Background: Chemokines induce cell motility during embryogenesis by activating specific receptors. While the orchestration of organogenesis is complex and requires the interaction of many morphoregulatory molecules that lead to coordinated organ development, limited knowledge exists regarding the human developmental biology of chemokines and their receptors. Such information on chemokine receptor expression could potentially enhance our understanding of organogenesis in the normal human fetus.
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