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      Bone Morphogenetic Protein-7 from Serum of Pregnant Mice Is Available to the Fetus through Placental Transfer during Early Stages of Development

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          Background: BMP-7 is an important mediator of metanephric mesenchyme differentiation during kidney development. Gene knockout studies have shown that BMP-7 null mutation mice die shortly after birth due to renal failure, although the induction of metanephric structures has initially occurred (E11–E13). Materials and Methods: Iodinated BMP-7 was injected into the tail vein of pregnant mice and its availability to tissues and fetuses was further analyzed by tissue uptake, LM autoradiography and SDS-PAGE electrophoresis. Results: Studies on the distribution of <sup>125</sup>I-BMP-7 injected through the tail vein of pregnant mice indicated that <sup>125</sup>I-BMP-7 passed across the placenta and localized in developing fetal organs, in particular kidneys, up to day 14 of gestation. At later stages of pregnancy <sup>125</sup>I-BMP-7 did not pass the trophoblasts of the placental barrier and did not enter the fetal blood vessels. Conclusion: The analysis of the distribution of <sup>125</sup>I-BMP-7 from pregnant mice to fetal organs, in particular the kidney, suggests a cross-over of maternal circulating BMP-7 to the fetus through the placental barrier.

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          Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

          Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
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            Induction of nephrogenic mesenchyme by osteogenic protein 1 (bone morphogenetic protein 7).

            The definitive mammalian kidney forms as the result of reciprocal interactions between the ureteric bud epithelium and metanephric mesenchyme. As osteogenic protein 1 (OP-1/bone morphogenetic protein 7), a member of the TGF-beta superfamily of proteins, is expressed predominantly in the kidney, we examined its involvement during metanephric induction and kidney differentiation. We found that OP-1 mRNA is expressed in the ureteric bud epithelium before mesenchymal condensation and is subsequently seen in the condensing mesenchyme and during glomerulogenesis. Mouse kidney metanephric rudiments cultured without ureteric bud epithelium failed to undergo mesenchymal condensation and further epithelialization, while exogenously added recombinant OP-1 was able to substitute for ureteric bud epithelium in restoring the induction of metanephric mesenchyme. This OP-1-induced nephrogenic mesenchyme differentiation follows a developmental pattern similar to that observed in the presence of the spinal cord, a metanephric inducer. Blocking OP-1 activity using either neutralizing antibodies or antisense oligonucleotides in mouse embryonic day 11.5 mesenchyme, cultured in the presence of metanephric inducers or in intact embryonic day 11.5 kidney rudiment, greatly reduced metanephric differentiation. These results demonstrate that OP-1 is required for metanephric mesenchyme differentiation and plays a functional role during kidney development.
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              Localization of osteogenic protein-1 (bone morphogenetic protein-7) during human embryonic development: high affinity binding to basement membranes.

               V Latin,  P. Chen,  T. Sampath (1994)
              Osteogenic protein-1 (OP-1) is a member of the bone morphogenetic protein subfamily of the transforming growth factor-beta (TGF-beta) superfamily. Since members of the TGF-beta superfamily have a role in tissue development the distribution of OP-1 in developing human embryos (gestational age 5-14 weeks) was examined by immunohistochemical methods. Positive staining for OP-1 was observed in: sclerotome, hypertrophied chondrocytes, osteoblasts, periosteum, epithelial cells of the adrenal "provisional cortex" and the convoluted tubules of developing kidneys. In the developing lungs, pancreas and skin, OP-1 was localized in basement membranes underlying the epithelium. In vitro binding studies of 125I-OP-1 to various extracellular matrix components revealed high affinity of OP-1 for type IV collagen and less for heparin, collagen types I and VI. Present findings suggest that, in addition to bone formation, OP-1 could have other important regulatory roles in human embryogenesis with high binding affinity to a basement membrane component.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                May 2004
                17 November 2004
                : 97
                : 1
                : e26-e32
                aDepartment of Anatomy, Medical School University of Zagreb, Zagreb, Croatia; bCreative BioMolecules, Inc., Hopkinton, Mass., USA
                77595 Nephron Exp Nephrol 2004;97:e26–e32
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 4, References: 22, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/77595
                Original Paper


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