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Transplacental thyroxine and fetal brain development

2003; American Society for Clinical Investigation; Volume: 111; Issue: 7 Linguagem: Inglês

10.1172/jci18236

1558-8238

R. Thomas Zoeller,

Birth, Development, and Health

in nature, I predict that mice with no heparan sulfate activity will develop thrombosis, supporting the concept that heparan sulfate is antithrombotic.These mice also should exhibit more profound intrauterine growth retardation than 3-OST-1 knockouts (15), thereby demonstrating a biological gradient for this unexpected finding depending on the extent to which heparan sulfate activity is reduced. SummaryWith their studies in 3-OST-1 knockout mice, HajMohammadi and colleagues (15) have advanced our understanding of the pathways that regulate thrombin.Antithrombin is critical for thrombin regulation because even partial deficiency is associated with thrombosis.In contrast, complete deficiency of heparan sulfate activity is necessary to provoke thrombosis.These findings suggest that small amounts of residual heparan sulfate activity are sufficient to catalyze antithrombin or that other vessel wall glycosaminoglycans can compensate for all but complete lack of heparan sulfate activity.