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Hypoglycemia-induced changes in VEGF, HIF-1 ฮฑ, and HIF-2ฮฑ protein expression in E9.5 embryonic heart.
Glucose is critical to the organogenesis-stage embryo and embryonic heart. Hypoglycemia (HG) interferes with normal development and function, and induces programmed cell death (PCD), in the embryonic heart. Increased levels of VEGF, HIF-1ฮฑ , and HIF-2ฮฑ have been noted in non-cardiac embryonic tissues in response to hypoglycemic stress. HIF-1ฮฑ and HIF-2ฮฑ are also known to induce PCD in non-cardiac tissues. In this study we investigated the effects of HG on microvasculature, VEGF, HIF-1ฮฑ, and HIF-2ฮฑ in E9.5 embryonic heart (plug = E0.5). Mouse embryos were exposed in vivo or in vitro for 24hr at E9.5 to hypoglycemia (40-60mg/dl glucose) or normoglycemia (150-180mg/dl glucose) and evaluated morphologically and by immunohistochemistry (IHC). Morphological analysis was performed to demonstrate changes in vasculature using transgenic embryos carrying a TIE2/LacZ construct and stained with X-gal. IHC analyses were performed on paraffin-embedded embryonic tissue sections for VEGF, HIF-1ฮฑ, and HIF-2 ฮฑ. TIE2/LacZ embryos revealed an increase in microvasculature after exposure to HG compared to normoglycemia. IHC demonstrated increased VEGF staining in hearts of embryos exposed to HG compared to normoglycemia. A dramatic increase in HIF-1ฮฑ staining, and a slight increase in HIF-2ฮฑ staining, was observed in hearts of embryos exposed to HG compared to normoglycemia. HG appears to induce a compensatory increase in VEGF and microvasculature in the embryo. The stress-inducible factors, HIF-1ฮฑ and HIF-2ฮฑ, may be involved in HG-induced cardiac PCD and malformations.
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