Showing papers by "Yaowu Zheng published in 2010"
TL;DR: An unexpected role for protease signaling in neural tube closure and the formation of the central nervous system is reported and a local protease network that may trigger Par2 signaling and monitor and regulate epithelial integrity is identified.
160 citations
TL;DR: In mouse model of LPS‐induced blood hypercoagulation, significant reduction of plasma thrombin‐antithrombin formation was observed in V EGF repressed mice, and tissues expressed different modes of damages, indicating that VEGF regulates coagulation cascade and may affect sepsis.
Abstract: VEGF is an important growth factor in embryonic development and functional maintenance of adult organs. Single allele inactivation of VEGF leads to embryonic lethality and many conditional disruptions show dramatic phenotypes or reduced viabilities. To overcome this burden, a reversible system, which was used in the regulation of VEGF expression and functional studies of many tissues and organs in adult, was developed. VEGF is known for expression in many tissues and high expression in platelets. Repression of VEGF expression showed significant defect in bleeding time and clotting time. In mouse model of LPS-induced blood hypercoagulation, significant reduction of plasma thrombin-antithrombin formation was observed in VEGF repressed mice, and tissues expressed different modes of damages. These results indicate that VEGF regulates coagulation cascade and may affect sepsis. This is the first genetic evidence of direct link between VEGF transcription and coagulation cascade. Studies using this system may help us to find out how VEGF regulates coagulation cascade and provide new strategies in treating coagulation related diseases.
16 citations
TL;DR: It is indicated that podocyte‐specific VEGF down‐regulation resulted in poor kidney performance and led mice to be more susceptible to further kidney damages.
Abstract: It is well-known that vascular endothelial growth factor (VEGF) plays a key role in development and pathology, but its function in normal adult tissues is rarely understood. Increased use of anti-angiogenic therapies targeting VEGF in human pathologies have shown more and more adverse effects. In this report, a conditional expression model (Tet-On system) was used to down-regulate podocyte VEGF in adult mice, which resulted in many kidney problems, characterized by glomerular morphological changes, proteinuria, reduced water consumption and urination, increased urine electro-conductivity, as well as high susceptibility to BSA stress. Our findings indicated that podocyte-specific VEGF down-regulation resulted in poor kidney performance and led mice to be more susceptible to further kidney damages.
10 citations
01 Jan 2010
TL;DR: This is the first genetic evidence of direct link between VEGF transcription and coagulation cascade and may affect sepsis.
Abstract: Summary VEGF is an important growth factor in embryonic development and functional maintenance of adult organs. Single allele inactivation of VEGF leads to embryonic lethality and many conditional disruptions show dramatic phenotypes or reduced viabilities. To overcome this burden, a reversible system, which was used in the regulation of VEGF expression and functional studies of many tissues and organs in adult, was developed. VEGF is known for expression in many tissues and high expression in platelets. Repression of VEGF expression showed significant defect in bleeding time and clotting time. In mouse model of LPS-induced blood hypercoagulation, significant reduction of plasma thrombin-antithrombin formation was observed in VEGF repressed mice, and tissues expressed different modes of damages. These results indicate that VEGF regulates coagulation cascade and may affect sepsis. This is the first genetic evidence of direct link between VEGF transcription and coagulation cascade. Studies using this system may help us to find out how VEGF regulates coagulation cascade and provide new strategies in treating coagulation related diseases. 2010 IUBMB IUBMB Life, 62(11): 819–824, 2010