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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The role of basic fibroblast growth factor in gastric ulceration

Hull, M. A. January 1997 (has links)
No description available.
2

Molecular analysis of the leukocyte cell-surface adhesion protein L-selectin

Nicholson, Martin William Michael January 1995 (has links)
No description available.
3

Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle

Baxter, Shannon A. 30 October 2010 (has links)
The homeobox transcription factor PROX1 is the mammalian ortholog of the Drosophila gene Prospero. Expression of PROX1 in a subset of venous endothelial cells changes their fate to lymphatic endothelial cells (LEC). PROX1 is required for lymphatic development as Prox1 null mice lack all lymphatic vasculature. PROX1 has been shown to have cell-type dependent roles in regulating the cell cycle. We hypothesize that PROX1 functions as a key cell cycle regulator in LECs and promotes their cell cycle progression. In this study, immunocytochemistry, western blotting and luciferase assays were used to characterize PROX1 mediated activation of the mouse Ccne1 promoter. Following deletion of the Prospero 1 domain (PD1∆), the resulting PROX1 protein is localized to both the nucleus and the cytoplasm. We have determined that PROX1 requires both E2F binding sites located in the Ccne1 promoter to activate transcription of the gene. We observed that siRNA knockdown of Prox1 reduced CYCLIN E1 protein levels as well as decreased cellular proliferation in LECs. In contrast, overexpression of a version of PROX1 in which the homeodomain and Prospero domain 2 (HDPD2Δ) were deleted increased CYCLIN E1 protein levels in human umbilical vein endothelial cells (HUVEC), but resulted in the arrest of cells in the G1 phase. We have also established that PROX1 is phosphorylated in primary human LECs. We have shown a role for the PD1 domain in mediating PROX1 subcellular localization and we have observed that the expression of the HDPD2Δ version of PROX1 blocks proliferation in HUVECs. We are the first to demonstrate a role for PROX1 as a transcriptional co-activator and to establish that PROX1 is phosphorylated in LECs.
4

Repression of the blood endothelial marker CD146 by the homeobox gene PROX1

OGUTCEN, EZGI 23 July 2010 (has links)
CD146 is a cell adhesion molecule that has been shown to regulate cell adhesion, migration and proliferation of different cell types. It is highly expressed in blood endothelial cells (BECs), but is only lowly expressed in lymphatic endothelial cells (LECs). The PROX1 homeobox gene is a master regulator of lymphangiogenesis and its expression is necessary and sufficient to drive venous endothelial cells into a LEC phenotype. The highly permeable nature of the lymphatic vessels may partially derive from PROX1 mediated repression of CD146 transcription. We hypothesize that PROX1 promotes lymphatic differentiation by repressing CD146 transcription. In gain of function studies, Human Umbilical Vein Endothelial Cells (HUVECs) were infected with adenoviruses encoding EGFP, wild type PROX1 (AdProx1) or a Homeo-Prospero domain deleted version of PROX1 (AdHDPD), which cannot bind DNA. In order to knockdown PROX1, LECs were transfected with PROX1 specific siRNA. When compared to EGFP infected HUVECs, AdProx1 infected HUVECs had decreased CD146 expression both at protein and mRNA levels. In contrast, AdHDPD infected HUVECs had increased levels of CD146 expression. In support of a role for PROX1 in repressing CD146, PROX1 siRNA transfected LECs express higher levels of CD146 as compared to mock transfected LECs or LECs transfected with control siRNA. Based on these results, we predict that CD146 expression is kept at basal levels by an unknown repressor bound to the CD146 promoter. By interacting with this unknown repressor, PROX1 further represses CD146 expression. On the other hand, the DNA binding-deficient ΔHDPD version of PROX1 binds the unknown repressor and sequesters it from the CD146 promoter, thereby relieving the repression of CD146 expression in ECs. Different levels of CD146 expression between BECs and LECs might reflect the structural and functional differences between blood and lymphatic vessels. Since CD146 plays a critical role in EC adhesion, regulation of CD146 expression in ECs might be one of the key factors regulating vessel permeability.
5

Mechanisms of PROX1 mediated regulation of the lymphatic endothelial cell cycle

Baxter, Shannon A. 30 October 2010 (has links)
The homeobox transcription factor PROX1 is the mammalian ortholog of the Drosophila gene Prospero. Expression of PROX1 in a subset of venous endothelial cells changes their fate to lymphatic endothelial cells (LEC). PROX1 is required for lymphatic development as Prox1 null mice lack all lymphatic vasculature. PROX1 has been shown to have cell-type dependent roles in regulating the cell cycle. We hypothesize that PROX1 functions as a key cell cycle regulator in LECs and promotes their cell cycle progression. In this study, immunocytochemistry, western blotting and luciferase assays were used to characterize PROX1 mediated activation of the mouse Ccne1 promoter. Following deletion of the Prospero 1 domain (PD1∆), the resulting PROX1 protein is localized to both the nucleus and the cytoplasm. We have determined that PROX1 requires both E2F binding sites located in the Ccne1 promoter to activate transcription of the gene. We observed that siRNA knockdown of Prox1 reduced CYCLIN E1 protein levels as well as decreased cellular proliferation in LECs. In contrast, overexpression of a version of PROX1 in which the homeodomain and Prospero domain 2 (HDPD2Δ) were deleted increased CYCLIN E1 protein levels in human umbilical vein endothelial cells (HUVEC), but resulted in the arrest of cells in the G1 phase. We have also established that PROX1 is phosphorylated in primary human LECs. We have shown a role for the PD1 domain in mediating PROX1 subcellular localization and we have observed that the expression of the HDPD2Δ version of PROX1 blocks proliferation in HUVECs. We are the first to demonstrate a role for PROX1 as a transcriptional co-activator and to establish that PROX1 is phosphorylated in LECs.
6

Repression of the blood endothelial marker CD146 by the homeobox gene PROX1

OGUTCEN, EZGI 23 July 2010 (has links)
CD146 is a cell adhesion molecule that has been shown to regulate cell adhesion, migration and proliferation of different cell types. It is highly expressed in blood endothelial cells (BECs), but is only lowly expressed in lymphatic endothelial cells (LECs). The PROX1 homeobox gene is a master regulator of lymphangiogenesis and its expression is necessary and sufficient to drive venous endothelial cells into a LEC phenotype. The highly permeable nature of the lymphatic vessels may partially derive from PROX1 mediated repression of CD146 transcription. We hypothesize that PROX1 promotes lymphatic differentiation by repressing CD146 transcription. In gain of function studies, Human Umbilical Vein Endothelial Cells (HUVECs) were infected with adenoviruses encoding EGFP, wild type PROX1 (AdProx1) or a Homeo-Prospero domain deleted version of PROX1 (AdHDPD), which cannot bind DNA. In order to knockdown PROX1, LECs were transfected with PROX1 specific siRNA. When compared to EGFP infected HUVECs, AdProx1 infected HUVECs had decreased CD146 expression both at protein and mRNA levels. In contrast, AdHDPD infected HUVECs had increased levels of CD146 expression. In support of a role for PROX1 in repressing CD146, PROX1 siRNA transfected LECs express higher levels of CD146 as compared to mock transfected LECs or LECs transfected with control siRNA. Based on these results, we predict that CD146 expression is kept at basal levels by an unknown repressor bound to the CD146 promoter. By interacting with this unknown repressor, PROX1 further represses CD146 expression. On the other hand, the DNA binding-deficient ΔHDPD version of PROX1 binds the unknown repressor and sequesters it from the CD146 promoter, thereby relieving the repression of CD146 expression in ECs. Different levels of CD146 expression between BECs and LECs might reflect the structural and functional differences between blood and lymphatic vessels. Since CD146 plays a critical role in EC adhesion, regulation of CD146 expression in ECs might be one of the key factors regulating vessel permeability.
7

In vitro studies on endothelial cells

Hunter, Nikolas Ross January 1987 (has links)
No description available.
8

In vitro studies of functional effects of antiendothelial cell autoantibodies

Carvalho, Maria Dulce Ribeiro January 1996 (has links)
No description available.
9

Validation of Rat Mesentery Culture Model for Time-Lapse Drug Evaluation and Cell Lineage Studies

January 2017 (has links)
acase@tulane.edu / An emerging need in the microcirculation research is the development of biomimetic angiogenesis models that recapitulate the complexity of a real tissue. Angiogenesis, defined as the growth of new vessels from pre-existing vessels, involves multiple cell types, such as endothelial and perivascular cells, in a multi-system setting since blood vessel networks are usually accompanied by lymphatic and nervous systems. Therefore, a need exists for a model of angiogenesis from intact microvascular networks that more closely reflects an in vivo scenario for the investigation of underlying mechanisms and the pre-clinical development of therapies. While other approaches have proven useful in identifying mechanistic signaling information, they are often limited in their complexity and capability to mimic physiologically relevant scenarios in one way or another and do not fully recapitulate the in vivo scenario. The first aim of this study was to demonstrate the ability for time-lapse comparisons of microvascular networks in angiogenesis scenarios to investigate the fate of vascular islands and investigate the endothelial cell plasticity. We developed a time-lapse angiogenesis model based on our previously introduced rat mesentery model. We demonstrated that time-lapse rat mesentery culture model is a powerful tool to study multi-cell, multi-system dynamics in microvascular networks. For the second aim of this study, we used the method developed in aim one to establish rat mesentery culture model as a novel anti-angiogenic drug screening tool. Using time-lapse model enabled tissue-specific comparisons before and after drug treatment to investigate its effects on entire microvascular networks. Validation of this method for anti-angiogenic drug testing was demonstrated using known angiogenesis inhibitor. Next, we showcased a potential application of the model for evaluating unknown effects of drug repositioning based on FDA-approved drug combinations. The results demonstrated the ability to identify concentration-dependent effects in an intact network scenario. The objective of the third aim was to showcase the capability of the rat mesentery culture model to study stem cell fate. We developed a protocol to deliver mesenchymal stem cells to mesentery tissues and culture for a period of time in a controlled environment. We confirmed the perivascular location of a subset of stem cells within capillaries, with morphologies resembling pericytes, and expressing pericyte markers. We also demonstrated that tracking stem cells within the microvascular networks is possible using the rat mesentery culture model. Furthermore, we reported a high variability in perivascular incorporation among cells from different donors. This work establishes for the first time, to the best of our knowledge, an ex vivo model to look at microvascular networks before and after growth. We confirmed, for the first time, vascular island incorporation as a new mode of angiogenesis using a novel method for time-lapse imaging of microvascular networks ex vivo. The results also establish this method for drug testing and stem cell tracking in a microvascular setting. / 1 / Mohammad Sadegh Azimi
10

The mechanism of endothelial cell specific gene expression of Von Willebrand Factor in vivo

Nassiri, Marjan 06 1900 (has links)
In vivo analyses of the Von Willebrand Factor (VWF) promoter previously demonstrated that a fragment spanning sequences -487 to +247 targets promoter activation to brain vascular endothelial cells. This fragment is active in all embryonic vessels of transgenic mice but in adult mice its activity is restricted to brain vascular endothelial cells, while endogenous VWF gene is expressed in vasculature of all major organs. In this study we demonstrate that a DNase I hypersensitive (HSS) sequences in intron 51 of the VWF gene contain cis-acting elements that are necessary for the VWF gene transcription in a subset of lung endothelial cells in vivo. Our results demonstrated that Nuclear Factor 1 (NF1) and Nuclear transcription Factor Y (NFY) repressors contribute to VWF organ-specific regulation. Mutation of the NF1 binding site resulted in promoter activation in lung and heart, while mutation of the repressor corresponding to a novel binding site for NFY resulted in promoter activation in kidney vasculature. / Experimental Medicine

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