Investigation of Integrated Effects of Hydroxyapatite and VEGF on Capillary Morphogenesis of Endothelial Cells

2019 ◽  
Vol 2 (6) ◽  
pp. 2339-2346
Author(s):  
Yang Wu ◽  
Rong Fu ◽  
Swetaparna Mohanty ◽  
Malak Nasser ◽  
Bingxin Guo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Capillary Morphogenesis

scholarly journals CYP1B1 expression promotes the proangiogenic phenotype of endothelium through decreased intracellular oxidative stress and thrombospondin-2 expression

Blood ◽  
2009 ◽  
Vol 113 (3) ◽  
pp. 744-754 ◽  
Author(s):  
Yixin Tang ◽  
Elizabeth A. Scheef ◽  
Shoujian Wang ◽  
Christine M. Sorenson ◽  
Craig B. Marcus ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Endothelial Cells ◽  
Retinopathy Of Prematurity ◽  
Cellular Responses ◽  
Retinal Endothelial Cells ◽  
Capillary Morphogenesis ◽  
Ischemic Retinopathy ◽  
Intracellular Oxidative Stress

Abstract Reactive species derived from cell oxygenation processes play an important role in vascular homeostasis and the pathogenesis of many diseases including retinopathy of prematurity. We show that CYP1B1-deficient (CYP1B1−/−) mice fail to elicit a neovascular response during oxygen-induced ischemic retinopathy. In addition, the retinal endothelial cells (ECs) prepared from CYP1B1−/− mice are less adherent, less migratory, and fail to undergo capillary morphogenesis. These aberrant cellular responses were completely reversed when oxygen levels were lowered or an antioxidant added. CYP1B1−/− ECs exhibited increased oxidative stress and expressed increased amounts of the antiangiogenic factor thrombospondin-2 (TSP2). Increased lipid peroxidation and TSP2 were both observed in retinas from CYP1B1−/− mice and were reversed by administration of an antioxidant. Reexpression of CYP1B1 in CYP1B1−/− ECs resulted in down-regulation of TSP2 expression and restoration of capillary morphogenesis. A TSP2 knockdown in CYP1B1−/− ECs also restored capillary morphogenesis. Thus, CYP1B1 metabolizes cell products that modulate intracellular oxidative stress, which enhances production of TSP2, an inhibitor of EC migration and capillary morphogenesis. Evidence is presented that similar changes occur in retinal endothelium in vivo to limit neovascularization.

scholarly journals HGF-induced capillary morphogenesis of endothelial cells is regulated by Src

2006 ◽  
Vol 344 (2) ◽  
pp. 617-622 ◽  
Author(s):  
Shigeru Kanda ◽  
Hiroshi Kanetake ◽  
Yasuyoshi Miyata
Keyword(s):  
Endothelial Cells ◽  
Capillary Morphogenesis

scholarly journals Sonic Hedgehog Induces Capillary Morphogenesis by Endothelial Cells through Phosphoinositide 3-Kinase

2003 ◽  
Vol 278 (10) ◽  
pp. 8244-8249 ◽  
Author(s):  
Shigeru Kanda ◽  
Yasushi Mochizuki ◽  
Takashi Suematsu ◽  
Yasuyoshi Miyata ◽  
Koichiro Nomata ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Sonic Hedgehog ◽  
Capillary Morphogenesis ◽  
Phosphoinositide 3 Kinase

Enforced expression of tissue inhibitor of matrix metalloproteinase-3 affects functional capillary morphogenesis and inhibits tumor growth in a murine tumor model

Blood ◽  
2002 ◽  
Vol 100 (9) ◽  
pp. 3361-3368 ◽  
Author(s):  
William W. Spurbeck ◽  
Catherine Y. C. Ng ◽  
Ted S. Strom ◽  
Elio F. Vanin ◽  
Andrew M. Davidoff
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Matrix Metalloproteinases ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Severe Combined Immunodeficiency ◽  
Melanoma Tumor ◽  
Vitro Assay ◽  
Capillary Morphogenesis

Abstract Homeostasis of the extracellular matrix is a delicate balance between degradation and remodeling, the balance being maintained by the interaction of activated matrix metalloproteinases (MMPs) and specific tissue inhibitors of matrix metalloproteinases (TIMPs). Up-regulation of MMP activity, favoring proteolytic degradation of the basement membrane and extracellular matrix, has been linked to tumor growth and metastasis, as well as tumor-associated angiogenesis, whereas inhibition of MMP activity appears to restrict these processes. We have used retroviral-mediated gene delivery to effect sustained autocrine expression of TIMP-3 in murine neuroblastoma and melanoma tumor cells in order to further examine the ability of TIMPs to inhibit angiogenesis in vivo. Growth of both histologic types of gene-modified tumor cells in severe combined immunodeficiency (SCID) mice was significantly restricted when compared with controls. Grossly, these tumors were small and had few feeding vessels. Histologic evaluation revealed that although tumors overexpressing TIMP-3 had an increased number of CD31+endothelial cells, these endothelial cells had not formed functional tubules, as evidenced by decreased vessel continuity and minimal pericyte recruitment. This effect appears to be mediated, in part, by decreased expression of vascular endothelial (VE)–cadherin by endothelial cells in the presence of TIMP-3 as seen both in an in vitro assay and in TIMP-3–overexpressing tumors. Taken together, these results demonstrate that overexpression of TIMP-3 can inhibit angiogenesis and associated tumor growth, and that the antiangiogenic effects of TIMP-3 appear to be mediated through the inhibition of functional capillary morphogenesis.

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