scholarly journals Effect of TLR2 monoclonal antibody on new blood vessels and immune rejection response after keratoplasty

2019 ◽  
Vol 18 (1) ◽  
pp. 19
Author(s):  
Wang Ji ◽  
Yuan Jianshu ◽  
Wen Feng
Keyword(s):  
Monoclonal Antibody ◽  
Blood Vessels ◽  
Immune Rejection ◽  
Rejection Response

scholarly journals An antagonist of integrin alpha v beta 3 prevents maturation of blood vessels during embryonic neovascularization

1995 ◽  
Vol 108 (7) ◽  
pp. 2655-2661 ◽  
Author(s):  
C.J. Drake ◽  
D.A. Cheresh ◽  
C.D. Little
Keyword(s):  
Experimental Data ◽  
Monoclonal Antibody ◽  
Blood Vessels ◽  
Chorioallantoic Membrane ◽  
Normal Pattern ◽  
Basal Surface ◽  
Lumen Formation ◽  
Vessel Development ◽  
Alpha V Beta 3 ◽  
Chicken Chorioallantoic Membrane

Experimental data in this study demonstrate that integrin alpha v beta 3 is fundamentally involved in the maturation of blood vessels during embryonic neovascularization (vasculogenesis). Integrin alpha v beta 3 was specifically expressed on the surface of angioblasts during vessel development in quail embryos and vitronectin, a ligand for alpha v beta 3, localized to the basal surface of these cells. More importantly, microinjection of the anti-alpha v beta 3 monoclonal antibody, LM609, disrupted the normal pattern of vascular development. After exposure to LM609 the angioblasts in experimental embryos appeared as clusters of rounded cells lacking normal cellular protrusions. This led to disruption of lumen formation and abnormal vessel patterning. These findings demonstrate that during vasculogenesis ligation of integrin alpha v beta 3 on the surface of primordial endothelial cells is critical for the differentiation and maturation of blood vessels. Similar studies on chicken chorioallantoic membrane showed that LM609 blocks angiogenesis. Together the two studies suggest that integrin alpha v beta 3 plays a role in neovascularization of tissues.

Antitumor Effects of a Monoclonal Antibody that Binds Anionic Phospholipids on the Surface of Tumor Blood Vessels in Mice

2005 ◽  
Vol 11 (4) ◽  
pp. 1551-1562 ◽  
Author(s):  
Sophia Ran ◽  
Jin He ◽  
Xianming Huang ◽  
Melina Soares ◽  
Douglas Scothorn ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Blood Vessels ◽  
Antitumor Effects ◽  
Anionic Phospholipids ◽  
Tumor Blood Vessels

LRP: a new adhesion molecule for endothelial and smooth muscle cells

2001 ◽  
Vol 281 (4) ◽  
pp. F739-F750 ◽  
Author(s):  
Chuan Hu ◽  
Juan A. Oliver ◽  
Michael R. Goldberg ◽  
Qais Al-Awqati
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Adhesion Molecule ◽  
Kidney Development ◽  
Target Location ◽  
Muscle Cells ◽  
Laminin Receptor

We recently generated a monoclonal antibody that disrupted the association of endothelial cells with their target location during kidney development. Here, we purified the antigen of this monoclonal antibody to homogeneity using rat mesangial cell cytosol. Sequence revealed that it is a previously identified protein, termed the “laminin receptor precursor” (LRP). We found that this protein is expressed in most tissues, but immunocytochemistry revealed that it is present largely or entirely in blood vessels where it is located underneath endothelial cells and in between smooth muscle cells of the vascular wall. Vascular smooth muscle cells such as mesangial cells produce and secrete LRP into their extracellular matrix where it is present in several molecular weight forms. Endothelial cells produce very little if any of the protein, but they bind avidly to LRP-coated dishes. Anti-LRP antibodies prevent the binding of smooth muscle cells to uncoated plates, implying that cells that secrete it use it for attachment. In an assay for heterologous cell-to-cell interaction, antibodies to LRP inhibited the binding of smooth muscle cells to endothelial cells. Maturation and differentiation of blood vessels require interaction between endothelial and smooth muscle cells. LRP is a new component of the mesangial matrix, and we propose that it is an adhesion molecule that mediates an interaction between smooth muscle cells and endothelia.

scholarly journals Induction of Protective Genes Leads to Islet Survival and Function

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Hongjun Wang ◽  
Christiane Ferran ◽  
Chiara Attanasio ◽  
Fulvio Calise ◽  
Leo E. Otterbein
Keyword(s):  
Islet Transplantation ◽  
Immunosuppressive Drugs ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Immune Rejection ◽  
Necrosis Factor Alpha ◽  
Protective Genes ◽  
Rejection Response ◽  
And Function ◽  
Islet Survival

Islet transplantation is the most valid approach to the treatment of type 1 diabetes. However, the function of transplanted islets is often compromised since a large number ofβcells undergo apoptosis induced by stress and the immune rejection response elicited by the recipient after transplantation. Conventional treatment for islet transplantation is to administer immunosuppressive drugs to the recipient to suppress the immune rejection response mounted against transplanted islets. Induction of protective genes in the recipient (e.g., heme oxygenase-1 (HO-1), A20/tumor necrosis factor alpha inducible protein3 (tnfaip3), biliverdin reductase (BVR), Bcl2, and others) or administration of one or more of the products of HO-1 to the donor, the islets themselves, and/or the recipient offers an alternative or synergistic approach to improve islet graft survival and function. In this perspective, we summarize studies describing the protective effects of these genes on islet survival and function in rodent allogeneic and xenogeneic transplantation models and the prevention of onset of diabetes, with emphasis on HO-1, A20, and BVR. Such approaches are also appealing to islet autotransplantation in patients with chronic pancreatitis after total pancreatectomy, a procedure that currently only leads to 1/3 of transplanted patients being diabetes-free.

scholarly journals Recognition of Bergmann glial and ependymal cells in the mouse nervous system by monoclonal antibody.

1981 ◽  
Vol 90 (2) ◽  
pp. 448-458 ◽  
Author(s):  
I Sommer ◽  
C Lagenaur ◽  
M Schachner
Keyword(s):  
Monoclonal Antibody ◽  
White Matter ◽  
Blood Vessels ◽  
Adult Mouse ◽  
Intact Animal ◽  
Ependymal Cells ◽  
Spleen Cells ◽  
Ventricular Cells ◽  
Cerebellar Astrocytes ◽  
Neurological Mutant Mice

A monoclonal antibody designated anti-Cl was obtained from a hybridoma clone isolated from a fusion of NS1 myeloma with spleen cells from BALB/c mice injected with homogenate of white matter from bovine corpus callosum. In the adult mouse neuroectoderm, C1 antigen is detectable by indirect immunohistology in the processes of Bergmann glial cells (also called Golgi epithelial cells) in the cerebellum and of Müller cells in the retina, whereas other astrocytes that express glial fibrillary acidic protein in these brain areas are negative for C1. In addition, C1 antigen is expressed in most, if not all, ependymal cells and in large blood vessels, but not capillaries. In the developing, early postnatal cerebellum, C1 antigen is not confined to Bergmann glial and ependymal cells but is additionally present in astrocytes of presumptive white matter and Purkinje cell layer. In the embryonic neuroectoderm, C1 antigen is already expressed at day 10, the earliest stage tested so far. The antigen is distinguished in radially oriented structures in telencephalon, pons, pituitary anlage, and retina. Ventricular cells are not labeled by C1 antibody at this stage. C1 antigen is not detectable in astrocytes of adult or nearly adult cerebella from the neurological mutant mice staggerer, reeler, and weaver, but is present in ependymal cells and large blood vessels. C1 antigen is expressed not only in the intact animal but also in cultured cerebellar astrocytes and fibroblastlike cells. It is localized intracellularly.

Fibrin Deposition in Squamous Cell Carcinomas of the Larynx and Hypopharynx

1998 ◽  
Vol 80 (11) ◽  
pp. 767-772 ◽  
Author(s):  
Helga Bárdos ◽  
Attila Juhász ◽  
Gábor Répássy ◽  
Róza Ádány
Keyword(s):  
Monoclonal Antibody ◽  
Connective Tissue ◽  
Tumor Cell ◽  
Blood Vessels ◽  
Squamous Cell ◽  
Close Association ◽  
Squamous Cell Carcinomas ◽  
Coagulation Cascade ◽  
Fibrin Deposition ◽  
Tumor Blood Vessels

SummaryExtravascular fibrin deposition is frequently observed within and around neoplastic tissue and has been implicated in various aspects of tumor growth. The distribution of fibrin deposits was investigated in squamous cell carcinomas representing different stages of tumor progression of the larynx (n = 25) and hypopharynx (n = 9) by immunofluorescent techniques. Double and treble labelings were used to detect fibrinogen and fibrin in combination with marker antigens for tumor cells (cytokeratin), endothelial cells (von Willebrand factor), macrophages (recognized by KiM7), as well as factor XIII subunit A (FXIIIA) and tenascin (an embryonic extracellular matrix protein newly expressed during tumorigenesis). All tissue samples showed specific staining for fibrinogen/fibrin. Fibrin deposition was localized almost exclusively in the connective tissue compartment of tumors with characteristic accumulation at the interface of connective tissue and the tumorous parenchyma. In certain tumor samples showing highly invasive characteristics, fibrin deposits were observed in close association with tumor blood vessels in the tumor cell nodules. The overlapping reactions with polyclonal antibody to fibrinogen/fibrin and monoclonal antibody to fibrin indicate the activation of the coagulation cascade resulting in in situ thrombin activation and fibrin formation. Fibrin was crosslinked and stabilized by FXIIIA as revealed by urea insolubility test. Accumulation of phagocytozing macrophages detected by Ki M7 monoclonal antibody could be seen in areas of fibrin deposition. The blood coagulation factor XIIIA was detected in and around the cells labeled with Ki M7 antibody. Tenascin and fibrin deposits were found in the same localization in the tumor stroma and in association with tumor blood vessels within the tumor cell nodules. Neither fibrin nor tenascin were detected in the histologically normal tissue adjacent to tumors. The close association between fibrin deposits and macrophage accumulation strongly suggests the active participation of tumor-associated macrophages in the formation of stabilized intratumoral fibrin that facilitates tumor matrix generation and tumor angiogenesis.

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