Selective killing of smooth muscle cells in culture by the ricin A-chain conjugated with monoclonal antibodies to a cell surface antigen via a dextran bridge

1985 ◽  
Vol 41 (10) ◽  
pp. 1342-1344 ◽  
Author(s):  
O. Yu. Printseva ◽  
A. I. Faerman ◽  
A. V. Maksimenko ◽  
A. G. Tonevitsky ◽  
O. B. Ilynsky ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Monoclonal Antibodies ◽  
Cell Surface ◽  
Smooth Muscle Cells ◽  
Surface Antigen ◽  
Muscle Cells ◽  
Ricin A Chain ◽  
A Cell ◽  
A Chain ◽  
Ricin A

A 90-kDa surface antigen of immature smooth muscle cells is ICAM-1

1991 ◽  
Vol 261 (4) ◽  
pp. L21-L22
Author(s):  
O. Yu. Printseva ◽  
M. M. Peclo ◽  
A. V. Tjurmin ◽  
A. M. Gown
Keyword(s):  
Monoclonal Antibody ◽  
Smooth Muscle ◽  
Monoclonal Antibodies ◽  
Smooth Muscle Cells ◽  
Molecular Mass ◽  
Surface Antigen ◽  
Muscle Cells ◽  
Human Aorta ◽  
Long Term Culture

A monoclonal antibody, designated 10F3, that reacts with an antigen of molecular mass 90,000 Da has been developed by immunization of BALB/c mice with smooth muscle cells in long-term culture. The cells were originally isolated from fetal human aorta. The 10F3 was identified as an antibody that reacts with the ICAM-1 molecule. ICAM-1 is a mesenchymal antigen that is lost during differentiation of cells other than endothelium but is reexpressed by the intimal cells of vessels involved in atherogenesis. atherosclerosis; monoclonal antibodies

scholarly journals Cytotoxicity of a cell-reactive immunotoxin containing ricin A chain is potentiated by an anti-immunotoxin containing ricin B chain.

1984 ◽  
Vol 160 (1) ◽  
pp. 341-346 ◽  
Author(s):  
E S Vitetta ◽  
R J Fulton ◽  
J W Uhr
Keyword(s):  
Cell Surface ◽  
Cell Line ◽  
Ricin A Chain ◽  
Daudi Cell ◽  
A Cell ◽  
A Chain ◽  
Ricin A

In vitro killing of the human Daudi cell line by either univalent [F(ab')] or divalent (IgG) forms of rabbit anti-human Ig (RAHIg) coupled to ricin A chain can be specifically potentiated by a "piggyback" treatment with ricin B chain coupled to goat anti-rabbit Ig (GARIg). When cells are treated with univalent immunotoxin (IT) [F(ab') RAHIg-A] and then cultured, IT can be detected on the cell surface for at least 5 h, since GARIg-B can still enhance killing at this time. These results provide a strategy for in vivo use of A chain- and B chain-containing IT.

A 90-kDa surface antigen of immature smooth muscle cells is ICAM-1

1991 ◽  
Vol 261 (4) ◽  
pp. 21-22
Author(s):  
O. Yu. Printseva ◽  
M. M. Peclo ◽  
A. V. Tjurmin ◽  
A. M. Gown
Keyword(s):  
Monoclonal Antibody ◽  
Smooth Muscle ◽  
Monoclonal Antibodies ◽  
Smooth Muscle Cells ◽  
Molecular Mass ◽  
Surface Antigen ◽  
Muscle Cells ◽  
Human Aorta ◽  
Long Term Culture

A monoclonal antibody, designated 10F3, that reacts with an antigen of molecular mass 90,000 Da has been developed by immunization of BALB/c mice with smooth muscle cells in long-term culture. The cells were originally isolated from fetal human aorta. The 10F3 was identified as an antibody that reacts with the ICAM-1 molecule. ICAM-1 is a mesenchymal antigen that is lost during differentiation of cells other than endothelium but is reexpressed by the intimal cells of vessels involved in atherogenesis. atherosclerosis; monoclonal antibodies

scholarly journals The role of membrane-membrane interactions in the regulation of endothelial cell growth.

1985 ◽  
Vol 100 (6) ◽  
pp. 1934-1940 ◽  
Author(s):  
R L Heimark ◽  
S M Schwartz
Keyword(s):  
Growth Rate ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Cell Surface ◽  
Smooth Muscle Cells ◽  
Inhibitory Activity ◽  
Surface Preparation ◽  
Muscle Cells ◽  
Inhibition Of Growth ◽  
A Cell

A cell surface preparation from confluent endothelial cells can inhibit DNA synthesis of actively growing endothelial cells. The decrease in the rate of [3H]thymidine incorporation is concentration dependent and levels off at 47% of the control. The preparation has no affect on the growth of vascular smooth muscle cells. A similar preparation from smooth muscle cells does not show inhibitory activity with either endothelial or smooth muscle cells. The inhibition of growth can also be demonstrated by a decrease in thymidine index and growth rate. The inhibition is transient and after 48 h, the growth rate is similar to that of the control. In a wound edge assay, both migration and proliferation are inhibited. The inhibitory activity is partially labile to trypsin and abolished by pepsin, heating at 100 degrees C, or reduction. Cell surface iodination and analysis of the proteins removed by urea treatment by SDS polyacrylamide gel electrophoresis show at least 11 bands with apparent molecular weights from 250,000 to 18,000. These radiolabeled proteins, as well as the active component of the cell surface preparation, are sedimentable at 100,000 g for 1 h. They are both solubilized in 30 mM octyl glucoside but not by treatment with 0.1 M sodium carbonate, pH 11.5. These results suggest that the activity is due to a cell-surface membrane fraction and may provide a basis for studying the mechanism of density-dependent inhibition of growth in a normal cell of defined origin.

Monoclonal Antibodies to Purified Ricin A-Chain: Production and Properties

Hybridoma ◽  
1987 ◽  
Vol 6 (2) ◽  
pp. 135-149 ◽  
Author(s):  
JOHN E. LEONARD ◽  
LAURA E. TANNEY ◽  
MORA L. COLLINS ◽  
IVOR ROYSTON ◽  
RAYMOND TAETLE
Keyword(s):  
Monoclonal Antibodies ◽  
Ricin A Chain ◽  
A Chain ◽  
Ricin A

scholarly journals Gene Expression Profiling of Leiomyoma and Myometrial Smooth Muscle Cells in Response to Transforming Growth Factor-β

Endocrinology ◽  
2005 ◽  
Vol 146 (3) ◽  
pp. 1097-1118 ◽  
Author(s):  
Xiaoping Luo ◽  
Li Ding ◽  
Jingxia Xu ◽  
Nasser Chegini
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Binding Protein ◽  
Muscle Cells ◽  
Time Dependent ◽  
Early Gene ◽  
A Cell

Altered expression of the TGF-β system is recognized to play a central role in various fibrotic disorders, including leiomyoma. In this study we performed microarray analysis to characterize the gene expression profile of leiomyoma and matched myometrial smooth muscle cells (LSMC and MSMC, respectively) in response to the time-dependent action of TGF-β and, after pretreatment with TGF-β type II receptor (TGF-βRII) antisense oligomer-blocking/reducing TGF-β autocrine/paracrine actions. Unsupervised and supervised assessments of the gene expression values with a false discovery rate selected at P ≤ 0.001 identified 310 genes as differentially expressed and regulated in LSMC and MSMC in a cell- and time-dependent manner by TGF-β. Pretreatment with TGF-βRII antisense resulted in changes in the expression of many of the 310 genes regulated by TGF-β, with 54 genes displaying a response to TGF-β treatment. Comparative analysis of the gene expression profile in TGF-βRII antisense- and GnRH analog-treated cells indicated that these treatments target the expression of 222 genes in a cell-specific manner. Gene ontology assigned these genes functions as cell cycle regulators, transcription factors, signal transducers, tissue turnover, and apoptosis. We validated the expression and TGF-β time-dependent regulation of IL-11, TGF-β-induced factor, TGF-β-inducible early gene response, early growth response 3, CITED2 (cAMP response element binding protein-binding protein/p300-interacting transactivator with ED-rich tail), Nur77, Runx1, Runx2, p27, p57, growth arrest-specific 1, and G protein-coupled receptor kinase 5 in LSMC and MSMC using real-time PCR. Together, the results provide the first comprehensive assessment of the LSMC and MSMC molecular environment targeted by autocrine/paracrine action of TGF-β, highlighting potential involvement of specific genes whose products may influence the outcome of leiomyoma growth and fibrotic characteristics by regulating inflammatory response, cell growth, apoptosis, and tissue remodeling.

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