Radiation induced endothelial cell retraction in vitro: Correlation with acute pulmonary edema

1999 ◽  
Vol 5 (1) ◽  
pp. 49-55 ◽  
Author(s):  
James M Onoda ◽  
Seema S Kantak ◽  
Clement A Diglio
Keyword(s):  
Endothelial Cell ◽  
Pulmonary Edema ◽  
Acute Pulmonary Edema ◽  
Radiation Induced ◽  
Endothelial Cell Retraction ◽  
Cell Retraction

The Inhibitor of VEGF-Receptors Tyrosine Kinase PTK-787 Blocks the Invasive Potential of Adult T-Cell Leukemia Cells through the Endothelium.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 84-84
Author(s):  
Ali Bazarbachi ◽  
Roa Harb ◽  
Hilda Khoury ◽  
Lara Haddad ◽  
Youmna Kfoury ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Conditioned Medium ◽  
Tube Formation ◽  
Adult T Cell Leukemia ◽  
Vegf Signaling ◽  
Anti Vegf ◽  
Endothelial Cell Retraction ◽  
Cell Retraction

Abstract Extravasation of tumor cells through the endothelial barrier is a critical step in cancer metastasis. HTLV-I associated adult T-cell leukemia/lymphoma (ATL) is an aggressive disease characterized by multiple organ invasion. We have shown that ATL-derived cells induce angiogenesis and communicate with endothelial cells through gap junctions. This results in induction of endothelial-derived metalloproteinases, sub-endothelial basement membrane degradation followed by endothelial cell retraction allowing neoplastic lymphocytes extravasation. In this study we have used the specific tyrosine kinase inhibitor of VEGF receptors PTK787, functional blocking antibodies against VEGF and the gap junction communication inhibitor18-a-G to dissect the respective role of VEGF signaling pathway and cell-to-cell communication in endothelial cell retraction and tumor cell extravasation. PTK787 has mild growth inhibitory and cytotoxic effects on both endothelial and tumor cells at a concentration of 50μM and significantly inhibited cell proliferation at 100μM. Hence, 20μM PTK787 which did not exhibit any cytotoxic or antiproliferative effects on both cell types was used in experiments that last 24 hours or longer (in vitro tube formation assay and invasion assay). Endothelial cells monolayers incubated with either ATL derived cells or their cell-free conditioned medium for 48 hours induced in vitro tube formation in Matrigel angiogenesis assay. This was inhibited by both anti-VEGF antibody and 18-a-G and to a greater extent and in a dose dependent manner by PTK787. Importantly, PTK787, and to a lesser extent anti-VEGF antibody and 18-alpha-G significantly attenuated the ability of ATL-derived cells to traverse endothelial cell monolayers in double compartment invasion assays. Signaling cascade that is activated upon VEGF stimulation of endothelial cells was investigated in confluent endothelial cells cocultured with ATL derived cells or cell-free conditioned medium in the absence or presence of PTK787 or anti-VEGF antibody, using phospho-specific antibodies against FAK Tyr 861, FAK Tyr 397, Src, ERK, PLCgamma, and Akt/PKB, known to be signal mediators in the Ras-Raf-MEKK-ERK signaling cascade. The addition of ATL derived cells or cell-free conditioned medium resulted in a transient activation of the above signal mediators with a peak increase at 15 minutes and gradual return to baseline after 60 minutes. This activation was down regulated in the presence of anti-VEGF antibody and to a greater extent in the presence of PTK787. This data establishes a novel role of VEGF signaling in tumor cell invasion and supports the potential use of PTK787 in the treatment of ATL and other hematological malignancies with angiogenic and invasive properties.

Enhanced Endothelial Cell Retraction Mediated by 12(S)-HETE: A Proposed Mechanism for the Role of Platelets in Tumor Cell Metastasis

1994 ◽  
Vol 210 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Kenneth V. Honn ◽  
Dean G. Tang ◽  
Irma M. Grossi ◽  
Colette Renaud ◽  
Zofia M. Duniec ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Tumor Cell ◽  
Cell Metastasis ◽  
Tumor Cell Metastasis ◽  
Endothelial Cell Retraction ◽  
Cell Retraction

Mechanisms of HER2-Induced Endothelial Cell Retraction

2007 ◽  
Vol 14 (10) ◽  
pp. 2971-2978 ◽  
Author(s):  
W. Bradford Carter ◽  
Guilian Niu ◽  
Michael D. Ward ◽  
Gregory Small ◽  
Julianne E. Hahn ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Endothelial Cell Retraction ◽  
Cell Retraction

Increased endothelial cell retraction and tumor cell invasion by soluble factors derived from pancreatic cancer cells

1997 ◽  
Vol 4 (4) ◽  
pp. 361-368 ◽  
Author(s):  
Shoji Nakamori ◽  
Hirotaka Okamoto ◽  
Toshiyuki Kusama ◽  
Kiyoko Shinkai ◽  
Mutsuko Mukai ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Endothelial Cell ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Soluble Factors ◽  
Pancreatic Cancer Cells ◽  
Endothelial Cell Retraction ◽  
Cell Retraction

scholarly journals Protective Effect of Atorvastatin on Radiation-induced Vascular Endothelial Cell Injury In Vitro

2010 ◽  
Vol 51 (5) ◽  
pp. 527-533 ◽  
Author(s):  
Xin-Ze RAN ◽  
Xi RAN ◽  
Zhao-Wen ZONG ◽  
Deng-Qun LIU ◽  
Gui-Ming XIANG ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Radiation Induced

scholarly journals 12(S)-HETE induces lymph endothelial cell retraction in�vitro by upregulation of SOX18

2018 ◽  
Author(s):  
Adryan Fristiohady ◽  
Daniela Milovanovic ◽  
Sigurd Krieger ◽  
Nicole Huttary ◽  
Chi Nguyen ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Endothelial Cell Retraction ◽  
Cell Retraction

Regulation of permeabilized endothelial cell retraction by myosin phosphorylation

1991 ◽  
Vol 261 (1) ◽  
pp. C32-C40 ◽  
Author(s):  
R. B. Wysolmerski ◽  
D. Lagunoff
Keyword(s):  
Endothelial Cell ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Specific Inhibitor ◽  
Light Chains ◽  
Myosin Light Chains ◽  
Inhibitory Peptide ◽  
Endothelial Cell Retraction ◽  
Cell Retraction ◽  
Gamma S

Permeabilized endothelial cell monolayers retracted on exposure to ATP and Ca2+. ADP, inosine triphosphate (ITP), GTP, adenosine 5'-(gamma-thio)triphosphate (ATP-gamma S), and 5'-adenylylimidodiphosphate failed to support retraction. However, ATP gamma S, a substrate for myosin light-chain kinase (MLCK) but not myosin adenosinetriphosphatase (ATPase), combined with ITP, a substrate for myosin ATPase but not MLCK, supported retraction. Two MLCK pseudosubstrate peptides, M5 and SM-1, inhibited endothelial cell retraction equally and more effectively than myosin kinase-inhibitory peptide with a sequence based on the phosphorylated site of myosin light chain. M5 was shown to inhibit thiophosphorylation of endothelial cell myosin light chains. Endothelial cells incubated with exogenous unregulated kinase in the presence of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetra-acetic acid retracted on addition of ATP. This retraction was accompanied by thiophosphorylation of the 19 kDa myosin light chains in the presence of ATP gamma 35S. The N-ethylmaleimide-modified subfragment 1 of myosin heads, a specific inhibitor of actin-myosin interaction, prevented retraction. These data add support to the proposal of a central role for MLCK activation of myosin in endothelial retraction.

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