Expression and Functional Significance of Adhesion Molecules on Cultured Endothelial Cells in Response to Ionizing Radiation

Prabhakarpandian, Balabhaskar; Goetz, Douglas J.; Swerlick, Robert A.; Chen, Xin; Kiani, Mohammad F.

doi:10.1111/j.1549-8719.2001.tb00182.x

Cited by 46 publications

(18 citation statements)

References 40 publications

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“…In addition, the ability of RT to shrinks tumor bulk dramatically and slow the rate of tumor cell proliferation could be enough to give the immune system an advantage (168). Irradiation may also increase trafficking of cells into tumor, as it does for normal tissues as a result of increased expression of adhesion molecules on the surface of endothelial cells involved in extravasation, such as ICAM-1, E-selectin, VCAM-1 and CD31 (169,170) (171)(172)(173). In tumors, the promotion of host cell trafficking may be offset by radiation damage to endothelial cells and the tortuous tumor vessels and defective angiogenesis, but the overall outcome may still be in favor of tumor control (174)(175)(176), as has been shown in some mouse tumor models (152).…”

Section: Radiation Therapymentioning

confidence: 99%

“…Others use gene therapy approaches to modify immunity within the tumor environment. The cytokines GM-CSF and IL-3 are thought to, in part, bring about some of their immune enhancing effects through generating DCs (173)(174)(175). Other approaches target using co-stimulator molecules such as B7.1 and B7.2 (334).…”

Section: Dendritic Cell and Macrophage Function And Subsetsmentioning

confidence: 99%

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Modification of the tumor microenvironment to enhance immunity

Liao

Schaue²,

McBride³

2007

Front Biosci

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The growth and spread of cancer depends as much on the host response to tumor as on the biological characteristics of the tumor itself. This interaction is at its most intimate and dynamic within the tumor microenvironment. It is here that the battle is fought that leads to mutual evolution of tumor and host cell phenotypes. Contributing to this evolutionary process are physiological changes distinctive for the tumor microenvironment, such as hypoxia, low nutrient levels, low extracellular pH, and high interstitial fluid pressure. These largely result from the chaotic intratumoral vasculature but are impacted by the nature of the tumor and the inflammatory and wound healing responses that are generated. Numerous infiltrating immune cells, including macrophages, lymphocytes, natural killer cells and dendritic cells infiltrate the tumor, contributing to high levels of growth factors, hormones, and cytokines. We suggest that the integrated interplay between host and tumor factors results in distinct phenotypes that determine the response to therapy as well as tumor behavior. Targeting the tumor microenvironment to awaken or reawaken immune cells, or to redirect it from a pro-tumor to an anti-tumor state, will require understanding of this phenotype. Current conventional therapies target tumors not tumor cells and clearly affect the host infiltrate and the physiological characteristics of the tumor microenvironment. This may an advantage that has yet to be effectively exploited due to lack of knowledge of existing phenotypes resulting from the tumor-host interactions. The same lack of knowledge impacts outcomes of clinical immunotherapy (IT) trials that have so far not broken through the ceiling of 10% success rate that seems to exist even in melanoma. It seems obvious that more could be achieved by combining therapies that tackle malignancies from multiple angles, with the tumor microenvironment conditioned to support a powerful effector arm generated by IT. The challenge is how to design combination therapies that modify the tumor microenvironment so as to promote immunity and better combat both local and systemic disease.

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Section: Radiation Therapymentioning

confidence: 99%

Section: Dendritic Cell and Macrophage Function And Subsetsmentioning

confidence: 99%

Modification of the tumor microenvironment to enhance immunity

Liao

Schaue²,

McBride³

2007

Front Biosci

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“…In previous studies, ionizing radiation was shown to affect the expression of ICAM‐1 in different human cell types such as endothelial cells, 9–13 colonic and gastric adenocarcinoma cells, 14 hepatoma cells 15 as well as HL60 and HeLa cells 16 . A radiation‐dependent upregulation of ICAM‐1 expression in human skin cells was also reported 10,16,24,25 .…”

Section: Discussionmentioning

confidence: 86%

“…Besides its constitutive expression on the cell surface of a wide variety of cell types including keratinocytes and fibroblasts, ICAM‐1 is upregulated in response to various inflammatory mediators 8 . Previous in vitro studies have shown that ICAM‐1 expression is increased after ionizing radiation in different cell types such as human endothelial cells, 9–13 carcinoma cell lines, 14 hepatoma cells 15 as well as HL60 and HeLa cells 16 . In addition, elevated ICAM‐1 expression levels after irradiation have been reported in vivo in mouse brain 17–20 and lung 21,22 …”

mentioning

confidence: 99%

Intercellular adhesion molecule-1: a consistent inflammatory marker of the cutaneous radiation reaction both in vitro and in vivo

Müller¹,

Köhn²,

Port³

et al. 2006

British Journal of Dermatology

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“…Ligand coated polystyrene microspheres (Duke Scientific, Fremont, CA) were used as model drug carriers (Prabhakarpandian et al, 2001). Red fluorescing polystyrene microspheres (2 mm in diameter) were coated with an IgG 2a mouse monoclonal antibody (mAb) RMP-1 to rat P-selectin (Kulidjian et al, 2002;Walter et al, 1997;Yuan et al, 2005).…”

Section: Preparation Of Ligand Coated Model Drug Carriersmentioning

confidence: 99%

Targeted delivery of antibody conjugated liposomal drug carriers to rat myocardial infarction

Scott

Wang

Nallamothu

et al. 2006

Biotech & Bioengineering

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Immunoliposome (IL) targeting to areas of inflammation after an acute myocardial infarction (MI) could provide the means by which pro-angiogenic compounds can be selectively targeted to the infarcted region. The adhesion of model drug carriers and ILs coated with an antibody to P-selectin was quantified in a rat model of MI following left coronary artery ligation. Anti-P-selectin coated model drug carriers showed a 140% and 180% increase in adhesion in the border zone of the MI 1 and 4 h post-MI, respectively. Radiolabeled anti-P-selectin ILs injected immediately post-MI and allowed to circulate 24 h showed an 83% increase in targeting to infarcted myocardium when compared to adjacent non-infarcted myocardium. Radiolabeled anti-P-selectin ILs injected 4 h post-MI and allowed to circulate for 24 h showed a 92% increase in accumulation in infarcted myocardium when compared to adjacent non-infarcted myocardium. Targeting to upregulated adhesion molecules on the endothelium provides a promising strategy for selectively delivering compounds to the infarct region of the myocardium using our liposomal-based drug delivery vehicle.

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Expression and Functional Significance of Adhesion Molecules on Cultured Endothelial Cells in Response to Ionizing Radiation

Abstract: These findings suggest that ICAM-1 is upregulated on irradiated HDMEC, HUVEC, and HMEC-1. E-selectin is upregulated to a functional level only on irradiated HDMEC, and not on irradiated HUVEC or HMEC-1.

Cited by 46 publications

References 40 publications

Modification of the tumor microenvironment to enhance immunity

Modification of the tumor microenvironment to enhance immunity

Intercellular adhesion molecule-1: a consistent inflammatory marker of the cutaneous radiation reaction both in vitro and in vivo

Targeted delivery of antibody conjugated liposomal drug carriers to rat myocardial infarction

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