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Interleukin-10 induces E-selectin on small and large blood vessel endothelial cells.

ABSTRACT: In vitro, expression of E-selectin is largely restricted to endothelial cells activated by inflammatory cytokines. Under activated conditions, cytokines such as interleukin (IL) 10, released by keratinocytes in large quantities, may also increase the expression of E-selectin on the dermal microvasculature. The aim of the present study was to investigate the expression of E-selectin on cultured human dermal microvascular endothelial cells (HDMEC) isolated from neonatal foreskins when exposed to IL-10. Expression of E-selectin was determined by immunofluorescence microscopy, FACS analysis, an HL-60 cell-binding assay, and quantitative polymerase chain reaction (PCR) analysis. For comparison with large blood vessel cells, the expression of E-selectin on human umbilical vein endothelial cells (HUVEC) was also determined in parallel by FACS and reverse transcriptase-PCR analysis under identical conditions. These studies demonstrate that IL-10 induces the expression of E-selectin on both HDMEC and HUVEC and that the level of expression of HDMEC is comparable with that induced by IL-1 beta and tumor necrosis factor-alpha. When HL-60 cells are incubated with HDMEC pretreated with IL-10, a consistent increase in adherence of HL-60 to endothelial cells is observed. This adherence was found to be mediated by L-selectin. PCR analysis and the quantification of E-selectin cDNA by a novel, highly sensitive and specific PCR-immunoassay demonstrate the induction of E-selectin mRNA at the transcriptional level. The induction of the expression of E-selectin by IL-10 on HDMEC may provide additional insights into the pathogenic mechanism of neutrophil accumulation at the site of inflammation in inflammatory skin diseases.

SUBMITTER: Vora M

PROVIDER: S-EPMC2192779 | biostudies-other | 1996 Sep

REPOSITORIES: biostudies-other

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Interleukin-10 induces E-selectin on small and large blood vessel endothelial cells.

Vora M M Romero L I LI Karasek M A MA

The Journal of experimental medicine 19960901 3

In vitro, expression of E-selectin is largely restricted to endothelial cells activated by inflammatory cytokines. Under activated conditions, cytokines such as interleukin (IL) 10, released by keratinocytes in large quantities, may also increase the expression of E-selectin on the dermal microvasculature. The aim of the present study was to investigate the expression of E-selectin on cultured human dermal microvascular endothelial cells (HDMEC) isolated from neonatal foreskins when exposed to I ...[more]

PMID: 9064342

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Project description:Lung cancer is a severe disease threatening human health worldwide. Distant hematogenous metastasis results in poor prognosis and death of lung cancer patients. In the present study, we investigated the effect of circulatory platelets (PLTs) on hematogenous metastasis of non-small cell lung carcinoma (NSCLC). Laser scanning confocal microscopy was employed to assay the expression of P-selectin in lung cancer tissue, paracancerous tissue and distant tissue, respectively. Meanwhile, fluorescence-activated cell sorting (FACS) was used to determine P-selectin activation in peripheral blood. Purified PLTs were co-cultured with A549 cells and human vascular endothelial cells (HuvECs). Subsequently, the formation of PLT-lung cancer cell complexes and their effects on rolling and adhesion of A549 on the surface of vascular endothelium were assayed. Integrin ?3, ?5, ?1, ICAM-1 and VCAM-1 mRNAs and proteins were measured by reverse RT-PCR and western blot analysis, respectively. The expression of P-selectin in lung adenocarcinoma tissue was significantly stronger compared to that in paracancerous and distant tissues. P-selectin activation in peripheral blood in lung adenocarcinoma was markedly enhanced. The rolling rate of A549 on HuvECs was significantly slowed down after co-culture of activated PLTs and A549 cells. The mRNA and protein levels of integrin ?3, ?5, ?1, ICAM-1 and VCAM-1 were significantly increased after the co-culture. In conclusion, the PLT-lung cancer cell complexes protected the lung cancer cells from mechanical injury under blood flow. Furthermore, up-regulated integrin ?3, ?5, ?1 and endothelial cell adhesion molecules ICAM-1 and VCAM-1 promoted the adhesion of A549 on vascular endothelial cells, which may be responsible for hematogenous metastasis of lung cancer.

Dataset Information

Interleukin-10 induces E-selectin on small and large blood vessel endothelial cells.

Publications

Interleukin-10 induces E-selectin on small and large blood vessel endothelial cells.

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