1999PubMedRequires access

[The role of ICAM-1 in leukocyte adherence to endothelial cells induced by hypoxia/reoxygenation].

Guan Qing Qian, H Liu, Yi Zhao

Open publisher page 0 citations

Abstract

OBJECTIVE: To determine whether intercellular adhesion molecule-1 (ICAM-1) mediats the polymorphonuclear leukocyte (PMN) adherence to endothelial cells elicited by hypoxia/reoxygenation (H/R). METHODS: Human umbilical vein endothelial cells (HUVEC) monolayers was exposed to hypoxia for 30 min or 120 min then reoxygenated. Count the number of PMN in adhesion assays. Expression of ICAM-1 and ICAM-1 mRNA was detected by immunohistochemical analysis and in situ hybridization. RESULTS: PMN adhesion to HUVEC exposed to H/R was significantly increased (1 fold) as compared with that of control (P < 0.01). H/R induced hyperadherence was significantly diminished by monoclonal antibodies directed at ICAM-1 or CD11a/CD18. The results showed an increased expression of ICAM-1 and ICAM-1 mRNA on HUVEC exposed to H/R. Hypoxic HUVEC might be responsible for PMN adesion. CONCLUSIONS: ICAM-1 mediated the adhesive interaction between PMN and VEC induced by hypoxia/reoxygenation.

About this research paper

What this paper is about

OBJECTIVE: To determine whether intercellular adhesion molecule-1 (ICAM-1) mediats the polymorphonuclear leukocyte (PMN) adherence to endothelial cells elicited by hypoxia/reoxygenation (H/R). METHODS: Human umbilical vein endothelial cells (HUVEC) monolayers was exposed to hypoxia for 30 min or 120 min then reoxygenated. Count the number of PMN in adhesion assays. Expression of ICAM-1 and ICAM-1 mRNA was detected by immunohistochemical analysis and in situ hybridization. RESULTS: PMN adhesion to HUVEC exposed to H/R was significantly increased (1 fold) as compared with that of control (P < 0.01). H/R induced hyperadherence was significantly diminished by monoclonal antibodies directed at ICAM-1 or CD11a/CD18. The results showed an increased expression of ICAM-1 and ICAM-1 mRNA on HUVEC exposed to H/R. Hypoxic HUVEC might be responsible for PMN adesion. CONCLUSIONS: ICAM-1 mediated the adhesive interaction between PMN and VEC induced by hypoxia/reoxygenation.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

OBJECTIVE: To determine whether intercellular adhesion molecule-1 (ICAM-1) mediats the polymorphonuclear leukocyte (PMN) adherence to endothelial cells elicited by hypoxia/reoxygenation (H/R). METHODS: Human umbilical vein endothelial cells (HUVEC) monolayers was exposed to hypoxia for 30 min or 120 min then reoxygenated. Count the number of PMN in adhesion assays. Expression of ICAM-1 and ICAM-1 mRNA was detected by immunohistochemical analysis and in situ hybridization. RESULTS: PMN adhesion to HUVEC exposed to H/R was significantly increased (1 fold) as compared with that of control (P < 0.01). H/R induced hyperadherence was significantly diminished by monoclonal antibodies directed at ICAM-1 or CD11a/CD18. The results showed an increased expression of ICAM-1 and ICAM-1 mRNA on HUVEC exposed to H/R. Hypoxic HUVEC might be responsible for PMN adesion. CONCLUSIONS: ICAM-1 mediated the adhesive interaction between PMN and VEC induced by hypoxia/reoxygenation.

Key concepts: CD11a, CD18, ICAM-1, Umbilical vein, Hypoxia (environmental), Intercellular Adhesion Molecule-1, Monoclonal antibody, Molecular biology

Related papers

Back to paper searchBrowse research topicsOriginal source
[The role of ICAM-1 in leukocyte adherence to endothelial cells induced by hypoxia/reoxygenation]. — Research Paper | ScholarLens