Objectives: Previous studies indicated the involvement of alpha2 (CD49b) integrin subunit in monocyte-laminin attachment in diabetes. The aim of the present study was to further investigate monocyte atherosclerosis related integrin subunit changes in relation to diabetes and hyperglycemia.
Design and methods: Monocytes were derived from 10 patients with type II diabetes and 10 age matched controls. Attachment to laminin-1 in the presence of anti-integrin subunit antibodies has been estimated by a solid phase assay while for the alpha2 integrin subunit density assessment, fluorescence spectrometry was used.
Results: Incubation of monocytes with monoclonal anti-alphaL (CD11a) and anti-beta2 (CD18) equalized the differences between diabetics and controls. Both glucose and insulin increased the alpha2 integrin subunit expression in relation to the controls.
Conclusions: The previously observed modified interaction between monocytes and laminin in diabetes mellitus may be attributed to changes not only in alpha2 but also in alphaL and beta2 integrin subunit changes.