Increased monocyte alphaL, alphaM and beta2 integrin subunits in diabetes mellitus

ObjectivesPrevious 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 methodsMonocytes 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.ResultsIncubation 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.ConclusionsThe 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.