Elevated plasma prostaglandins and acetylated histone in monocytes in Type 1 diabetes patients
SSH Chen, AJ Jenkins, H Majewski - Diabetic medicine, 2009 - Wiley Online Library
SSH Chen, AJ Jenkins, H Majewski
Diabetic medicine, 2009•Wiley Online LibraryAims/hypothesis Inflammation is implicated in diabetes and cyclooxygenase (COX) is
involved in vascular inflammatory processes, participating in both atherosclerosis and
thrombosis. The aims were to determine whether levels of monocyte COX and plasma COX
metabolites are increased in Type 1 diabetic patients and to determine whether these could
be linked to histone hyperacetylation. Materials and methods Monocytes from 19 Type 1
diabetic and 39 non‐diabetic control subjects were probed for COX and acetylated histone …
involved in vascular inflammatory processes, participating in both atherosclerosis and
thrombosis. The aims were to determine whether levels of monocyte COX and plasma COX
metabolites are increased in Type 1 diabetic patients and to determine whether these could
be linked to histone hyperacetylation. Materials and methods Monocytes from 19 Type 1
diabetic and 39 non‐diabetic control subjects were probed for COX and acetylated histone …
Abstract
Aims/hypothesis Inflammation is implicated in diabetes and cyclooxygenase (COX) is involved in vascular inflammatory processes, participating in both atherosclerosis and thrombosis. The aims were to determine whether levels of monocyte COX and plasma COX metabolites are increased in Type 1 diabetic patients and to determine whether these could be linked to histone hyperacetylation.
Materials and methods Monocytes from 19 Type 1 diabetic and 39 non‐diabetic control subjects were probed for COX and acetylated histone H4 proteins by immunoblotting. Plasma COX metabolite levels [thromboxane B2 (TXB2) and prostaglandin E2 (PGE2)] were determined by enzyme immunoassay.
Results Monocyte COX‐2 expression was significantly up‐regulated (1.3‐fold) in diabetic relative to the non‐diabetic control subjects and plasma PGE2 was markedly elevated (2.7‐fold). In diabetic subjects, monocyte acetylated histone H4 levels were significantly elevated; sub‐group analysis indicated that the increased histone acetylation was found only in the complication‐free group.
Conclusions Results support increased inflammatory activity in Type 1 diabetes that involves COX‐2 and increased prostaglandin production, which may predispose patients to cardiovascular events. The observation of elevated histone acetylation only in complication‐free diabetic subjects suggests that this may be a protective mechanism. This merits further investigation as histone hyperacetylation has been associated with reduced expression of factors involved in vascular injury and remodelling.
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