[HTML][HTML] Immunohistochemical analysis of the relationship between islet cell proliferation and the production of the enteroviral capsid protein, VP1, in the islets of�…

A Willcox, SJ Richardson, AJ Bone, AK Foulis…�- Diabetologia, 2011 - Springer
A Willcox, SJ Richardson, AJ Bone, AK Foulis, NG Morgan
Diabetologia, 2011Springer
Aims/hypothesis The enteroviral capsid protein, VP1, was recently shown to be present in
some beta cells in more than 60% of patients with recent-onset type 1 diabetes but in very
few age-matched controls. The rate of proliferation of islet cells was also markedly increased
in the type 1 diabetic patients. As it has been suggested that enteroviruses replicate most
efficiently in proliferating cells, we have investigated whether VP1 is preferentially present in
proliferating beta cells in type 1 diabetes. Methods Combined immunoperoxidase and�…
Aims/hypothesis
The enteroviral capsid protein, VP1, was recently shown to be present in some beta cells in more than 60% of patients with recent-onset type 1 diabetes but in very few age-matched controls. The rate of proliferation of islet cells was also markedly increased in the type 1 diabetic patients. As it has been suggested that enteroviruses replicate most efficiently in proliferating cells, we have investigated whether VP1 is preferentially present in proliferating beta cells in type 1 diabetes.
Methods
Combined immunoperoxidase and immunofluorescence staining was used to record the presence of enteroviral VP1, insulin and Ki67 in the islets of recent-onset type 1 diabetic patients.
Results
From a total of 1,175 islets, 359 (30.5%) contained insulin. VP1-producing endocrine cells were found in 72 islets (6.1% of total), all of which retained insulin. Ki67+ endocrine cells were present in 52 (4.4%) islets, with 44 (84.6%) of these being insulin-positive. Overall, 28 of 1,175 (2.4%) islets contained both Ki67+ cells and VP1+ cells. Dual positivity of these markers accounted for 38.9% of the total VP1+ islets and 53.8% of the total Ki67+ islets. No individual islet cells were dual-positive for Ki67 and VP1.
Conclusions/interpretation
Ki67+ cells were frequently observed in islets that also contained VP1+ cells, suggesting that the factors facilitating viral replication may also drive islet cell proliferation. However, in an individual cell, VP1 production does not require concurrent beta cell proliferation.
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