Stimulation of Endothelial Cell Growth by Sera From Diabetic Patients With Retinopathy

Petty, R.; Morgan, D; Pearson, J; Mahler, R.F.

doi:10.1016/s0140-6736(88)91064-1

Cited by 31 publications

(3 citation statements)

References 22 publications

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“…However, the role of elevated blood glucose in diabetic complications remains unsettled. For example, good glycemic control does not totally avert the vascular complications of diabetes, while on the contrary some patients with poor metabolic control do not have these complications [34]. Another concern is that we have no evidence of microvascular disease, because we did not assess this complication.…”

Section: Figmentioning

confidence: 97%

Basic Fibroblast Growth Factor Stimulates Angiogenesis in the Hindlimb of Hyperglycemic Rats

Stark

Baffour

Garb

et al. 1998

Journal of Surgical Research

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Section: Figmentioning

confidence: 97%

Basic Fibroblast Growth Factor Stimulates Angiogenesis in the Hindlimb of Hyperglycemic Rats

Stark

Baffour

Garb

et al. 1998

Journal of Surgical Research

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“…The lack of any correlation between LJM and either plasma or serum PDGF concentrations suggests that microvascular complications of diabetes are unlikely to be influenced by systemic PDGF concentrations. Serum factors with different physical properties from PDGF have previously been implicated in diabetic retinopathy [18].…”

Section: Discussionmentioning

confidence: 99%

Immunoassay of platelet-derived growth factor in the blood of patients with diabetes mellitus

1994

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Summary Platelet-derived growth factor (PDGF) is a powerful mitogen for many cell types, and is believed to play a major role in wound healing when released from platelets at sites of injury. In diabetes mellitus, it has been proposed that premature release of PDGF from platelets impairs the ability of platetets to initiate healing, and also accelerates the development of diabetic complications such as angiopathy by increasing plasma-borne PDGE However, plasma samples from diabetic patients have not previously been assayed for PDGF using suitable techniques. A sensitive monoclonal enzyme-linked immunoassay for PDGF was applied to plasma and serum samples fiom 18 healthy control subjects and 60 diabetic patients. Neither plasma nor serum PDGF concentrations differed significantly between control subjects, insulin-dependent, and non-insulin-dependent diabetic patients. However, 23 % of the diabetic subjects had serum PDGF levels above the control range. Limited joint mobility, which is characterised by joint contractures and collagen deposition in the skin, and is associated with microvascular disease, was used as a marker of diabetic complications. Limited joint mobility affected 43 % of the diabetic subjects. Patients with moderate limited joint mobility bad had diabetes significantly longer than those without limited joint mobility (means 17years and 9 years, respectively, p = 0.008). However, limited joint mobility was not associated with elevated serum or plasma PDGF in insulin-dependent or non-insulin-dependent diabetes. We conclude that complications of diabetes are unlikely to be caused by changes in systemic levels of PDGE The delayed healing associated with diabetes is not due to a deficit in PDGF available from platelets. [Diabetologia (1994[Diabetologia ( ) 37: 1142[Diabetologia ( -1146

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“…Others have provided evidence of the pres ence in diabetic serum of an endothelial cell proliferation factor that is independent of carbohydrate and lipid metabolism. 6 The overall impression of these and many other studies is that even extremely good metabolic control of the diabetes does not completely protect patients from the complications of late diabetes. Therefore it would be reasonable to search for basic physiologic factors not directly linked to the metabolic disturbance in order to understand better the progression of widespread mi crovascular disease in late diabetes.…”

mentioning

confidence: 94%

Induction and Possible Role of Fibrinolysis in Diabetes Mellitus

Gram¹,

Jespersen²

1991

Semin Thromb Hemost

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This article reviews the evidence supporting a relationship between an enhanced tissue injury, increased fibrin formation, defective fibrinolysis, and the evolution of the complications of late diabetic disease. Particular attention is drawn to the role of a defective endothelial cell mediated fibrinolysis with respect to increased fibrin formation and a delayed tissue repair in diabetic patients. Reviewed are studies that indicate that it is possible in patients with diabetes by means of sulfonylurea compounds to increase endothelial cell-produced t-PA without affecting PAI-1. It is advocated that potent compounds should be searched for, with the capability to modify the hemostatic process of the diabetic endothelial cell in order to express more fibrinolytic activity independent of the patient's metabolic state in an attempt to delay the complications of late diabetes.

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Stimulation of Endothelial Cell Growth by Sera From Diabetic Patients With Retinopathy

Cited by 31 publications

References 22 publications

Basic Fibroblast Growth Factor Stimulates Angiogenesis in the Hindlimb of Hyperglycemic Rats

Basic Fibroblast Growth Factor Stimulates Angiogenesis in the Hindlimb of Hyperglycemic Rats

Immunoassay of platelet-derived growth factor in the blood of patients with diabetes mellitus

Induction and Possible Role of Fibrinolysis in Diabetes Mellitus

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