Impaired Retinal Angiogenesis in Diabetes

Stitt, Alan W.; McGoldrick, Ciara; Rice-McCaldin, A.; McCance, David R.; Glenn, Josephine V.; Hsu, Daniel K.; Liu, Fu‐Tong; Thorpe, Suzanne R.; Gardiner, Tom

doi:10.2337/diabetes.54.3.785

Cited by 102 publications

(78 citation statements)

References 53 publications

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“…HUVEC suspended in gels containing rat tail collagen at 3.75-5.0 μg/ml form lumen-containing CLS within 24 hr, structures that are maintained over several days (Davis and Camarillo, 1996;Kamei et al, 2006;Salazar et al, 1999). Similar morphogenesis is observed with bovine aortic and microvascular endothelial cells plated in gels of diluted Matrigel or type I collagen (Stitt et al, 2005;A.G. and Tony Walshe, unpublished observations).…”

Section: Morphogenesismentioning

confidence: 54%

In vitro assays of angiogenesis for assessment of angiogenic and anti-angiogenic agents

Goodwin¹

2007

Microvascular Research

259

208

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Blood vessels, either in insufficient numbers or in excess, contribute to the pathogenesis of many diseases. Agents that stimulate angiogenesis can improve blood flow in patients with ischemic diseases, whereas anti-angiogenic agents are used to treat disorders ranging from macular degeneration to cancer. In this review I describe in vitro assays that can be used to assess the activity of agents that affect angiogenesis. Means of quantifying endothelial cell matrix degradation, migration, proliferation, apoptosis and morphogenesis are discussed, as are embryoid body, aortic ring and metatarsal assays of vessel outgrowth. Strengths and limitations of these techniques are also addressed.

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Section: Morphogenesismentioning

confidence: 54%

In vitro assays of angiogenesis for assessment of angiogenic and anti-angiogenic agents

Goodwin¹

2007

Microvascular Research

259

208

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“…Lgals3 gene deletion effectively prevented early retinal changes associated with streptozotocin-induced diabetes [75], whereas it abolished the AGE-mediated increase in retinal ischemia and restored the neovascular response to that seen in controls [76].…”

Section: Galectin-3 As a Disease Mediator: Animal Studiesmentioning

confidence: 99%

Galectin-3 in diabetic patients

Pugliese

Iacobini

Ricci

et al. 2014

Clinical Chemistry and Laboratory Medicine (CCLM)

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Galectin-3 is a versatile molecule which exerts several and sometimes opposite functions in various pathophysiological processes. Recently, galectin-3 has gained attention as a powerful predictor of heart failure and mortality, thus becoming a useful prognostic marker in clinical practice. Moreover, though not specifically investigated in diabetic cohorts, plasma levels of galectin-3 correlated with the prevalence of diabetes and related metabolic conditions, thus suggesting that pharmacological blockade of this lectin might be successful for treating heart failure especially in subjects suffering from these disorders. Indeed, galectin-3 is considered not only as a marker of heart failure, but also as a mediator of the disease, due to its pro-fibrotic action, though evidence comes mainly from studies in galectin-3 deficient mice. However, these studies have provided contrasting results, with either attenuation or acceleration of organ fibrosis and inflammation, depending on the experimental setting and particularly on the levels of advanced glycation endproducts (AGEs)/advanced lipoxidation endproducts (ALEs), of which galectin-3 is a scavenging receptor. In fact, under conditions of increased AGE/ALE levels, galectin-3 ablation was associated with tissue-specific outcomes, reflecting the AGE/ALE-receptor function of this lectin. Conversely, in experimental models of acute inflammation and fibrosis, galectin-3 deficiency resulted in attenuation of tissue injury. There is a need for prospective studies in diabetic patients specifically investigating the relation of galectin-3 levels with complications and for further animal studies in order to establish the effective role of this lectin in organ damage before considering its pharmacological blockade in the clinical setting.

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“…In experimental in vitro and in vivo models of retinal angiogenesis assays, Stitt et al (1) discovered that sera of type 2 diabetic patients have strong antiangiogenic effects. The poorer the glycemic control of patients, the more evident the inhibition of angiogenesis.…”

Section: Research Design Andmentioning

confidence: 99%

“…It is responsible for diabetic retinopathy, nephropathy, and neuropathy (1). Moreover, diabetes leads to reduced collateralization in ischemic tissues, which causes impaired wound healing, exacerbation of peripheral limb ischemia, and a three-to fourfold increase in cardiac mortality in comparison with nondiabetic patients (2,3).…”

mentioning

confidence: 99%