Molecular size distribution of somatostatin-like immunoreactivity in the cerebroventricular fluid of neurosurgical patients

Rißler, Klaus; S, Jost; Mohadjer, M.; Mundinger, F.; Cramer, H.

doi:10.1016/s0921-8696(87)80008-7

Cited by 3 publications

(3 citation statements)

References 42 publications

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“…There is no information available concerning the molecular forms of somatostatin synthesized by the human retina. However, in the human brain, somatostatin-14 is primarily secreted by cortical neurons, whereas somatostatin-28 is the predominant form in cells at the subcortical and hypothalamic levels (23,24). In the retina, somatostatin is synthesized in GABAergic amacrine cells, which are localized in the neuroretina (5,25).…”

Section: Discussionmentioning

confidence: 99%

Somatostatin Molecular Variants in the Vitreous Fluid

et al. 2005

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OBJECTIVE -There is growing evidence to indicate that somatostatin could be added to the list of natural antiangiogenic factors that exist in the vitreous fluid. In addition, a deficit of intravitreous somatostatin-like immunoreactivity (SLI) has been found in diabetic patients with proliferative diabetic retinopathy (PDR). In the present study, we have determined the main molecular variants of somatostatin (somatostatin-14 and somatostatin-28) in the vitreous fluid and plasma of nondiabetic control subjects and diabetic patients with PDR. In addition, the contribution of cortistatin, a neuropeptide with strong structural similarities to somatostatin, to SLI and its levels in vitreous and plasma in both nondiabetic and diabetic patients has also been measured. RESERCH DESIGN AND METHODS-Plasma and vitreous fluid from 22 diabetic patients with PDR and 22 nondiabetic control subjects were analyzed. Somatostatin-14, somatostatin-28 and cortistatin were measured by radioimmunoassay but separation by highperformance liquid chromatography was required to measure somatostatin-14.RESULTS -The predominant molecular form of somatostatin within the vitreous fluid was somatostatin-28 (fivefold higher than somatostatin-14 in control subjects and threefold higher in patients with PDR). Cortistatin significantly contributed to SLI and its intravitreous levels were higher than those detected in plasma (nondiabetic control subjects: 147 vs. 78 [24 -32] pg/ml; patients with PDR: 187 vs. 62 [24 -472] pg/ml; P ϭ 0.01 for both). Intravitreous somatostatin-14 was similar in both subjects with PDR and the control group (P ϭ 0.87). By contrast, somatostatin-28 concentration was lower in patients with PDR than in nondiabetic control subjects (350 Ϯ 32 vs. 595 Ϯ 66 pg/ml; P ϭ 0.004).CONCLUSIONS -Somatostatin-28 is the main molecular variant in the vitreous fluid. The intravitreous SLI deficit detected in patients with PDR is mainly due to somatostatin-28. Cortistatin is abundant in the vitreous fluid and significantly contributes to SLI. These findings could open up new strategies for PDR treatment. Diabetes Care 28:1941-1947, 2005P roliferative diabetic retinopathy (PDR) represents a highly prevalent cause of visual loss in western countries and is the leading cause of new-onset blindness among people of working age (1). There is now ample evidence to suggest that the development of diabetic retinopathy is a multifactorial process in which it is not just the angiogenic factors alone but the balance between angiogenic and antiangiogenic factors that is crucial. Inhibition of angiogenesis has therefore become a target for the treatment of retinal neovascularization.Several pilot studies using the somatostatin analog octreotide in patients with early proliferative and severe non-PDR have revealed decreased incidence of progression into proliferative retinopathy needing panretinal laser treatment (2,3). In addition, the incidence of vitreous hemorrhage and the need for vitreoretinal surgery was also significantly reduced in octreotide-tr...

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Section: Discussionmentioning

confidence: 99%

Somatostatin Molecular Variants in the Vitreous Fluid

et al. 2005

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“…There is no information about the molecular forms of SS synthesized by the human retina. In the human brain, SS-14 is primarily secreted by cortical neurons, whereas SS-28 is synthesized at the subcortical and hypothalamic levels [395,396]. Because the neuroretina and hypothalamus have the same embryologic origin [397,398] it might be that in both tissues -as well as in the vitreous fluid-the predominant SS form will be SS-28.…”

Section: Somatostatinmentioning

confidence: 99%

Angiogenic and Antiangiogenic Factors in Proliferative Diabetic Retinopathy

Simó

Carrasco²,

Garcia-Ramírez³

et al. 2006

CDR

328

236

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Diabetic retinopathy continues to be the leading cause of legal blindness among working-age individuals. The earliest histological features of diabetic retinopathy include neuroretinal damage, capillary basement membrane thickening, loss of pericytes and loss of endothelial cells. At advanced stages, neovascularization, the hallmark of proliferative diabetic retinopathy (PDR) occurs, and blindness can result from relentless abnormal fibrovascular proliferation with subsequent bleeding and retinal detachment. Macular oedema is another retinal complication of diabetes that is responsible for a major part of vision loss, particularly in type 2 diabetes. The breakdown of the blood retinal barrier and the consequent vascular leakage and thickening of retina are the main events involved in its pathogenesis. Although a tight control of both blood glucose levels and hypertension are essential to prevent or arrest progression of the disease, the recommended goals are difficult to achieve in many patients. Laser photocoagulation treatment soon after the onset of PDR significantly reduces the incidence of severe vision loss. However, the optimal timing for laser treatment is frequently passed and, in addition, it is not uniformly successful in halting visual decline. For all these reasons, new pharmacological treatments based on the understanding of the pathophysiological mechanisms of diabetic retinopathy have been developed in recent years. There is mounting evidence to suggest that angiogenic factors play a crucial role in PDR development, vascular endothelial growth factor (VEGF) being the most relevant. Other growth factors or cytokines such as insulin-like growth factor I (IGF-1), hepatocyte growth factor (HGF), basic fibroblast growth factor (b-FGF), platelet derived growth factor (PDGF), pro-inflammatory cytokines and angiopoetins, are also involved in the pathogenesis of PDR. However, the intraocular synthesis of angiogenic factors is counterbalanced by the synthesis of antiangiogenic factors. Therefore, the balance between the angiogenic and antiangiogenic factors rather than angiogenic factors themselves will be crucial in determining the progression of PDR. The main antiangiogenic factor is the pigment epithelium derived factor (PEDF) but the transforming growth factor beta (TGF-beta), thrombospondin (TSP) and somatostatin are also among the intraocullary synthesized antiangiogenic factors.

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“…This receptor downregulation is paradoxical in view of the decreased SS tissue concentration and the lower SS concentration in the cerebrospinal fluid [12,20,[70][71][72][73][74][75][76][77][78][79][80][81], Whereas some investi gators have not reported any significant dif ference in cerebrospinal fluid SS concentra tion between early-onset and late-onset AD patients [82], McDonald et al [83] docu mented a correlation between the cerebrospi nal fluid SS concentration and the severity of dementia. According to others, reduced SS concentrations in the cerebrospinal fluid are not specific for dementia but can also be observed in patients with depression and schizophrenia [84], In contrast to these find ings, only few reports show SS increases in the substantia innominata/nucleus basalis and in the striatum/putamcn [62,85], Hypothalamic SS concentrations in de mented patients have been reported to be unchanged, increased or slightly decreased [85][86][87], More recent studies have shown that the cortical neurons secreting SS-14 are more sus ceptible to degeneration than the neurons at subcortical and hypothalamic levels which se crete SS-28 [88][89][90][91][92][93],…”

Section: Somatostatinmentioning

confidence: 99%

Neuropeptide Changes in Dementia: Pathogenetic Implications and Diagnostic Value

Valenti¹

1996

Gerontology

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The main object of this review is to describe the most significant alterations of neuropeptide patterns occurring in the brain and in the cerebral spinal fluid of demented patients and particularly of elderly patients with Alzheimer type dementia. The changes in concentration in the different brain areas are described along with their peripheral endocrine implications. Alterations in the synthesis and release of neuropeptides may play a significant role in the pathogenesis of dementia in elderly patients, in addition to the well known changes in classical neurotransmitter systems. Measurements of neuropeptide levels in cerebrospinal fluid or postmortem brain material as alleged biological markers for the diagnostic purpose, however, have produced controversial results. Neuropeptide changes in the demented brain show regional differences and are not specific and selective enough to differentiate between senile dementia, Alzheimer type dementia and other degenerative disorders.

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Molecular size distribution of somatostatin-like immunoreactivity in the cerebroventricular fluid of neurosurgical patients

Cited by 3 publications

References 42 publications

Somatostatin Molecular Variants in the Vitreous Fluid

Somatostatin Molecular Variants in the Vitreous Fluid

Angiogenic and Antiangiogenic Factors in Proliferative Diabetic Retinopathy

Neuropeptide Changes in Dementia: Pathogenetic Implications and Diagnostic Value

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