Immunohistochemical Study of Cellular Fibronectin in Preretinal Membranes

Ohsato, Masahiko; Shiga, Sousuke; Kato, Hitoshi; Hayashi, Hideyuki; Oshima, Kenji

doi:10.1097/00006982-199414050-00007

Cited by 5 publications

(4 citation statements)

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“…It was suggested that cFN is involved in the pathogenesis of epiretinal membrane formations. 21 A study using human cFN antibodies has shown a diffuse distribution of cFN within membranes extracted from patients with PVR and proliferative DRP, and a localised distribution in neovascular vessels in proliferative DRP membranes. 20 40 However, elevated cFN levels in the vitreous of our DM patients without membranes strongly suggest local production of cFN irrespectively of membrane formation.…”

Section: Discussionmentioning

confidence: 99%

“…In vitreoretinal membranes, the production of cFN was, next to the endothelium of neovessels, also ascribed to (migrated) RPE cells. 21 44 45 It was proved that RPE cells can synthesise FN, but the distinction between which FN types (cellular or soluble) has not yet been performed. TGF-b has been reported to be a potent stimulator of FN release by RPE cells, 44 and human serum (as a model of vascular leakage in vivo) has been reported to contain substances stimulating FN synthesis in cultured human RPE cells.…”

Section: Discussionmentioning

confidence: 99%

“…[16][17][18] Besides being produced by endothelial cells, cellular FN (cFN) can also be secreted by a variety of cultured cells including fibroblasts, smooth muscle cells, and possibly also by retinal pigment epithelial (RPE) cells and retinal glia. [19][20][21][22][23] Elevated plasma levels of circulating cFN have been described in diverse clinical syndromes with endothelial activation, including systemic vasculitis, and diabetes mellitus, and cFN has been reported as a specific marker for endothelial cell injury. 16 24-26 We hypothesise and show that intraocular levels of cFN reflect intraocular vascular damage and that cFN is locally produced in the eye.…”

mentioning

confidence: 99%

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Intraocular and plasma levels of cellular fibronectin in patients with uveitis and diabetes mellitus

Probst

Fijnheer²,

Schellekens³

et al. 2004

British Journal of Ophthalmology

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Aim: To determine intraocular and plasma levels of cellular fibronectin (cFN) in patients with uveitis or diabetes mellitus (DM) and to assess the association with disease activity, macular oedema, and vascular leakage on fluorescein angiography. In addition, to examine whether cFN is locally produced in the eye. Methods: Intraocular and plasma levels of cFN were determined by ELISA in 39 patients with uveitis (23 active, 16 non-active), in 11 patients with DM (eight with and three without diabetic retinopathy) and in 17 control patients. The influence of diabetic retinopathy, inflammatory activity, vascular leakage, and macular oedema (MO) on intraocular and plasma cFN levels was studied. Local production of cFN was determined by calculating absolute and relative intraocular to plasma ratios. Aqueous and vitreous levels of cFN were compared. Results: No differences in plasma cFN levels were found between patients with uveitis, DM, or controls. Intraocular cFN levels were significantly raised in patients with uveitis and DM, specifically in those with active disease (active uveitis and active diabetic retinopathy versus controls: p = 0.001 and 0.002 respectively). Further, intraocular cFN levels were significantly elevated in patients with macular oedema or vascular leakage, irrespectively of whether associated with uveitis or DM (p = 0.001 and 0.002). Intraocular cFN levels were consistently higher in the vitreous than the aqueous. Intraocular production of cFN was documented by elevated absolute and relative intraocular to plasma ratios in nine out of 11 patients tested. Conclusions: Elevated intraocular cFN levels were found in uveitis and DM, especially in those with active processes, intraocular vascular damage, and MO. These results suggest that locally produced cFN levels reflect intraocular vascular damage. M acular oedema (MO), an excess of fluid within the retinal tissue, is caused by leakage from retinal or choroidal vessels and represents a final common pathway of various pathological conditions associated with the disruptions of the blood-retinal barrier (BRB).1-4 MO is a dreaded complication and a major cause of visual loss in uveitis, diabetes mellitus (DM), retinal vascular occlusions, following intraocular surgery, and in other conditions affecting the vasculature of the retina. 5-8Vasculitis, with subsequent vascular leakage on fluorescein angiography (FA), is an intraocular inflammatory condition of diverse aetiology, reflecting the activity of the intraocular inflammation. Although commonly idiopathic, it has strong associations with systemic inflammatory diseases. Vascular leakage on FA in patients with DM is caused by pathological vascular wall changes leading to loss of vascular integrity. Vascular leakage and MO are usually investigated with FA, fluorophotometry, or optical coherence tomography (OCT). 9-12Fibronectins (FN) refer to a large family of glycoproteins (440-500 kD), which are major components of the extracellular matrix and play an important part in cell to cell and cell to mat...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Intraocular and plasma levels of cellular fibronectin in patients with uveitis and diabetes mellitus

Probst

Fijnheer²,

Schellekens³

et al. 2004

British Journal of Ophthalmology

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“…Cellular fibronectin of the epiretinal membrane which is distributed diffusely, is produced by the membrane itself, can promote cell proliferation and migration [23].…”

Section: Membranementioning

confidence: 99%

Autonomic Regulation of the Function of the Vitreous Body and Retina

Edward¹,

Eugine²,

Иванович³

et al. 2018

CTOY

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The data of the literature on the structure and physiology of the vitreous body and the retina in normal and pathological conditions are presented. The mechanism of vitreous detachment and its role in the development of vitreoretinal proliferation are described. Described adren-choline-peptide and NO-ergic mechanisms in signal transduction of the vitreous body and retina. Pharmacological and surgical methods of treatment of vitreoretinal proliferation are briefly described.

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