A novel co-culture model of the blood-retinal barrier based on primary retinal endothelial cells, pericytes and astrocytes

Wisniewska-Kruk, Joanna; Hoeben, Kees A.; Vogels, I. M. C.; Gaillard, Pieter J.; Noorden, C. J. F. Van; Schlingemann, Reinier O.; Klaassen, Ingeborg

doi:10.1016/j.exer.2011.12.003

Cited by 85 publications

(75 citation statements)

References 49 publications

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“…VEGF is considered to induce transcellular transport via caveolae (22). In previous studies, exposure to exogenous VEGF led to an increase in the number of pinocytotic vesicles at the lumenal side of retinal capillaries, and to increased levels of PLVAP in caveolae (23,53). To mimic the in vivo pathophysiology of DME, bovine retinal ECs (BRECs) were stimulated with VEGF, which led to an increase in the mRNA expression levels of caveolin-1 and PLVAP (22).…”

Section: Plvap and Diseasesmentioning

confidence: 82%

“…Increased retinal VEGF levels are associated with BRB breakdown in diabetic rodents, primates and humans (22,23,34). VEGF is considered to induce transcellular transport via caveolae (22).…”

Section: Plvap and Diseasesmentioning

confidence: 99%

“…To mimic the in vivo pathophysiology of DME, bovine retinal ECs (BRECs) were stimulated with VEGF, which led to an increase in the mRNA expression levels of caveolin-1 and PLVAP (22). In addition, a cell-based enzyme-linked immunosorbent assay detected a significant increase in the PLVAP content of BRECs at 72 h following VEGF treatment (23). …”

Section: Plvap and Diseasesmentioning

confidence: 99%

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Plasmalemma vesicle-associated protein: A crucial component of vascular homeostasis

Guo

Zhang

Hou

et al. 2016

Experimental and Therapeutic Medicine

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Endothelial subcellular structures, including caveolae, fenestrae and transendothelial channels, are crucial for regulating microvascular function. Plasmalemma vesicle-associated protein (PLVAP) is an endothelial cell-specific protein that forms the stomatal and fenestral diaphragms of blood vessels and regulates basal permeability, leukocyte migration and angiogenesis. Loss of PLVAP in mice leads to premature mortality due to disrupted homeostasis. Evidence from previous studies suggested that PLVAP is involved in cancer, traumatic spinal cord injury, acute ischemic brain disease, transplant glomerulopathy, Norrie disease and diabetic retinopathy. Specifically, PLVAP expression has been demonstrated to be upregulated in these diseases, accompanied by pro-angiogenic or pro-inflammatory responses. Therefore, PLVAP is considered a novel therapeutic target, in addition to an endothelial cell marker. The present review summarizes the structure and functions of PLVAP, and its roles in pathophysiological processes.

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Section: Plvap and Diseasesmentioning

confidence: 82%

Section: Plvap and Diseasesmentioning

confidence: 99%

Section: Plvap and Diseasesmentioning

confidence: 99%

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Plasmalemma vesicle-associated protein: A crucial component of vascular homeostasis

Guo

Zhang

Hou

et al. 2016

Experimental and Therapeutic Medicine

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“…Consequently, it is important to study their pathophysiological mechanisms in experimental contests where the interactions between these two cell types are preserved. Even though some studies in the literature used EC-pericyte co-cultures [16][17][18], in our knowledge this is the first time in which pericytes and EC of human origin have been utilized.…”

Section: Discussionmentioning

confidence: 99%

Human pericyte–endothelial cell interactions in co-culture models mimicking the diabetic retinal microvascular environment

et al. 2012

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“…They typically surround and communicate with the endothelial cells lining the vessels, help to lay down the basement membrane matrix [2], regulate vascular flow [3,4], secrete cytokines to inhibit endothelial proliferation [5], and tighten the endothelial permeability barrier [5–7]. Regarding the latter, pericytes are crucial for maintaining the integrity of the blood-brain barrier, especially in the retina.…”

Section: Introductionmentioning

confidence: 99%

Ascorbic acid prevents high glucose-induced apoptosis in human brain pericytes

May

Jayagopal

et al. 2014

Biochemical and Biophysical Research Communications

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High glucose concentrations due to diabetes increase apoptosis of vascular pericytes, impairing vascular regulation and weakening vessels, especially in brain and retina. We sought to determine whether vitamin C, or ascorbic acid, could prevent such high glucose-induced increases in pericyte apoptosis. Culture of human microvascular brain pericytes at 25 mM compared to 5 mM glucose increased apoptosis measured as the appearance of cleaved caspase 3. Loading the cells with ascorbate during culture decreased apoptosis, both at 5 and 25 mM glucose. High glucose-induced apoptosis was due largely to activation of the receptor for advanced glycation end products (RAGE), since it was prevented by specific RAGE inhibition. Culture of pericytes for 24 hours with RAGE agonists also increased apoptosis, which was completely prevented by inclusion of 100 μM ascorbate. Ascorbate also prevented RAGE agonist-induced apoptosis measured as annexin V binding in human retinal pericytes, a cell type with relevance to diabetic retinopathy. RAGE agonists decreased intracellular ascorbate and GSH in brain pericytes. Despite this evidence of increased oxidative stress, ascorbate prevention of RAGE-induced apoptosis was not mimicked by several antioxidants. These results show that ascorbate prevents pericyte apoptosis due RAGE activation. Although RAGE activation decreases intracellular ascorbate and GSH, the prevention of apoptosis by ascorbate may involve effects beyond its function as an antioxidant.

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A novel co-culture model of the blood-retinal barrier based on primary retinal endothelial cells, pericytes and astrocytes

Cited by 85 publications

References 49 publications

Plasmalemma vesicle-associated protein: A crucial component of vascular homeostasis

Plasmalemma vesicle-associated protein: A crucial component of vascular homeostasis

Human pericyte–endothelial cell interactions in co-culture models mimicking the diabetic retinal microvascular environment

Ascorbic acid prevents high glucose-induced apoptosis in human brain pericytes

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