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

Tarallo, Sonia; Beltramo, Elena; Berrone, Elena; Porta, Massimo

doi:10.1007/s00592-012-0390-5

Cited by 30 publications

(23 citation statements)

References 41 publications

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“…A C C E P T E D ACCEPTED MANUSCRIPT 60 retinopathy in vitro and in vivo (Beltramo et al, 2009;Berrone et al, 2006;Hammes et al, 2003;Tarallo et al, 2012). A clinical trial tested the ability of benfotiamine to reduce plasma and urinary AGEs but showed no benefit (Alkhalaf et al, 2012) and in T1D patients, 24 month treatment with benfotiamine demonstrated no change in peripheral nerve function or soluble inflammatory biomarkers (Fraser et al, 2012).…”

Section: Therapeutic Options In Diabetic Retinopathymentioning

confidence: 99%

The progress in understanding and treatment of diabetic retinopathy

Stitt

Curtis

Chen

et al. 2016

Progress in Retinal and Eye Research

825

657

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Section: Therapeutic Options In Diabetic Retinopathymentioning

confidence: 99%

The progress in understanding and treatment of diabetic retinopathy

Stitt

Curtis

Chen

et al. 2016

Progress in Retinal and Eye Research

825

657

View full text Add to dashboard Cite

“…Benfotiamine, a lipid soluble thiamine (vitamin B1), prevents hyperglycemiainduced pericyte-endothelial cell interactions [87]. In diabetic rats, Benfotiamine has been shown to inhibit the development of histopathology characteristic of diabetic retinopathy via inhibiting the major biochemical pathways implicated in its pathogenesis [88].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Oxidative stress, mitochondrial damage and diabetic retinopathy

Kowluru

Mishra

2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

272

246

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Diabetes has emerged as an epidemic of the 21st century, and retinopathy remains the leading cause of blindness in young adults and the mechanism of this blinding disease remains evasive. Diabetes-induced metabolic abnormalities have been identified, but a causal relationship between any specific abnormality and the development of this multi-factorial disease is unclear. Reactive oxygen species (ROS) are increased and the antioxidant defense system is compromised. Increased ROS result in retinal metabolic abnormalities, and these metabolic abnormalities can also produce ROS. Sustained exposure to ROS damages the mitochondria and compromises the electron transport system (ETC), and, ultimately, the mitochondrial DNA (mtDNA) is damaged. Damaged mtDNA impairs its transcription, and the vicious cycle of ROS continues to propagate. Many genes important in generation and neutralization of ROS are also epigenetically modified further increasing ROS, and the futile cycle continues to fuel in. Antioxidants have generated beneficial effects in ameliorating retinopathy in diabetic rodents, but limited clinical studies have not been encouraging. With the ongoing use of antioxidants for other chronic diseases, there is a need for a controlled trial to recognize their potential in ameliorating the development of this devastating disease.

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“…However, insulin treatment cannot fully prevent the development of the severe chronic complications related to diabetes, such as kidney failure, coronary heart disease, retinopathy, and neuropathy [3–7]. Islet transplantation is a relatively low-invasive procedure that has been shown to normalize glycemia and effectively counteract the development of diabetic complications [8–13].…”

Section: Introductionmentioning

confidence: 99%

Co-transplantation of autologous MSCs delays islet allograft rejection and generates a local immunoprivileged site

et al. 2015

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Aims Mesenchymal stem cells (MSCs) are multipotent cells with immunomodulatory properties. We tested the ability of MSCs to delay islet allograft rejection. Methods Mesenchymal stem cells were generated in vitro from C57BL/6 and BALB/c mice bone marrow, and their immunomodulatory properties were tested in vitro. We then tested the effect of a local or systemic administration of heterologous and autologous MSCs on graft survival in a fully allogeneic model of islet transplantation (BALB/c islets into C57BL/6 mice). Results In vitro, autologous, but not heterologous, MSCs abrogated immune cell proliferation in response to alloantigens and skewed the immune response toward a Th2 profile. A single dose of autologous MSCs co-transplanted under the kidney capsule with allogeneic islets delayed islet rejection, reduced graft infiltration, and induced long-term graft function in 30 % of recipients. Based on ex vivo analysis of recipient splenocytes, the use of autologous MSCs did not appear to have any systemic effect on the immune response toward graft alloantigens. The systemic injection of autologous MSCs or the local injection of heterologous MSCs failed to delay islet graft rejection. Conclusion Autologous, but not heterologous, MSCs showed multiple immunoregulatory properties in vitro and delayed allograft rejection in vivo when co-transplanted with islets; however, they failed to prevent rejection when injected systemically. Autologous MSCs thus appear to produce a local immunoprivileged site, which promotes graft survival.

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

Abstract: Background: Pericytes regulate vascular tone, perfusion pressure and endothelial cell (EC)

Cited by 30 publications

References 41 publications

The progress in understanding and treatment of diabetic retinopathy

The progress in understanding and treatment of diabetic retinopathy

Oxidative stress, mitochondrial damage and diabetic retinopathy

Co-transplantation of autologous MSCs delays islet allograft rejection and generates a local immunoprivileged site

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