Changes in cultured endothelial cell glycosaminoglycans under hyperglycemic conditions and the effect of insulin and heparin

Han, Juying; Zhang, Fuming; Xie, Jin; Linhardt, Robert J.; Hiebert, Linda M.

doi:10.1186/1475-2840-8-46

Cited by 29 publications

(19 citation statements)

References 41 publications

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“…In agreement with our results, the percentage of total GAGs in high glucose-treated medium was significantly increased compared to glucose-free medium (Han et al, 2009). One explanation of increased GAGs is presented by Takeda et al (2001) who reported that, high glucose stimulates GAGs production through activation of protein kinase C and TGF-beta cascade.…”

Section: Discussionsupporting

confidence: 92%

“…One explanation of increased GAGs is presented by Takeda et al (2001) who reported that, high glucose stimulates GAGs production through activation of protein kinase C and TGF-beta cascade. Hyperglycemia may also lead to the release of GAGs from cell proteoglycan core proteins because cultured endothelial cells treated with high glucose showed a reduction in total GAGs, while medium GAGs was increased (Han et al, 2009). We can conclude that alteration of GAGs synthesized by cells is an important pathological mechanism, which can be correlated with cell injury by hyperglycemia.…”

Section: Discussionmentioning

confidence: 76%

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Serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) as diagnostic markers for early hepatocellular carcinoma in cirrhotic patients with or without diabetes

Ibrahim¹

2013

J. Med. Lab. Diagn.

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The significance of serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) in early screening of hepatocellular carcinoma in cirrhotic patients was evaluated. The effect of diabetes on GAGs and IGF-1 levels was also estimated. Fifty cirrhotic patients with early stage Hepatocellular carcinoma (HCC) (22 were diabetic), thirty control cirrhotic patients without HCC (11 were diabetic) and twenty normal control subjects, were enrolled to the study. Serum α-fetoprotein (AFP), the commonly used marker for HCC, was measured in all HCC patients. Serum GAGs increased significantly, while IGF-1 was reduced in patients with cirrhosis and early stage HCC compared to normal control (P < 0.001). There was a significant reduction in GAGs and IGF-1 levels in control cirrhotic group compared to HCC group (P < 0.05). HCC patients who had normal AFP showed significantly increased GAGs and reduced IGF-1 levels compared to normal control. In comparison with corresponding non-diabetic patients, diabetic patients showed a significant increase in serum GAGs in both cirrhotic control and HCC (P < 0.01), while a significant decrease was observed in serum IGF-1 only in HCC (P < 0.05). Concomitant determination and monitoring of serum GAGs and IGF-1 could be used as a simple, low cost and non-invasive marker for HCC in cirrhotic patients.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 76%

Serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) as diagnostic markers for early hepatocellular carcinoma in cirrhotic patients with or without diabetes

Ibrahim¹

2013

J. Med. Lab. Diagn.

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“…57 Increased levels of HSPG and of AAV2 co-receptors are not unexpected in DR and may contribute to its progression. High glucose levels upregulate cell-associated proteoglycans in retinal pericytes 58 and promote the secretion of HS chains by endothelial cells, 59 and VEGF increases the retinal expression of the HS side chains of HSPGs. 60 Perlecan binds FGFs, 61,62 and the intraretinal stores of immunoreactive bFGF and HSPG increase in patients with DR. 63 Of note, abnormal HSPG expression and structure can contribute to vascular leakage and to the release of pro-angiogenic factors in DR, 64 whereas bFGF, αvβ5 integrin, and HGF can signal to promote angiogenesis in DR. 65 However, contrary to what is expected from our findings using rats after 6 weeks of STZ, the mRNA levels of perlecan, the [ 35 S] sulfate incorporation into HSPG, 66 and the immunolocalization of HSPG 67 decrease in the retina of diabetic rats at 5 and 11 months after STZ treatment, respectively.…”

Section: Aav2 Vectors Reverse Diabetic Retinal Alterations N Díaz-lezmentioning

confidence: 99%

Diabetes enhances the efficacy of AAV2 vectors in the retina: therapeutic effect of AAV2 encoding vasoinhibin and soluble VEGF receptor 1

Díaz‐Lezama

Adán‐Castro

et al. 2016

Laboratory Investigation

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Adeno-associated virus (AAV) vector-mediated delivery of inhibitors of blood-retinal barrier breakdown (BRBB) offers promise for the treatment of diabetic macular edema. Here, we demonstrated a reversal of blood-retinal barrier pathology mediated by AAV type 2 (AAV2) vectors encoding vasoinhibin or soluble VEGF receptor 1 (sFlt-1) when administered intravitreally to diabetic rats. Efficacy and safety of the AAV2 vasoinhibin vector were tested by monitoring its effect on diabetes-induced changes in the retinal vascular bed and thickness, and in the electroretinogram (ERG). Also, the transduction of AAV2 vectors and expression of AAV2 receptors and co-receptors were compared between the diabetic and the non-diabetic rat retinas. AAV2 vasoinhibin or AAV2 sFlt-1 vectors were injected intravitreally before or after enhanced BRBB due to diabetes induced by streptozotocin. The BRBB was examined by the Evans blue method, the vascular bed by fluorescein angiography, expression of the AAV2 EGFP reporter vector by confocal microscopy, and the AAV2 genome, expression of transgenes, receptors, and co-receptors by quantitative PCR. AAV2 vasoinhibin and sFlt-1 vectors inhibited the diabetes-mediated increase in BRBB when injected after, but not before, diabetes was induced. The AAV2 vasoinhibin vector decreased retinal microvascular abnormalities and the diabetes-induced reduction of the B-wave of the ERG, but it had no effect in non-diabetic controls. Also, retinal thickness was not altered by diabetes or by the AAV2 vasoinhibin vector. The AAV2 genome, vasoinhibin and sFlt-1 transgenes, and EGFP levels were higher in the retinas from diabetic rats and were associated with an elevated expression of AAV2 receptors (syndecan, glypican, and perlecan) and co-receptors (fibroblast growth factor receptor 1, αvβ5 integrin, and hepatocyte growth factor receptor). We conclude that retinal transduction and efficacy of AAV2 vectors are enhanced in diabetes, possibly due to their elevated cell entry. AAV2 vectors encoding vasoinhibin and sFlt-1 may be desirable gene therapeutics to target diabetic retinopathy and macular edema.

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“…8 Osteopontin (OPN) is a secreted phosphoprotein normally expressed in bone and epithelial cells including the lung bronchi and renal tubules. Overexpression is observed in many cancers, 9 and it is associated with invasion and metastasis, including in lung cancer. 10 Cisplatin is a cytotoxic chemotherapeutic agent routinely used in the treatment of solid malignancies, including renal cell carcinoma (RCC) and non-small-cell lung adenocarcinoma (ADC).…”

mentioning

confidence: 99%

Differential effects of sevoflurane on the metastatic potential and chemosensitivity of non-small-cell lung adenocarcinoma and renal cell carcinoma in vitro

Ciechanowicz

Zhao

Chen

et al. 2018

British Journal of Anaesthesia

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Changes in cultured endothelial cell glycosaminoglycans under hyperglycemic conditions and the effect of insulin and heparin

Cited by 29 publications

References 41 publications

Serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) as diagnostic markers for early hepatocellular carcinoma in cirrhotic patients with or without diabetes

Serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) as diagnostic markers for early hepatocellular carcinoma in cirrhotic patients with or without diabetes

Diabetes enhances the efficacy of AAV2 vectors in the retina: therapeutic effect of AAV2 encoding vasoinhibin and soluble VEGF receptor 1

Differential effects of sevoflurane on the metastatic potential and chemosensitivity of non-small-cell lung adenocarcinoma and renal cell carcinoma in vitro

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