Gene Therapy of Endothelial Nitric Oxide Synthase and Manganese Superoxide Dismutase Restores Delayed Wound Healing in Type 1 Diabetic Mice

Luo, Jia; Wang, Yingying; Fu, Weiling; Wu, Jun; Chen, Alex F.

doi:10.1161/01.cir.0000137969.87365.05

Cited by 172 publications

(177 citation statements)

References 50 publications

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“…Thereafter, to further confirm the role of DA D 1 receptors on diabetic wound healing, experiments were undertaken in DA D 1 receptor knockout C57BL/6 mice (KOD 1 STZDiab). 29 As expected, in contrast to those in the wild-type STZ-Diab mice, the specific DA D 1 receptor agonists had no effects on promoting wound healing in these KOD1 STZ-Diab mice ( Figure 1A). On day 11, the percent healing values in these animals were approximately 60 in the SKF38393-treated group and approximately 66 in the SKF81297-treated group ( Figure 1B), thereby further confirming the role of DA D 1 receptors in regulating diabetic wound healing (Figure 1, A and B).…”

Section: Stimulation Of Da D 1 Receptor Accelerates Dermal Wound Healsupporting

confidence: 68%

“…29 Our results indicated that in contrast to nontreated diabetic controls, in mice treated with a specific DA D 1 receptor agonistdSKF38393 or SKF81297 (i.p. 10 mg/kg per day for 5 days)dsignificantly improved the rate of wound healing in these animals (P < 0.05), with intact surface new skin occurring by day 11 ( Figure 1A).…”

Section: Stimulation Of Da D 1 Receptor Accelerates Dermal Wound Healmentioning

confidence: 59%

“…Mice with a glucose concentration >300 mg/dL were considered diabetic. 29 For the creation of cutaneous wound, diabetic C57BL/6, db/db mice and DA D 1 receptor knockout mice were anesthetized by i.p. injection of ketamine/xylazine mixture (100/10 mg).…”

Section: Induction Of Diabetes and Creation Of Woundmentioning

confidence: 99%

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Activation of Dopamine D1 Receptors in Dermal Fibroblasts Restores Vascular Endothelial Growth Factor-A Production by These Cells and Subsequent Angiogenesis in Diabetic Cutaneous Wound Tissues

Chakroborty

Sarkar

et al. 2016

The American Journal of Pathology

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Section: Stimulation Of Da D 1 Receptor Accelerates Dermal Wound Healsupporting

confidence: 68%

Section: Stimulation Of Da D 1 Receptor Accelerates Dermal Wound Healmentioning

confidence: 59%

See 1 more Smart Citation

Activation of Dopamine D1 Receptors in Dermal Fibroblasts Restores Vascular Endothelial Growth Factor-A Production by These Cells and Subsequent Angiogenesis in Diabetic Cutaneous Wound Tissues

Chakroborty

Sarkar

et al. 2016

The American Journal of Pathology

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“…The full thickness excisional wounds were created as previously described (18). Briefly, 1 wk after blood glucose reached 250 mg/dL, mice were anesthetized with a 10% chloral hydrate, and the dorsum was depilated with 8% Na 2S.…”

Section: Animalsmentioning

confidence: 99%

Folic Acid Promotes Wound Healing in Diabetic Mice by Suppression of Oxidative Stress

Zhao

Zhou

Chen

et al. 2018

Journal of Nutritional Science and Vitaminology

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SummaryThe aim of this study was to investigate the effects of folic acid on impaired wound healing in diabetic mice. Male mice were divided into three groups: group 1, the non-diabetic mice (control); group 2, the streptozotocin (STZ)-induced type 1 diabetic mice; and group 3, the diabetic mice that received a daily dose of 3 mg/kg folic acid via oral gavage. Full-thickness excision wounds were created with 8-mm skin biopsy punches. Each wound closure was continuously evaluated until the wound healed up. Wound healing was delayed in diabetic mice compared with the non-diabetic mice. There were significantly reduced levels of hydroxyproline content (indicator of collagen deposition) and glutathione in diabetic wounds, whereas levels of lipid peroxidation and protein nitrotyrosination were increased. Daily supplementation with folic acid restored diabetes-induced healing delay. Histopathology showed that folic acid supplementation accelerated granulation tissue formation, proliferation of fibroblasts, and tissue regeneration in diabetic mice. Interestingly, folic acid alleviated diabetes-induced impaired collagen deposition in wounds. Moreover, folic acid significantly decreased levels of lipid peroxidation, protein nitrotyrosination and glutathione depletion in diabetic wounds. In conclusion, our results indicate that folic acid supplementation may improve impaired wound healing via suppressing oxidative stress in diabetic mice.

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“…6 -8 Last, recent experimental studies have shown that gene therapy to restore eNOS uncoupling or expression effectively restores diabetic endothelial dysfunction. 9,10 Thus, a dysfunctional eNOS/NO system is a major mediator of endothelial dysfunction in diabetes.…”

mentioning

confidence: 99%

Deficiency of Endothelial Nitric-Oxide Synthase Confers Susceptibility to Diabetic Nephropathy in Nephropathy-Resistant Inbred Mice

Kanetsuna

Takahashi

Nagata

et al. 2007

The American Journal of Pathology

166

150

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Recent studies have implicated dysfunctional endothelial nitric-oxide synthase (eNOS) as a common pathogenic pathway in diabetic vascular complications. However, functional consequences are still incompletely understood. To determine the role of eNOS-derived nitric oxide (NO) in diabetic nephropathy, we induced diabetes in eNOS knockout (KO) and wild-type (WT) mice on the C57BL6 background, using low-dose streptozotocin injection, and we investigated their glomerular phenotype at up to 20 weeks of diabetes. Although the severity of hyperglycemia in diabetic eNOS KO mice was similar to diabetic WT mice, diabetic eNOS KO mice developed overt albuminuria, hypertension, and glomerular mesangiolysis, whereas diabetic WT and nondiabetic control mice did not. Glomerular hyperfiltration was also significantly reduced in diabetic eNOS KO mice. Electron micrographs from diabetic eNOS KO mice revealed an injured endothelial morphology, thickened glomerular basement membrane, and focal foot process effacement. Furthermore, the anionic sites at glomeru- Nitric oxide (NO) is a free radical that mediates diverse functions in a range of biological systems.1 NO is produced by a family of nitric-oxide synthase (NOS) enzymes to catalyze the stoichiometric five-electron oxidation of the terminal quanidino group of L-arginine to produce NO and L-citrulline. Three NOS isoforms have been distinguished in mammalian species: neuronal NOS, inducible NOS, which is expressed in a variety of activated tissues, and endothelial NOS (eNOS).1 In the vasculature, NO is mostly generated by eNOS, and the generated NO plays a crucial role in maintaining vascular homeostasis, including vascular tone, leukocyte adhesion to endothelium, proliferation of vascular smooth muscle cells, and platelet aggregation and adhesion to the vessel wall.

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Gene Therapy of Endothelial Nitric Oxide Synthase and Manganese Superoxide Dismutase Restores Delayed Wound Healing in Type 1 Diabetic Mice

Cited by 172 publications

References 50 publications

Activation of Dopamine D1 Receptors in Dermal Fibroblasts Restores Vascular Endothelial Growth Factor-A Production by These Cells and Subsequent Angiogenesis in Diabetic Cutaneous Wound Tissues

Activation of Dopamine D1 Receptors in Dermal Fibroblasts Restores Vascular Endothelial Growth Factor-A Production by These Cells and Subsequent Angiogenesis in Diabetic Cutaneous Wound Tissues

Folic Acid Promotes Wound Healing in Diabetic Mice by Suppression of Oxidative Stress

Deficiency of Endothelial Nitric-Oxide Synthase Confers Susceptibility to Diabetic Nephropathy in Nephropathy-Resistant Inbred Mice

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