Periodontal treatment modulates gene expression of endothelial progenitor cells in diabetic patients

2017 ◽  
Vol 44 (12) ◽  
pp. 1253-1263 ◽  
Author(s):  
Yi Wang ◽  
Hin Nam Liu ◽  
Zhe Zhen ◽  
Kai Hang Yiu ◽  
Hung Fat Tse ◽  
...  
Endocrine ◽  
2014 ◽  
Vol 49 (2) ◽  
pp. 415-421 ◽  
Author(s):  
Maria Ida Maiorino ◽  
Giuseppe Bellastella ◽  
Michela Petrizzo ◽  
Elisabetta Della Volpe ◽  
Rosanna Orlando ◽  
...  

2021 ◽  
Author(s):  
Siqi He ◽  
Tanaya Walimbe ◽  
Hongyuan Chen ◽  
Kewa Gao ◽  
Priyadarsini Kumar ◽  
...  

AbstractDiabetic ischemic wound treatment remains a critical clinical challenge. Strategies that enhance angiogenesis and improve ischemic pathology may promote the healing of poor wounds, particularly diabetic wounds in highly ischemic condition. We previously identified a cyclic peptide LXW7 that specifically binds to integrin αvβ3 on endothelial progenitor cells (EPCs) and endothelial cells (ECs), activates VEGF receptors, and promotes EC growth and maturation. In this study, we designed and synthesized a pro-angiogenic molecule LXW7-DS-SILY by conjugating LXW7 to a collagen-binding proteoglycan mimetic DS-SILY and further employed this novel bifunctional ligand to functionalize extracellular matrix (ECM) scaffolds, promote neovascularization and accelerate ischemic wound healing. We established a Zucker Diabetic Fatty (ZDF) rat ischemic skin flap model and found the wounds treated by LXW7-DS-SILY-functionalized ECM scaffolds, with or without EPCs, significantly improved wound healing, enhanced neovascularization and modulated collagen fibrillogenesis. These functionalized ECM scaffolds also significantly promoted EPC attachment, growth and survival in the ischemic environment. Altogether, this study provides a promising novel treatment to accelerate diabetic ischemic wound healing, thereby reducing limb amputation and mortality of diabetic patients.


2013 ◽  
Vol 168 (2) ◽  
pp. 153-161 ◽  
Author(s):  
Barbara Głowińska-Olszewska ◽  
Marcin Moniuszko ◽  
Andrzej Hryniewicz ◽  
Marta Jeznach ◽  
Małgorzata Rusak ◽  
...  

ObjectiveThe low number of circulating endothelial progenitor cells (EPCs) has emerged as a biomarker of cardiovascular (CV) risk in adults. Data regarding EPCs in paediatric populations with CV risk factors are limited. The aim of the study was to estimate the EPC number and its relationship with vascular function and structure in children with type 1 diabetes mellitus (T1DM).Design and methodsWe performed a comparative analysis of 52 children with T1DM (mean age 14.5 years; diabetes duration, 6.0 years; HbA1c level, 8.5%) and 36 healthy age- and gender-matched control children. EPCs were identified and analysed by flow cytometry with the use of MABs directed against CD34, CD144 (VE-cadherin) and CD309 (VEGFR-2). sICAM-1, hsCRP, thrombomodulin and adiponectin levels were also assessed. We evaluated vascular function (flow-mediated dilation (FMD)) and structure (carotid intima–media thickness (IMT)) ultrasonographically.ResultsFrequencies of CD34+ cells were similar in both groups (P=0.30). In contrast, frequencies of CD34+VE-cadherin+ cells were significantly higher in diabetic children compared with the healthy group (P=0.003). Similarly, diabetic patients tended to present with higher frequencies of CD34+VEGFR+ cells (P=0.06). FMD was lower (6.9 vs 10.5%, P=0.002) and IMT was higher (0.50 vs 0.44 mm, P=0.0006) in diabetic children. We demonstrated a significant relationship between CD34+VEGFR-2+ cells and BMI (r=0.3, P=0.014), HDL (r=−0.27, P=0.04), sICAM-1 (r=0.47, P=0.023) and FMD (r=−0.45, P<0.001). Similarly, frequencies of CD34+VE-cadherin+ cells were significantly correlated with BMI (r=0.32, P=0.02) and FMD (r=−0.31, P=0.03).ConclusionsWe demonstrated here that increased frequencies of EPCs observed in diabetic children are negatively correlated with endothelial function. Further studies are warranted to assess whether this phenomenon might result from effective mobilisation of EPCs in order to repair damaged endothelium in children at increased risk for atherosclerosis.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Cai-Guo Yu ◽  
Ning Zhang ◽  
Sha-Sha Yuan ◽  
Yan Ma ◽  
Long-Yan Yang ◽  
...  

Despite being featured as metabolic disorder, diabetic patients are largely affected by hyperglycemia-induced vascular abnormality. Accumulated evidence has confirmed the beneficial effect of endothelial progenitor cells (EPCs) in coronary heart disease. However, antivascular endothelial growth factor (anti-VEGF) treatment is the main therapy for diabetic retinopathy and nephropathy, indicating the uncertain role of EPCs in the pathogenesis of diabetic microvascular disease. In this review, we first illustrate how hyperglycemia induces metabolic and epigenetic changes in EPCs, which exerts deleterious impact on their number and function. We then discuss how abnormal angiogenesis develops in eyes and kidneys under diabetes condition, focusing on “VEGF uncoupling with nitric oxide” and “competitive angiopoietin 1/angiopoietin 2” mechanisms that are shared in both organs. Next, we dissect the nature of EPCs in diabetic microvascular complications. After we overview the current EPCs-related strategies, we point out new EPCs-associated options for future exploration. Ultimately, we hope that this review would uncover the mysterious nature of EPCs in diabetic microvascular disease for therapeutics.


2017 ◽  
Vol 10 ◽  
pp. 117955141774398 ◽  
Author(s):  
Roberto Negro ◽  
Eupremio Luigi Greco ◽  
Giacomo Greco

Background: It is postulated that the ability of dipeptidyl peptidase-4 inhibitors (DPP-4-i) to increase circulating endothelial progenitor cells (EPCs) may be at least partly mediated by active stromal cell–derived factor 1α (SDF-1α) (a pivotal mediator of stem cell mobilization from the bone marrow). As other DPP-4-i were demonstrated to increase EPC concentrations, in this study, we sought to investigate the ability of the DPP-4-i alogliptin in modifying EPCs and SDF-1α, in patients with good and poor diabetes control. Methods: Two groups of diabetic patients on metformin were divided by hemoglobin A1c (HbA1c): Group A—those with HbA1c ≤6.5% (28 patients) and Group B—those with HbA1c 7.5% to 8.5% (31 patients). Both groups received alogliptin 25 mg/daily for 4 months. At baseline and 4 months later, clinical, laboratory parameters, EPCs, and active SDF-1α were determined. Results: After 4-month treatment with alogliptin, either Group A or Group B showed reduced HbA1c levels and concomitant similar increase in EPCs and active SDF-1α. Conclusions: Alogliptin showed significant benefits in increasing EPCs and active SDF-1α either in good or poor diabetes control. The study demonstrated that similar to other DPP-4-i, also alogliptin is able to increase EPC concentrations, suggesting the existence of a class effect mediated by SDF-1α. The extent of increase in EPCs is independent from baseline diabetes control.


2015 ◽  
Vol 67-69 ◽  
pp. 21-29 ◽  
Author(s):  
Gian Paolo Fadini ◽  
Mauro Rigato ◽  
Federico Boscari ◽  
Roberta Cappellari ◽  
Lisa Menegazzo ◽  
...  

2020 ◽  
Vol 9 (3) ◽  
Author(s):  
Mirta T. Ito ◽  
Sueli M. da Silva Costa ◽  
Letícia C. Baptista ◽  
Gabriela Q. Carvalho‐Siqueira ◽  
Dulcinéia M. Albuquerque ◽  
...  

Background The clinical aspects of sickle cell anemia ( SCA ) are heterogeneous, and different patients may present significantly different clinical evolutions. Almost all organs can be affected, particularly the central nervous system. Transient ischemic events, infarcts, and cerebral hemorrhage can be observed and affect ≈25% of the patients with SCA . Differences in the expression of molecules produced by endothelial cells may be associated with the clinical heterogeneity of patients affected by vascular diseases. In this study, we investigated the differential expression of genes involved in endothelial cell biology in SCA patients with and without stroke. Methods and Results Endothelial progenitor cells from 4 SCA patients with stroke and 6 SCA patients without stroke were evaluated through the polymerase chain reaction array technique. The analysis of gene expression profiling identified 29 differentially expressed genes. Eleven of these genes were upregulated, and most were associated with angiogenesis (55%), inflammatory response (18%), and coagulation (18%) pathways. Downregulated expression was observed in 18 genes, with the majority associated with angiogenesis (28%), apoptosis (28%), and cell adhesion (22%) pathways. Remarkable overexpression of the MMP 1 (matrix metalloproteinase 1) gene in the endothelial progenitor cells of all SCA patients with stroke (fold change: 204.64; P =0.0004) was observed. Conclusions Our results strongly suggest that angiogenesis is an important process in sickle cell stroke, and differences in the gene expression profile of endothelial cell biology, especially MMP 1 , may be related to stroke in SCA patients.


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