scholarly journals Adiponectin Enhances Biological Functions of Vascular Endothelial Progenitor Cells Through the mTOR-STAT3 Signaling Pathway

2018 ◽  
pp. 563-570 ◽  
Author(s):  
X. DONG ◽  
X. YAN ◽  
W. ZHANG ◽  
S. TANG
Keyword(s):  
Protein Expression ◽  
Mrna Expression ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Vascular Endothelial ◽  
Biological Functions ◽  
Endothelial Progenitor ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Adiponectin (APN), an adipose tissue-excreted adipokine, plays protective roles in metabolic and cardiovascular diseases. In this study, the effects and mechanisms of APN on biological functions of rat vascular endothelial progenitor cells (VEPCs) were investigated in vitro. After administrating APN in rat VEPCs, the proliferation was measured by methyl thiazolyl tetrazolium (MTT) method, the apoptotic rate was test by Flow cytometry assay, mRNA expression of B-cell lymphoma-2 (Bcl-2) and vascular endothelial growth factor (VEGF) was determined by real-time reverse transcriptase polymerase chain reaction (RT-PCR), and protein expression of mechanistic target of rapamycin (mTOR), signal transducer and activator of transcription 3 (STAT3) and phospho-STAT3 (pSTAT3) was analyzed by Western blot. It was suggested that APN promoted the optical density (OD) value of VEPCs, enhanced mRNA expression of Bcl-2 and VEGF, and inhibited cell apoptotic rate. Furthermore, protein expression of pSTAT3 was also increased in the presence of APN. Moreover, APN changed-proliferation, apoptosis and VEGF expression of VEPCs were partially suppressed after blocking the mTOR-STAT3 signaling pathway by the mTOR inhibitor XL388. It was indicated that APN promoted biological functions of VEPCs through targeting the mTOR-STAT3 signaling pathway.

scholarly journals DPP4 inhibitors promote biological functions of human endothelial progenitor cells by targeting the SDF-1/CXCR4 signaling pathway

2016 ◽  
Vol 68 (1) ◽  
pp. 207-216 ◽  
Author(s):  
Feng Liu ◽  
Guo-Dong Huang ◽  
Jia-Zhen Tang ◽  
Yu-Huan Peng
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Hypoglycemic Agents ◽  
Dependent Manner ◽  
Biological Functions ◽  
Endothelial Progenitor ◽  
Cxcr4 Signaling ◽  
Dpp4 Inhibitors

Dipeptidyl peptidase 4 (DPP4) inhibitors(oral hypoglycemic agents)have beneficial effects during the early stages of diabetes. In this study, we evaluated the role of DPP4inhibitorsonthe biological functions of cultured human endothelial progenitor cells (EPCs). After treating EPCs with the DPP4 inhibitors sitagliptin and vildagliptin, we examined the mRNA expression of DPP4, vascular endothelial growth factor (VEGF),VEGF receptor 2 (VEGFR-2),endothelial nitric oxide synthase (eNOS), caspase-3,stromal cell-derived factor-1 (SDF-1), chemokine (C-X-C motif) receptor 4 (CXCR4) were measured by RT-PCR. The protein expression of SDF-1 and CXCR4 was determined by Western blot; cell proliferation was tested by the MTT method, and DPP4 activity was determined by a DPP4 assay. Our results revealed that DPP4 expression and activity were inhibited following the treatment with various doses of DPP4 inhibitors. Cell proliferation and the expression of VEGF, VEGFR-2andeNOS were up regulated, while cell apoptosis was inhibited by DPP4 inhibitors in a dose-dependent manner. DPP4 inhibitors activated the SDF-1/CXCR4 signaling pathway, shown by the elevated expression of SDF-1/CXCR4. This further proved that after the SDF-1/CXCR4 signaling pathway was blocked by its inhibitor ADM3100, the effects of DPP4 inhibitors on the proliferation and apoptosis, and the expression of VEGF, VEGFR-2and eNOS of EPCs were significantly reduced. These findings suggest that DPP4 inhibitors promote the biological functions of human EPCs by up regulating the SDF-1/CXCR4 signaling pathway.

scholarly journals MicroRNA-21 Regulates the Proliferation, Differentiation, and Apoptosis of Human Renal Cell Carcinoma Cells by the mTOR-STAT3 Signaling Pathway

2016 ◽  
Vol 24 (5) ◽  
pp. 371-380 ◽  
Author(s):  
Tao Liang ◽  
Xiao-Yong Hu ◽  
Yong-Hui Li ◽  
Bin-Qiang Tian ◽  
Zuo-Wei Li ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Renal Cell ◽  
Caspase 3 ◽  
Human Renal Cell Carcinoma ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

MicroRNA-21 (miRNA-21), a kind of short, noncoding RNAs, functioned as a tumor marker and was upregulated in renal cell carcinoma (RCC). However, the underlying mechanisms of miRNA-21 in RCC were uncertain. Therefore, the effects and mechanisms of miRNA-21 on the proliferation, differentiation, and apoptosis of cultured human RCC cells were further investigated in this study. After slicing miRNA-21 in RCC cells, the viability, mRNA expression of C/EBPα and PPARγ, caspase 3 activity, and protein expression of mTOR, STAT3, and pSTAT3 were determined. It was found that knockdown of miRNA-21 downregulated the optical density (OD) value of cells, inhibited mRNA expression of PPARγ and C/EBPα, and enhanced activity of caspase 3. Furthermore, protein expression of pSTAT3 was also decreased in the absence of miRNA-21. Notably, miRNA-21-changed proliferation, differentiation, and apoptosis of human RCC cells were partially regulated following the block of the mTOR-STAT3 signaling pathway by the mTOR inhibitor (XL388). It was indicated that miRNA-21 promoted proliferation and differentiation and decreased apoptosis of human RCC cells through the activation of the mTOR-STAT3 signaling pathway.

scholarly journals Suppression of microRNA-135b-5p protects against myocardial ischemia/reperfusion injury by activating JAK2/STAT3 signaling pathway in mice during sevoflurane anesthesia

2017 ◽  
Vol 37 (3) ◽  
Author(s):  
Xiao-Juan Xie ◽  
Dong-Mei Fan ◽  
Kai Xi ◽  
Ya-Wei Chen ◽  
Peng-Wei Qi ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Inhalation Anesthesia ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Myocardial Ischemia Reperfusion

The study aims to explore the effects of miR-135b-5p on myocardial ischemia/reperfusion (I/R) injuries by regulating Janus protein tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription (STAT) signaling pathway by mediating inhalation anesthesia with sevoflurane. A sum of 120 healthy Wistar male mice was assigned into six groups. Left ventricular ejection fraction (LVEF) and left ventricular shortening fraction (LVSF) were detected. Cardiomyocyte apoptosis was determined by terminal dexynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) assay. MiR-135b-5p expression, mRNA and protein expression of p-STAT3, p-JAK2, STAT3, JAK2, B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein B (Bax) were detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Target relationship between miR-135b-5p and JAK2 was confirmed by dual-luciferase reporter assay. The other five groups exhibited increased cardiomyocyte necrosis, apoptosis, miR-135b-5p and Bax expression, mRNA expression of JAK2 and STAT3, and protein expression of p-STAT3 and p-JAK2 compared with the sham group, but showed decreased LVEF, LVFS, and Bcl-2 expression. Compared with the model and AG490 + Sevo groups, the Sevo, inhibitor + Sevo and inhibitor + AG490 + Sevo groups displayed reduced cardiomyocyte necrosis, apoptosis, miR-135b-5p and Bax expression, but displayed elevated mRNA expression of JAK2 and STAT3, protein expression of p-STAT3 and p-JAK2, LVEF, LVFS and Bcl-2 expression. Compared with the Sevo and inhibitor + AG490 + Sevo groups, the AG490 + Sevo group showed decreased LVEF, LVFS, Bcl-2 expression, mRNA expressions of JAK2 and STAT3, and protein expressions of p-STAT3 and p-JAK2, but increased cardiomyocyte necrosis, apoptosis, and Bax expressions. MiR-135b-5p negatively targetted JAK2. Inhibition of miR-135b-5p can protect against myocardial I/R injury by activating JAK2/STAT3 signaling pathway through mediation of inhalation anesthesia with sevoflurane.

A cardiac rehabilitation program increases the acute respond of endothelial progenitor cells after maximum exercise in patients with chronic heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Kourek ◽  
E Karatzanos ◽  
D Delis ◽  
M Alshamari ◽  
V Linardatou ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Cardiac Rehabilitation ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Rehabilitation Program ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Maximum Exercise

Abstract Background Chronic heart failure (CHF) remains a leading cause of morbidity and mortality and it is characterized by vascular endothelial dysfunction. During the last decades, endothelial progenitor cells (EPCs) are being used as an index of the endothelium restoration potential, therefore reflecting the vascular endothelial function. Exercise training has been shown to stimulate the mobilization of EPCs at rest in CHF patients. However, the effect of exercise training on the acute respond of EPCs after maximum exercise in CHF patients remains unknown. Purpose The purpose of the study was to assess the effect of a cardiac rehabilitation (CR) program on the acute respond of EPCs after maximum exercise in patients with CHF. Methods Forty-four consecutive patients (35 males) with stable CHF [mean±SD, Age (years): 56±10, BMI (kg/m2): 28.7±5.2, EF (%): 33±8, Peak VO2 (ml/kg/min): 18.4±4.4, Peak work rate (watts): 101±39] enrolled a 36-session CR program based on high-intensity interval exercise training. All patients underwent an initial symptom limited maximal cardiopulmonary exercise testing (CPET) on an ergometer before the CR program and a final maximal CPET after the CR program. Venous blood was drawn before and after each CPET. Five circulating endothelial populations were identified and quantified by flow cytometry; CD34+/CD45-/CD133+, CD34+/CD45-/CD133+/VEGFR2, CD34+/CD133+/VEGFR2, CD34+/CD45-/CD133- and CD34+/CD45-/CD133-/VEGFR2. EPCs values are expressed as cells/million enucleated cells in medians (25th-75th percentiles). Results The acute mobilization of EPCs after the final CPET was higher than after the initial CPET in 4 out of 5 circulating endothelial populations. Most specifically, difference of the acute mobilization of CD34+/CD45-/CD133+ cells [initial CPET: 25 (15–46) vs final CPET: 49 (26–71), p=0.002], CD34+/CD45-/CD133+/VEGFR2 cells [initial CPET: 3 (2–5) vs final CPET: 8 (5–12), p<0.001], CD34+/CD45-/CD133- cells [initial CPET: 129 (52–338) vs final CPET: 250 (129–518), p=0.03] and CD34+/CD45-/CD133-/VEGFR2 cells [initial CPET: 2 (1–4) vs final CPET: 6 (3–9), p<0.001] increased after the final CPET. The acute mobilization of CD34+/CD133+/VEGFR2 cells [initial CPET: 3 (−1–7) vs final CPET: 5 (0–15), p=0.441] did not differ between the 2 CPETS. Conclusion A 36-session cardiac rehabilitation program increases the acute respond of endothelial progenitor cells after maximum cardiopulmonary exercise training in patients with chronic heart failure, therefore indicating the beneficial effect of exercise training on the vascular endothelial function. Funding Acknowledgement Type of funding source: Public grant(s) – EU funding. Main funding source(s): Co-financed by Greece and the European Union (European Social Fund- ESF) through the Operational Programme “Human Resources Development, Education and Lifelong Learning” in the context of the project

Endothelial progenitor cells and hypertension: current concepts and future implications

2016 ◽  
Vol 130 (22) ◽  
pp. 2029-2042 ◽  
Author(s):  
Shengyuan Luo ◽  
Wenhao Xia ◽  
Cong Chen ◽  
Eric A. Robinson ◽  
Jun Tao
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Current Knowledge ◽  
Circulatory System ◽  
Essential Element ◽  
Future Research ◽  
Chronic Hypertension ◽  
Vascular Endothelial ◽  
Endothelial Progenitor ◽  
Endothelial Integrity

The discovery of endothelial progenitor cells (EPCs), a group of cells that play important roles in angiogenesis and the maintenance of vascular endothelial integrity, has led to considerable improvements in our understanding of the circulatory system and the regulatory mechanisms of vascular homoeostasis. Despite lingering disputes over where EPCs actually originate and how they facilitate angiogenesis, extensive research in the past decade has brought about significant advancements in this field of research, establishing EPCs as an essential element in the pathogenesis of various diseases. EPC and hypertensive disorders, especially essential hypertension (EH, also known as primary hypertension), represent one of the most appealing branches in this area of research. Chronic hypertension remains a major threat to public health, and the exact pathologic mechanisms of EH have never been fully elucidated. Is there a relationship between EPC and hypertension? If so, what is the nature of such relationship–is it mediated by blood pressure alterations, or other factors that lie in between? How can our current knowledge about EPCs be utilized to advance the prevention and clinical management of hypertension? In this review, we set out to answer these questions by summarizing the current concepts about EPC pathophysiology in the context of hypertension, while attempting to point out directions for future research on this subject.

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