Electroacupuncture pretreatment promotes angiogenesis via hypoxia-inducible factor 1α and vascular endothelial growth factor in a rat model of chronic myocardial ischemia

2020 ◽  
pp. 096452842093837
Author(s):  
Yimeng Fu ◽  
Jia Li ◽  
Song Wu ◽  
Hua Wang
Keyword(s):  
Myocardial Infarction ◽  
Protein Expression ◽  
Hypoxia Inducible Factor ◽  
Serum Levels ◽  
Left Ventricular ◽  
Vascular Endothelial ◽  
Vascular Regeneration ◽  
Endothelial Growth Factor ◽  
Masson Staining ◽  
Chronic Myocardial Ischemia

Objective: Electroacupuncture (EA) pretreatment appears useful in the treatment of chronic myocardial ischemia (CMI). The goal of this study was to investigate the effect of EA preconditioning on the regulation of hypoxia-inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) proteins in a CMI model of vascular regeneration. Methods: A CMI model was established by subcutaneous injection of isoprinosine hydrochloride (ISO) for 14 days in 45 Wistar rats, which had been randomly divided into a model group ( n = 15), a CMI group pretreated with sham EA for 21 days (CMI + Sham group, n = 15) and a CMI group pretreated with verum EA for 21 days (CMI + EA, n = 15) prior to modeling. An additional 15 Wistar rats received 0.9% sodium chloride via intraperitoneal injection for 14 consecutive days (control group). Serum levels of VEGF and HIF-1α were measured by ELISA, while protein expression of VEGF and HIF-1α in the area of myocardial infarction was measured by Western blotting. The area of myocardial infarction and fibrosis of the myocardial tissue in the study groups were visualized by hematoxylin-eosin (HE) staining and Masson staining, respectively. Results: EA pretreatment improved cardiac function by regulating left ventricular end-diastolic diameter and left ventricular end-systolic diameter, left ventricular ejection fraction and the ST segment voltage of the electrocardiogram. EA pretreatment promoted vascular regeneration by increasing serum levels of VEGF and HIF-1α and by increasing protein expression of HIF-1α and VEGF in the infarcted region of the myocardium, leading to a reduction in the area of myocardial infarction on HE staining and reduction of myocardial fibrosis on Masson staining. Conclusion: EA pretreatment promotes protein expression of HIF-1α and VEGF in areas of ischemic myocardium, which may represent useful biomarkers for coronary collateral establishment and offer potential targets for therapeutic angiogenesis in patients with CMI.

Serum Levels of Vascular Endothelial Growth Factor in Patients with Acute Myocardial Infarction Undergoing Reperfusion Therapy

1997 ◽  
Vol 92 (5) ◽  
pp. 453-454 ◽  
Author(s):  
Yoshinori Seko ◽  
Yasushi Imai ◽  
Shin Suzuki ◽  
Shuichi Kamijukkoku ◽  
Kazuya Hayasaki ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Serum Levels ◽  
Reperfusion Therapy ◽  
Vascular Endothelial ◽  
Early Reperfusion ◽  
Healthy Control ◽  
Endothelial Growth Factor

1. Vascular endothelial growth factor, a potent angiogenic mitogen, is known to be induced in response to ischaemia as well as being secreted from tumour cells. However, the precise mechanism of vascular endothelial growth factor release in acute myocardial infarction and the effects of coronary reperfusion on the circulating levels of vascular endothelial growth factor are still unknown. 2. Nineteen patients with acute myocardial infarction who underwent early reperfusion therapy were studied. Serum levels of vascular endothelial growth factor before reperfusion were markedly increased as compared with those in 19 healthy control subjects [252.4 ± 158.1 pg/ml (mean ± SD) compared with undetectable]. After reperfusion, the serum vascular endothelial growth factor levels rapidly returned almost completely to the normal control range. 4. These data strongly suggest that the serum level of vascular endothelial growth factor is one of the most sensitive indicators of myocardial ischaemia.

Serum levels of endostatin, vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in patients with acute myocardial infarction undergoing early reperfusion therapy

2004 ◽  
Vol 106 (5) ◽  
pp. 439-442 ◽  
Author(s):  
Yoshinori SEKO ◽  
Shuichi FUKUDA ◽  
Ryozo NAGAI
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Growth Factor ◽  
Serum Levels ◽  
Reperfusion Therapy ◽  
Vascular Endothelial ◽  
Early Reperfusion ◽  
Ischaemia Reperfusion ◽  
Endothelial Growth Factor ◽  
Hepatocyte Growth

Angiogenesis is controlled by anti-angiogenic factors as well as by angiogenic factors, such as VEGF (vascular endothelial growth factor) and HGF (hepatocyte growth factor). Endostatin, a potent endogenous angiogenesis inhibitor, is known to inhibit endothelial proliferation and suppress tumour growth. However, to date, little is known about the pathophysiology of endostatin in ischaemia/reperfusion. To investigate the mechanisms of angiogenesis induced by myocardial ischaemia/reperfusion in more detail, we studied the circulating levels of endostatin, VEGF and HGF in 17 patients with acute myocardial infarction, who underwent early reperfusion therapy. In all patients, serum endostatin, VEGF and HGF levels before reperfusion were increased significantly compared with those in 17 control subjects (endostatin, 49.2±11.7 ng/ml, but not detectable in controls; VEGF, 685.6±150.3 pg/ml compared with 173.7±33.6 pg/ml; HGF, 3638±1285 pg/ml compared with 59±13 pg/ml; values are means±S.E.M.). After reperfusion, the serum endostatin and VEGF levels decreased significantly, but still remained higher than those in control subjects (endostatin, 19.6±7.0 ng/ml; VEGF, 284.2±90.2 pg/ml). In contrast, serum HGF levels increased significantly (15 146±2230 pg/ml) after reperfusion. These data indicated that serum levels of endostatin changed in parallel with those of VEGF in response to myocardial ischaemia/reperfusion, and the marked increase in serum HGF levels after reperfusion seemed to be, at least in part, due to heparin administration. Our data offer a possible anti-endostatin therapy in patients with acute myocardial infarction to facilitate collateral vessel formation.

scholarly journals Melatonin Reduces Angiogenesis in Serous Papillary Ovarian Carcinoma of Ethanol-Preferring Rats

2017 ◽  
Author(s):  
Luiz Gustavo De Almeida Chuffa ◽  
Yohan Ricci Zonta ◽  
Marcelo Martinez ◽  
Isabel Cristina Cherici Camargo ◽  
Raquel Fantin Domeniconi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Serum Levels ◽  
Ethanol Consumption ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Chemically Induced ◽  
Therapeutic Opportunity ◽  
Endothelial Growth Factor

Angiogenesis is a hallmark of ovarian cancer (OC) it promotes rapid cell growth and the associated metastasis. Identifying new bioactive compounds to target angiogenesis may provide valuable paradigms as therapeutic strategies. Melatonin is a well-characterized indoleamine that possesses important anti-angiogenic properties in a set of aggressive solid tumors. Herein, we evaluated the role of melatonin therapy on the angiogenic signaling pathway in OC of an ethanol-preferring rat model that mimics the same pathophysiological conditions occurring in women. OC was chemically induced with a single injection of 7,12-dimethylbenz(a)anthracene (DMBA) under the ovarian bursa. After the rats developed serous papillary OC, half of the animals received i.p. injections of melatonin (200 µg/100 g body weight/day) for 60 days. Serum levels of melatonin were higher following therapy, and the expression of its receptor MT1R was significantly increased in OC-bearing rats, regardless of ethanol intake. TGFB1, a transforming growth factor-beta1, was reduced only after melatonin treatment. Importantly, vascular endothelial growth factor (VEGF) was severely reduced after melatonin therapy in animals given or not given ethanol. Conversely, the levels of VEGF receptor 1 (VEGFR1) was diminished after ethanol consumption, regardless of melatonin therapy, and VEGFR2 was only reduced following melatonin. Hypoxia-inducible factor (HIF)-1α was augmented with ethanol consumption, and notably, melatonin significantly reduced their levels. Collectively, our results suggest that melatonin attenuates angiogenesis in OC of an animal model of ethanol consumption; this provides a possible complementary therapeutic opportunity for concurrent OC chemotherapy.

scholarly journals Circulating MiRNA-195-5p and -451a in Transient and Acute Ischemic Stroke Patients in an Emergency Department

2019 ◽  
Vol 8 (2) ◽  
pp. 130 ◽  
Author(s):  
Mauro Giordano ◽  
Tiziana Ciarambino ◽  
Michele D’Amico ◽  
Maria Trotta ◽  
Alessandra Di Sette ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Serum Level ◽  
Acute Ischemic Stroke ◽  
Hypoxia Inducible Factor ◽  
Serum Levels ◽  
Vascular Endothelial ◽  
Circulating Mirna ◽  
Elevated Expression ◽  
Ischemic Attack ◽  
Endothelial Growth Factor

We have evaluated circulating miRNAs (-195-5p and -451a) in subjects with acute ischemic stroke (AIS) and in patients with transient ischemic attack (TIA). In this study, 18 subjects with AIS and 18 patients with TIA were enrolled and examined at admission (T0) and at 24 h and 48 h after admission, and compared to 20 controls (C). At T0, circulating miRNA-195-5p and -451a were significantly upregulated in both AIS and TIA patients, compared to C. We also observed a progressive reduction of circulating miRNA levels at 24 h and 48 h in both AIS and TIA patients. Hypoxia inducible factor 1alpha (HIF-1α) serum level was significantly increased at T0, in both AIS and TIA patients, in comparison to C (both p < 0.01 vs. C) and it decreased in both AIS and TIA patients at 24 h and at 48 h, in comparison to T0 (both p < 0.01 vs. T0). Vascular endothelial growth factor (VEGF) serum level was significantly decreased at T0, in both AIS and TIA patients, if compared to C (both p < 0.01 vs. C) and increased, in both AIS and TIA patients, at 24 h and 48 h, if compared to T0 (both p < 0.01 vs. T0). The elevated expression of miRNA-195-5p and miRNA-451a significantly decreased over time at 24 h and 48 h, and it is associated with decreased HIF-α levels and increased VEGF serum levels. These data may suggest a role for this miRNAs as biomarker in the pathogenesis and prognosis of AIS patients and for the first time also in TIA patients.

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