Expression of vascular endothelial growth factor in patients with acute myocardial infarction

Hojo, Yukihiro; Ikeda, Uichi; Zhu, Yun; Okada, Motoi; Ueno, Shu‐ichi; Arakawa, Hiroshi; Fujikawa, Hideyuki; Katsuki, Takaaki; Shimada, Kazuyuki

doi:10.1016/s0735-1097(99)00632-4

Cited by 147 publications

(109 citation statements)

References 27 publications

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“…In vitro experimental studies have shown that VEGF, Ang-2, and Tie-2 but not Ang-1 expression is upregulated in ischemic myocardium, 3,5 whereas clinical studies in patients with ACS (AMI patients) have shown increased peripheral blood VEGF. [7][8][9][10][11] The present study shows that in addition to raised VEGF and Tie-2 levels, Ang-2 levels were also raised in ACS patients within 24 hours of presentation, although Ang-1 levels were not different compared with those of healthy control subjects and SA patients. Patients with evidence of myocardial damage (ie, AMI) had the highest levels of Ang-2, VEGF, and Tie-2 compared with other groups.…”

Section: Discussionmentioning

confidence: 43%

“…11 Two studies have shown significant correlations between VEGF and peak CK levels, 7,9 suggesting that the extent of myocardial damage may be linked to elevated circulating VEGF levels. We confirm this aspect in the present study, adding the novel finding that Tie-2 and Ang-2 are also significantly correlated with peak total CK levels in patients with AMI.…”

Section: Discussionmentioning

confidence: 99%

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Plasma Angiopoietin-1, Angiopoietin-2, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor Levels in Acute Coronary Syndromes

2004

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Background— Angiopoietin (Ang) -1 and -2, their receptor Tie-2, and vascular endothelial growth factor (VEGF) regulate angiogenesis and may be important in myocardial collateral development. Elevated levels of growth factors and their receptors are reported in myocardial infarction (MI), but changes after an acute coronary event are unknown. Methods and Results— Plasma Ang-1, Ang-2, Tie-2, and VEGF levels were measured on admission (baseline) and at 48 hours (acute stage) in 126 patients with acute coronary syndrome (82 MI, 44 unstable angina pectoris). Baseline levels were compared with those of 40 patients with stable angina and 40 healthy controls. Measurements were repeated in 38 MI patients at 6 and 18 weeks (chronic stage). Baseline Ang-2 and Tie-2 levels were highest in MI patients ( P <0.001). Patients with MI and unstable angina pectoris had higher VEGF levels compared with stable angina patients and healthy control subjects ( P <0.001). In patients with acute MI, serial changes in all indexes from baseline to 18 weeks were observed (all P <0.001). Ang-1 levels were unchanged from baseline to 6 weeks but were elevated at 18 weeks. Ang-2 changes followed a biphasic pattern, being higher at baseline and 6 weeks but lower at 48 hours and 18 weeks. Tie-2 levels increased from baseline and remained elevated in the chronic phase. VEGF peaked at 6 weeks and then decreased toward baseline at 18 weeks. Conclusions— Plasma Ang-2, Tie-2, and VEGF levels but not Ang-1 levels were increased in patients with acute coronary syndrome. Serial changes in the plasma levels and interrelationships among Ang-1, Ang-2, Tie-2, and VEGF levels from the acute to the chronic stages in MI may reflect the progressive stages of angiogenesis activity in the ischemic-necrotic myocardium in vivo.

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Section: Discussionmentioning

confidence: 43%

Section: Discussionmentioning

confidence: 99%

Plasma Angiopoietin-1, Angiopoietin-2, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor Levels in Acute Coronary Syndromes

2004

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“…MNCs and ECs have been shown to produce and release VEGF, a potent angiogenic cytokine (Hojo et al, 2000;Namiki et al, 1995). In the present study, A, Exogenous addition of rhVEGF (10 ng/mL) significantly enhanced the differentiation of PB-MNCs into EPC-like AT cells.…”

Section: Discussionmentioning

confidence: 52%

“…Human MNCs produce and secrete VEGF protein (Hojo et al, 2000), which could modulate the differentiation of PB-MNCs into EPCs through an autocrine mechanism (Risau, 1995). We examined the role of VEGF released from PB-MNCs on the differentiation of PB-MNCs into EPCs.…”

Section: Role Of Autocrine Vegf In Epc Differentiationmentioning

confidence: 99%

Hypoxic Preconditioning Augments Efficacy of Human Endothelial Progenitor Cells for Therapeutic Neovascularization

Akita

Murohara

Ikeda

et al. 2003

Laboratory Investigation

121

100

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SUMMARY:A subset of human peripheral blood mononuclear cells (PB-MNCs) differentiate into endothelial progenitor cells (EPCs) that participate in postnatal neovascularization. Although tissue ischemia can mobilize EPCs from bone marrow, the effects of hypoxia on differentiation and angiogenic function of EPCs are little known. We examined whether hypoxic conditioning would modulate differentiation and function of human PB-MNC-derived EPCs. A subset of PB-MNCs gave rise to EPC-like attaching (AT) cells under either normoxic or hypoxic conditions. However, hypoxia much enhanced the differentiation of AT cells from PB-MNCs compared with normoxia. AT cells released vascular endothelial growth factor (VEGF) protein and expressed CD31 and kinase insert domain receptor/VEGFR-2, endothelial lineage markers, on their surface, which were also enhanced by hypoxia. Both a neutralizing anti-VEGF mAb and a KDR-specific receptor tyrosine kinase inhibitor, SU1498, suppressed PB-MNC differentiation into EPC-like AT cells in a dose-dependent manner. Migration of AT cells in response to VEGF as examined by a modified Boyden chamber apparatus was also enhanced by hypoxia. Finally, in vivo neovascularization efficacy was significantly enhanced by in vitro hypoxic conditioning of AT cells when cells were transplanted into the ischemic hindlimb of immunodeficient nude rats. In conclusion, hypoxia directly stimulated differentiation of EPC-like AT cells from human PB-MNC culture. Moreover, hypoxic preconditioning of AT cells before in vivo transplantation is a useful means to enhance therapeutic vasculogenesis. (Lab Invest 2003, 83:65-73).

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“…VEGFhas been shown to be an important factor in the pathogenesis of vascularrelated diseases, including the growth of tumors, vascular dysfunction in diabetes mellitus, and atherosclerosis of the coronary arteries (13,27,28). The increased VEGFproduction found in OSASpatients might contribute to new vessel formation in ischemic and atherosclerotic vascular regions.…”

Section: Discussionmentioning

confidence: 99%

Effects of Oxygen Administration on the Circulating Vascular Endothelial Growth Factor (VEGF) Levels in Patients with Obstructive Sleep Apnea Syndrome

et al. 2003

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Expression of vascular endothelial growth factor in patients with acute myocardial infarction

Abstract: The extent of myocardial damage contributes to the elevation of serum VEGF levels in AMI. VEGF produced by PBMCs may play an important role in the improvement of left ventricular function by promoting angiogenesis and reendothelialization after AMI.

Cited by 147 publications

References 27 publications

Plasma Angiopoietin-1, Angiopoietin-2, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor Levels in Acute Coronary Syndromes

Plasma Angiopoietin-1, Angiopoietin-2, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor Levels in Acute Coronary Syndromes

Hypoxic Preconditioning Augments Efficacy of Human Endothelial Progenitor Cells for Therapeutic Neovascularization

Effects of Oxygen Administration on the Circulating Vascular Endothelial Growth Factor (VEGF) Levels in Patients with Obstructive Sleep Apnea Syndrome

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