The effects of acute and intermittent hypoxia on the expressions of HIF-1α and VEGF in the left and right ventricles of the rabbit heart

Tekin, Demet; Dursun, Ali Doğan; Baştuğ, Metin; Karaorman, Gökhan; Ficicilar, Hakan

doi:10.5152/akd.2011.104

Cited by 8 publications

(6 citation statements)

References 25 publications

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“…On the other hand, intermittent hypoxia did not affect VEGF expression in the left ventricle in the present study. Recently, we have shown that both acute and intermittent normobaric hypoxia increased the VEGF mRNA expression in the left ventricle in rabbits ( 15 ). The duration and intensity of exposed hypoxia as well as the animal species were different in the two studies.…”

Section: Discussionmentioning

confidence: 99%

“…HIF-1alpha mRNA is also up-regulated in patients with acute ischemia or early infarction, followed by VEGF increase in patients with infarction ( 14 ). Furthermore, acute and intermittent hypoxia has been shown to increase cardiac HIF-1 and VEGF levels in animal experiments ( 15 - 17 ). On the other hand, in patients with diabetes, VEGF is decreased and angiogenesis is impaired by hyperglycemia.…”

Section: Introductionmentioning

confidence: 99%

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Effect of intermittent hypoxia on the cardiac HIF-1/VEGF pathway in experimental type 1 diabetes mellitus

Güzel¹,

Dursun²,

Ficicilar³

et al. 2015

Anatol J Cardiol

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Objective:High altitude and hypoxic preconditioning have cardioprotective effects by increasing coronary vascularity, reducing post-ischemic injury, and improving cardiac function. Our purpose was to examine if intermittent hypoxia treatment has any restoring effects related to the possible role of the HIF-1/VEGF pathway on diabetic cardiomyopathy.Methods:Wistar Albino male rats (n=34) were divided into four groups: control (C), intermittent hypoxia (IH), diabetes mellitus (DM), and diabetes mellitus plus intermittent hypoxia (DM+IH). Following a streptozotocin (STZ) injection (50 mg/kg, i.p.), blood glucose levels of 250 mg/dL and above were considered as DM. IH and DM+IH groups were exposed to hypoxia 6 h/day for 42 days at a pressure corresponding to 3000 m altitude. Twenty-four hours after the IH protocol, hearts were excised. Hematoxylin and eosin-stained apical parts of the left ventricles were evaluated. Hypoxia inducible factor-1 (HIF-1), vascular endothelial growth factor 164 (VEGF164), and VEGF188 polymerase chain reaction products were run in agarose gel electrophoresis. Band density analysis of UV camera images was performed using Image J. The data were compared by one-way ANOVA, repeated measures two-way ANOVA, and the Kruskal-Wallis test.Results:The percent weight change was lower in the DM group than in the controls (p=0.004). The tissue injury was the highest in the DM group and the least in the IH group. Diabetes decreased, whereas the IH treatment increased the vascularity. A decrease was observed in the VEGF188 mRNA levels in the DM+IH group compared with the C group, but there were no difference in HIF-1α and VEGF164 mRNA levels between the groups.Conclusion:The IH treatment restored the diabetic effects on the heart by reducing tissue injury and increasing the capillarity without transcriptional changes in HIF-1/VEGF correspondingly.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of intermittent hypoxia on the cardiac HIF-1/VEGF pathway in experimental type 1 diabetes mellitus

Güzel¹,

Dursun²,

Ficicilar³

et al. 2015

Anatol J Cardiol

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“…Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that functions as the master regulator of gene expression in response to hypoxia. HIF-1α may function to regulate cell death or cell survival via downstream proteins such as heme oxygenase-1, inducible nitric oxide synthase, cyclooxygenase-2 and vascular endothelial growth factor [5,[11][12][13][14][15][16], the Bcl-2 family member Bcl-2/adenovirus E1B 19-kDa protein interacting protein 3 (BNIP3), and insulin growth factor binding protein 3 (IGFBP3) [13,[17][18][19]. This study identified HIF-1α as a key regulator of BNIP3 and IGFBP3 in cardiomyocytes.…”

Section: Introductionmentioning

confidence: 97%

Tetramethylpyrazine Ameliorated Hypoxia-Induced Myocardial Cell Apoptosis via HIF-1α/JNK/p38 and IGFBP3/BNIP3 Inhibition to Upregulate PI3K/Akt Survival Signaling

Lin

Kuo²,

Jiang

et al. 2015

Cell Physiol Biochem

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Background: Hemorrhagic shock (HS) is the major cause of death from trauma. Hemorrhagic shock may lead to cellular hypoxia and organ damage. Our previous findings showed that HS induced a cardiac apoptosis pathway and synergistically caused myocardial cell damage in diabetic rats under trauma-induced HS. Tetramethylpyrazine (TMP) is a major biologically active ingredient purified from the rhizome of Ligusticum wallichii (called Chuang Xiong in Chinese). Chuan Xiong rescued cells from synergistic cardiomyoblast cell injury under high-glucose (HG) conditions plus hypoxia. TMP is one of the most important active ingredients that elevated the survival rate in ischemic brain injury and prevented inducible NO synthase expression to have anti-inflammatory effects against cell damage in different cell types. Method: Here, we further investigate whether TMP can protect against hypoxic (<1% oxygen) conditions in H9c2 cardiomyoblast cells for 24 hrs. Results: Our results showed that hypoxia mediated through HIF-1α/JNK/p38 activation significantly elevated the levels of the hypoxia-related proteins HIF-1α, BNIP3 and IGFBP3, further enhanced the pro-apoptotic protein Bak and upregulated downstream Caspase 9 and 3, resulting in cell death. All of these phenomena were fully recovered under TMP treatment. We observed that TMP exerted this effect by activating the IGF1 receptor survival pathway, dependent primarily on PI3K/Akt. When PI3K (class I) was blocked by specific siRNA, the hypoxia-induced activated caspase 3 and cell apoptosis could not be reversed by TMP treatment. Conclusion: Our results strongly suggest that TMP could be used to restore hypoxia-induced myocardial cell apoptosis and cardiac hypoxic damage.

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“…In physiological conditions, HIF-1α expression is significantly higher in the right than in the left ventricle (114). RV HIF-1α expression is increased in a number of animal models of PH, including MCT rats (115), hypoxia-exposed (HOX) rats (116), pulmonary artery-banded (PAB) rats (117), SuHx rats (117), and pulmonary embolism (PE) rats (118).…”

Section: Therapeutic Potential Of Hif Targeting In Phmentioning

confidence: 99%

Hypoxia-inducible factor signaling in pulmonary hypertension

Pullamsetti

Mamazhakypov

Weißmann

et al. 2020

Journal of Clinical Investigation

147

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The effects of acute and intermittent hypoxia on the expressions of HIF-1α and VEGF in the left and right ventricles of the rabbit heart

Cited by 8 publications

References 25 publications

Effect of intermittent hypoxia on the cardiac HIF-1/VEGF pathway in experimental type 1 diabetes mellitus

Effect of intermittent hypoxia on the cardiac HIF-1/VEGF pathway in experimental type 1 diabetes mellitus

Tetramethylpyrazine Ameliorated Hypoxia-Induced Myocardial Cell Apoptosis via HIF-1α/JNK/p38 and IGFBP3/BNIP3 Inhibition to Upregulate PI3K/Akt Survival Signaling

Hypoxia-inducible factor signaling in pulmonary hypertension

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