Angiotensin II-induced process of angiogenesis is mediated by spleen tyrosine kinase via VEGF receptor-1 phosphorylation

Buharalioğlu, C. Kemal; Song, Chi Young; Yaghini, Fariborz A.; Ghafoor, Hafiz U; Motiwala, Mustafa; Adris, Tusita; Estes, Anne M.; Malik, Kafait U.

doi:10.1152/ajpheart.01018.2010

Cited by 39 publications

(32 citation statements)

References 38 publications

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“…This is consistent with that shown in other vascular beds (Kou et al, 2007;Buharalioglu et al, 2011).…”

Section: Discussionsupporting

confidence: 93%

“…The proangiogenic effect of AngII has been reported previously (Hu et al, 2007;Buharalioglu et al, 2011). In hCMECs, there was a significantly increased rate of tube formation in response to AngII 1 ƒM treatment (Fig.…”

Section: Candesartan Has a Proangiogenic Effect In Hcmecssupporting

confidence: 80%

“…et al, 2011) or coronary artery endothelial cells (Fujiyama et al, 2001;Hu et al, 2007), and none of them evaluated the effect of AngII or AngII and ARBs in hCMECs, which are phenotypically different from other endothelial cells (Feletou, 2011). In addition, the majority of the studies focused on the involvement of VEGF (Buharalioglu et al, 2011), angiopoietins (Herr et al, 2008), and EGFR transactivation (Fujiyama et al, 2001) in the angiogenic response to AngII. This ignores the possible role of other angiogenic mediators, such as BDNF, which has been shown to induce VEGF expression (Caporali and Emanueli, 2009) and produce an angiogenic response comparable to that of VEGF in endothelial cells (Li et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Similar to its proliferative effect, AngII has been reported to affect the migration of cells in vitro (Buharalioglu et al, 2011). Because we have found a proliferative effect of candesartan on AngII-treated hCMECs, we were interested in assessing the effect of this dose of candesartan on two critical steps of angiogenesis: migration and tube formation in AngII-treated hCMECs.…”

Section: Candesartan Modulates the Migration Rate Of Hcmecsmentioning

confidence: 97%

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AT1 Receptor Antagonism Is Proangiogenic in the Brain: BDNF a Novel Mediator

Alhusban

Kozák

Ergul

et al. 2012

J Pharmacol Exp Ther

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Candesartan is an angiotensin II type 1 receptor blocker (ARB) that has been to shown to limit ischemic stroke and improve stroke outcome. In experimental stroke, candesartan induces a proangiogenic effect that is partly attributable to vascular endothelial growth factor. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family that has been reported to have angiogenic effects and play an important role in recovery after stroke. The purpose of this investigation was to determine the role of BDNF in the proangiogenic effect of candesartan in the brain under hypertensive conditions. Accordingly, spontaneously hypertensive rats were treated with candesartan, and brain tissue samples were collected for quantification of BDNF expression. In addition, human cerebromicrovascular endothelial cells were treated with either low-dose (1 ƒM) or high-dose (1 mM) angiotensin II alone or in combination with candesartan (0.16 mM) to assess the effect of candesartan treatment and BDNF involvement in the behavior of endothelial cells. Candesartan significantly increased the expression of BDNF in the SHR (P , 0.05). In addition, candesartan reversed the antiangiogenic effect of the 1-mM dose of AngII (P 5 0.0001). The observed effects of candesartan were ablated by neutralizing the effects of BDNF. Treatment with the AT2 antagonist PD-123319 significantly reduced tube-like formation in endothelial cells. AT2 stimulation induced the BDNF expression and migration (P , 0.05). In conclusion, candesartan exerts a proangiogenic effect on brain microvascular endothelial cells treated with angiotensin II. This response is attributable to increased BDNF expression and is mediated through stimulation of the AT2 receptor.

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“…This is consistent with that shown in other vascular beds (Kou et al, 2007;Buharalioglu et al, 2011).…”

Section: Discussionsupporting

confidence: 93%

Section: Candesartan Has a Proangiogenic Effect In Hcmecssupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Candesartan Modulates the Migration Rate Of Hcmecsmentioning

confidence: 97%

See 2 more Smart Citations

AT1 Receptor Antagonism Is Proangiogenic in the Brain: BDNF a Novel Mediator

Alhusban

Kozák

Ergul

et al. 2012

J Pharmacol Exp Ther

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“…Aortic DDAH-1 expression decreased in line with VEGF-A and eNOS suppression, but DDAH-2 expression was even more enhanced in the BAY-treated group. Although the role of Syk in angiotensin II-induced VEGF-mediated vasculogenesis has been established, 47 there is still inadequate evidence to speculate about the effect of Syk on DDAH-1 and DDAH-2 in the pathogenesis of LCWE-induced CALs. DDAH-2 might exert some additional effects to overcome LCWE-induced in-VEGF-A and DDAH-1 upregulation was significantly suppressed by Syk inhibition (Figure 7C).…”

mentioning

confidence: 99%

Vascular Endothelial Growth Factor-A in <i>Lactobacillus Casei </i>Cell Wall Extract-Induced Coronary Arteritis of a Murine Model

Lin

Sheen

Tain

et al. 2014

Circ J

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Exosomes secreted by hypoxic cardiosphere‐derived cells enhance tube formation and increase pro‐angiogenic miRNA

Namazi¹,

Mohit²,

Namazi

et al. 2018

J of Cellular Biochemistry

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Exosomes are required for the regenerative effects of human cardiosphere-derived cells (CDCs). Studies show that they mimic the cardioprotective benefits of CDCs in rodents and porcine myocardial infarction (MI) models. Hypoxic preconditioning of stem cells increases the cardioprotective effects of exosomes in MI models by enhancing angiogenesis. Several exosomal microRNAs (miRNAs) up-regulate in response to hypoxia and play a role in cardioprotective and pro-angiogenic effects. In this study, we have demonstrated that human CDCs secreted exosomes under hypoxic conditions (1% O for 2 days) enhanced tube formation by human umbilical vein endothelial cells (HUVECs) at a concentration of 25 µg/mL. Pro-angiogenic exosomal miRNAs including miR-126, miR-130a, and miR-210 showed a substantial increase (>2-, >2-, and >4-fold, respectively) in the hypoxic exosomes compared to normoxic CDC-derived exosomes. Our study suggested a significant benefit of hypoxic CDC exosomes for the treatment of cardiac diseases by induction of angiogenesis via enrichment of pro-angiogenic exosomal miRNAs.

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Angiotensin II-induced process of angiogenesis is mediated by spleen tyrosine kinase via VEGF receptor-1 phosphorylation

Abstract: Buharalioglu CK, Song CY, Yaghini FA, Ghafoor HU, Motiwala M, Adris T, Estes AM, Malik KU. Angiotensin II-induced process of angiogenesis is mediated by spleen tyrosine kinase via VEGF receptor-1 phosphorylation.

Cited by 39 publications

References 38 publications

AT1 Receptor Antagonism Is Proangiogenic in the Brain: BDNF a Novel Mediator

AT1 Receptor Antagonism Is Proangiogenic in the Brain: BDNF a Novel Mediator

Vascular Endothelial Growth Factor-A in <i>Lactobacillus Casei </i>Cell Wall Extract-Induced Coronary Arteritis of a Murine Model

Exosomes secreted by hypoxic cardiosphere‐derived cells enhance tube formation and increase pro‐angiogenic miRNA

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