Heparin Cofactor II, a Serine Protease Inhibitor, Promotes Angiogenesis via Activation of the AMP-activated Protein Kinase-Endothelial Nitric-oxide Synthase Signaling Pathway

Ikeda, Yasumasa; Aihara, Ken‐ichi; Yoshida, Sumiko; Igarashi, Takashi; Tajima, Soichiro; Izawa‐Ishizawa, Yuki; Kihira, Yoshitaka; Ishizawa, Keisuke; Tomita, Shuhei; Tsuchiya, Koichiro; Sata, Masataka; Akiyama, Masashi; Kato, Shigeaki; Matsumoto, Toshio; Takahashi, Toshiaki

doi:10.1074/jbc.m112.353532

Cited by 31 publications

(33 citation statements)

References 45 publications

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“…The cellular effects which are mediated by protease‐activated receptors include tube formation, migration and proliferation of endothelial cells. Hence, HCII is required for maintenance of angiogenesis . No significant differences were detected between MS and HI or in relation to DMTs and MRI outcomes.…”

Section: Discussionmentioning

confidence: 87%

Hemostasis biomarkers in multiple sclerosis

Ziliotto

Bernardi

Jakimovski

et al. 2018

Euro J of Neurology

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Section: Discussionmentioning

confidence: 87%

Hemostasis biomarkers in multiple sclerosis

Ziliotto

Bernardi

Jakimovski

et al. 2018

Euro J of Neurology

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“…The principal AMPK catalytic subunit isoform contributing to AMPK activity in endothelial cells is the α 1 isoform . Previous studies have shown that AMPK induces phosphorylation of eNOS at serine‐1177 and activates NO generation in endothelial cells . A recent study also found that high concentrations of AMPK agonist also dilate resistance arteries through activation of SERCA and BKCa channels in smooth muscle .…”

Section: Discussionmentioning

confidence: 99%

Irisin Lowers Blood Pressure by Improvement of Endothelial Dysfunction via AMPK‐Akt‐eNOS‐NO Pathway in the Spontaneously Hypertensive Rat

Han

Wang

et al. 2016

JAHA

117

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BackgroundExercise is a major nonpharmacological treatment for hypertension, but its underlying mechanisms are still not completely elucidated. Irisin, a polypeptide containing 112 amino acids, which is secreted mainly by skeletal muscle cells during exercise, exerts a protective role in metabolic diseases, such as diabetes mellitus and obesity. Because of the close relationship between irisin and metabolic diseases, we hypothesized that irisin may play a role in the regulation of blood pressure.Methods and ResultsBlood pressures of male Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs) were monitored through the carotid artery. Our study found that acute intravenous injection of irisin reduced blood pressure in SHRs, but not WKY rats. Irisin, by itself, had no direct vasorelaxing effect in phenylephrine‐preconstricted mesenteric arteries from SHRs. However, irisin augmented the acetylcholine‐induced vasorelaxation in mesenteric arteries from SHRs that could be reversed by Nω‐nitro‐l‐arginine‐methyl ester (L‐NAME; 100 μmol/L), indicating a role of nitric oxide (NO) in this action. Indeed, irisin increased NO production and phosphorylation of endothelial nirtic oxide synthase (eNOS) in endothelial cells. 5′‐AMP‐activated protein kinase (AMPK) was involved in the vasorelaxing effect of irisin because compound C (20 μmol/L), an AMPK inhibitor, blocked the irisin‐mediated increase in phosphorylation of eNOS and protein kinase B (Akt) in endothelial cells and vasodilation in mesenteric arteries.ConclusionsWe conclude that acute administration of irisin lowers blood pressure of SHRs by amelioration of endothelial dysfunction of the mesenteric artery through the AMPK‐Akt‐eNOS‐NO signaling pathway.

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“…The top 50 upregulated and downregulated genes are depicted in a heatmap ( Figure 3B; blue: antitumorigenic genes are indicated by arrows, and antiangiogenic genes are indicated by arrowheads; pink: tumorigenic genes are indicated by arrows, and angiogenic genes are indicated by arrowheads) and are presented in full detail in Supplemental hi TECs characterized by a Th1-TME. Among the most strongly downregulated genes, tumorigenic genes such as LAMC2 (31), leupaxin (32), or ADAM12 (33), and angiogenic genes, such as SERPIND1 (34), HEY2 (35), or EDIL3 (36) were detected. Accordingly, gene expression in the TECs within the GBP-1 hi group reflected the intertumoral activity (angiostatic and antitumorigenic) associated with the Th1-TME in CRC.…”

Section: Pure Tumor Ecs Can Be Isolated From Crcs With Different Progmentioning

confidence: 99%

Matricellular protein SPARCL1 regulates tumor microenvironment–dependent endothelial cell heterogeneity in colorectal carcinoma

Naschberger¹,

Liebl²,

Schellerer³

et al. 2016

Journal of Clinical Investigation

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Heparin Cofactor II, a Serine Protease Inhibitor, Promotes Angiogenesis via Activation of the AMP-activated Protein Kinase-Endothelial Nitric-oxide Synthase Signaling Pathway

Cited by 31 publications

References 45 publications

Hemostasis biomarkers in multiple sclerosis

Hemostasis biomarkers in multiple sclerosis

Irisin Lowers Blood Pressure by Improvement of Endothelial Dysfunction via AMPK‐Akt‐eNOS‐NO Pathway in the Spontaneously Hypertensive Rat

Matricellular protein SPARCL1 regulates tumor microenvironment–dependent endothelial cell heterogeneity in colorectal carcinoma

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