Enzymatic Measurement of Tryptase-Like Protease Release from Isolated Perfused Guinea Pig Heart during Ischemia-Reperfusion

Matsui, Nobuaki; Okikawa, Tomoko; Imajo, Naoki; Yasui, Yumiko; Fukuishi, Nobuyuki; Akagi, Masaaki

doi:10.1248/bpb.28.2149

Cited by 6 publications

(3 citation statements)

References 9 publications

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“…After primary PCI, tryptase levels quickly decreased. This is concordant with a previous study in the isolated perfused guinea pig heart, which showed that tryptase was released into the coronary effluent during ischemia, but not during reperfusion (Matsui et al, 2005).…”

Section: Discussionsupporting

confidence: 93%

“…Mast cell degranulation is an early event in ischemia/ reperfusion (I/R) injury. Tryptase and histamine were rapidly released from heart during ischemia within 10 min (Matsui et al, 2005). In the study by Filipiak et al, persistent tryptase elevation has been detected in patients with nonallergic acute coronary syndromes, both in the acute phase and at follow-up.…”

Section: Discussionmentioning

confidence: 98%

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Dynamic changes and clinical significance of serum tryptase levels in STEMI patients treated with primary PCI

Chen

Cui

et al. 2014

Biomarkers

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Dynamic changes and clinical significance of serum tryptase levels in STEMI patients treated with primary PCI

Chen

Cui

et al. 2014

Biomarkers

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“…Several of the known stimulators of PAR-2 are upregulated or increased by ischemia-reperfusion, including cytokines (TNF-␣) (29,30) and tissue factor (11,12,20,22). In addition, PAR-2 may be activated by endogenous proteases, most likely mast cell tryptase released in the AAR myocardium, thereby exerting local cardioprotection (27).…”

Section: Discussionmentioning

confidence: 99%

PAR-2 activation at the time of reperfusion salvages myocardium via an ERK1/2 pathway in in vivo rat hearts

Jiang

Zatta

Kin

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Protease-activated receptor-2 (PAR-2) may have proinflammatory effects in some tissues and protective effects in other tissues. The role of PAR-2 in in vivo myocardial ischemia-reperfusion has not yet been determined. This study tested the hypothesis that PAR-2 activation with the PAR-2 agonist peptide SLIGRL (PAR-2 AP) reduces myocardial infarct size when given at reperfusion in vivo, and this cardioprotection involves the ERK1/2 pathway. Anesthetized rats were randomly assigned to the following groups with 30 min of regional ischemia and 3 h reperfusion: 1) control with saline; 2) vehicle (DMSO); 3) PAR-2 AP, 1 mg/kg given intravenously 5 min before reperfusion; 4) scrambled peptide (SP), 1 mg/kg; 5) the ERK1/2 inhibitor PD-98059 (PD), 0.3 mg/kg given 10 min before reperfusion; 6) the phosphatidylinositol 3-kinase inhibitor LY-294002 (LY), 0.3 mg/kg given 10 min before reperfusion; 7) PD + PAR-2 AP, 0.3 mg/kg PD given 5 min before PAR-2 AP; 8) LY + PAR-2 AP, 0.3 mg/kg LY given 5 min before PAR-2 AP; 9) chelerythrine (Chel) alone, 5 mg/kg given 10 min before reperfusion; and 10) Chel + PAR-2 AP, Chel was given 5 min before PAR-2 AP (10 min before reperfusion). Activation of ERK1/2, ERK5, Akt, and the downstream targets of ERK1/2 [P90 RSK and bcl-xl/bcl-2-associated death promoter (BAD)] was determined by Western blot analysis in separate experiments. PAR-2 AP significantly reduced infarct size compared with control (36 +/- 2% vs. 53 +/- 1%, P< 0.05), and SP had no effect on infarct size (53 +/- 3%). PAR-2 AP significantly increased phosphorylation of ERK1/2, p90RSK, and BAD but not Akt or ERK5. Accordingly, the infarct-size sparing effect of PAR-2 AP was abolished by PD (PAR-2 AP, 36 +/- 2% vs. PD + PAR-2 AP, 50 +/- 1%; P < 0.05) and by Chel (Chel + PAR-2 AP, 58 +/- 2%) but not by LY (PAR-2 AP, 36 +/- 2% vs. LY + PAR-2 AP, 38 +/- 3%; P > 0.05). Therefore, PAR-2 activation is cardioprotective in the in vivo rat heart ischemia-reperfusion model, and this protection involves the ERK1/2 pathway and PKC.

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Cardio- and Vasoprotective Effects of Quinacrine in an In Vivo Rat Model of Myocardial Ischemia/Reperfusion Injury

Sonin,

Pochkaeva,

Papayan

et al. 2024

Bull Exp Biol Med

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Enzymatic Measurement of Tryptase-Like Protease Release from Isolated Perfused Guinea Pig Heart during Ischemia-Reperfusion

Cited by 6 publications

References 9 publications

Dynamic changes and clinical significance of serum tryptase levels in STEMI patients treated with primary PCI

Dynamic changes and clinical significance of serum tryptase levels in STEMI patients treated with primary PCI

PAR-2 activation at the time of reperfusion salvages myocardium via an ERK1/2 pathway in in vivo rat hearts

Cardio- and Vasoprotective Effects of Quinacrine in an In Vivo Rat Model of Myocardial Ischemia/Reperfusion Injury

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