Effects of thromboxane analog U46619 on endothelial damaged canine coronary arteries in vivo

Bové, Alfred A.; Safford, Robert E.; Brum, José M.; Sufan, Qian; Dewey, Jerry

doi:10.1016/0090-6980(86)90189-9

Cited by 8 publications

(4 citation statements)

References 38 publications

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“…The compounds were then added to each at 10 X the desired concentration (30 μL, n = 3 rings for 8 concentrations of each compound). The compounds in this study included (all purchased from Sigma-Aldrich, St. Louis, MO): vasodilators blebbistatin 30 , forskolin 35 , and verapamil; 36 and vasoconstrictors norepinephrine 31 , phenylephrine 37 , and U46619 38 . Blebbistatin, verapamil, and U46619 were dissolved in 1% dimethylsulfoxide (DMSO), while forskolin, norepinephrine, and phenylephrine were dissolved in phosphate buffered saline (PBS).…”

Section: Methodsmentioning

confidence: 99%

A high-throughput in vitro ring assay for vasoactivity using magnetic 3D bioprinting

Tseng

Gage

Haisler

et al. 2016

Sci Rep

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Vasoactive liabilities are typically assayed using wire myography, which is limited by its high cost and low throughput. To meet the demand for higher throughput in vitro alternatives, this study introduces a magnetic 3D bioprinting-based vasoactivity assay. The principle behind this assay is the magnetic printing of vascular smooth muscle cells into 3D rings that functionally represent blood vessel segments, whose contraction can be altered by vasodilators and vasoconstrictors. A cost-effective imaging modality employing a mobile device is used to capture contraction with high throughput. The goal of this study was to validate ring contraction as a measure of vasoactivity, using a small panel of known vasoactive drugs. In vitro responses of the rings matched outcomes predicted by in vivo pharmacology, and were supported by immunohistochemistry. Altogether, this ring assay robustly models vasoactivity, which could meet the need for higher throughput in vitro alternatives.

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Section: Methodsmentioning

confidence: 99%

A high-throughput in vitro ring assay for vasoactivity using magnetic 3D bioprinting

Tseng

Gage

Haisler

et al. 2016

Sci Rep

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“…In smooth muscle cells, TXA 2 promotes proliferation and migration contributing to neointima formation (11). TXA 2 is the most potent vasoconstrictor known, producing substantial narrowing of coronary arteries and resistance vessels and mediating cyclic coronary fl ow variations in experimental models of myocardial infarction and unstable angina (11)(12)(13). Indeed, thromboxane A 2 receptor (TP) blockers and TXA 2 synthase (TXA 2 S) inhibitors attenuate the eff ect of and the damage caused by ischemic injury and infl ammation in several organs, including heart (11).…”

mentioning

confidence: 99%

“…Indeed, thromboxane A 2 receptor (TP) blockers and TXA 2 synthase (TXA 2 S) inhibitors attenuate the eff ect of and the damage caused by ischemic injury and infl ammation in several organs, including heart (11). TP expression and plasma levels of TP ligands are elevated, both locally and systemically, in several vascular and thrombotic diseases, including unstable angina, myocardial infarction, and various vasculopathies (11,12,14).…”

mentioning

confidence: 99%

Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection

Ashton

Mukherjee

Nagajyothi

et al. 2007

The Journal of Experimental Medicine

125

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Chagas' disease is caused by infection with the parasite Trypanosoma cruzi. We report that infected, but not uninfected, human endothelial cells (ECs) released thromboxane A2 (TXA2). Physical chromatography and liquid chromatography-tandem mass spectrometry revealed that TXA2 is the predominant eicosanoid present in all life stages of T. cruzi. Parasite-derived TXA2 accounts for up to 90% of the circulating levels of TXA2 in infected wild-type mice, and perturbs host physiology. Mice in which the gene for the TXA2 receptor (TP) has been deleted, exhibited higher mortality and more severe cardiac pathology and parasitism (fourfold) than WT mice after infection. Conversely, deletion of the TXA2 synthase gene had no effect on survival or disease severity. TP expression on somatic cells, but not cells involved in either acquired or innate immunity, was the primary determinant of disease progression. The higher intracellular parasitism observed in TP-null ECs was ablated upon restoration of TP expression. We conclude that the host response to parasite-derived TXA2 in T. cruzi infection is possibly an important determinant of mortality and parasitism. A deeper understanding of the role of TXA2 may result in novel therapeutic targets for a disease with limited treatment options.

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“…TXA 2 is the most potent vasoconstrictor known, producing substantial narrowing of coronary arteries and resistance vessels and mediating cyclic coronary fl ow variations in experimental models of myocardial infarction and unstable angina (11)(12)(13). Indeed, thromboxane A 2 receptor (TP) blockers and TXA 2 synthase (TXA 2 S) inhibitors attenuate the eff ect of and the damage caused by ischemic injury and infl ammation in several organs, including heart (11).…”

mentioning

confidence: 99%

Thromboxane A₂is a key regulator of pathogenesis duringTrypanosoma cruziinfection

Ashton¹,

Mukherjee²,

Nagajyothi³

et al. 2007

J Cell Biol

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Chagas' disease is caused by infection with the protozoan parasite Trypanosoma cruzi. This parasite has a complex life cycle that involves mammalian hosts and insect vectors (1). The vectors become infected after taking a blood meal from an infected host that has circulating, nondividing, blood form trypomastigotes (BFT). The BFT transform into epimastigotes, which multiply extracellularly, inside the insect midgut and diff erentiate into nondividing metacyclic trypomastigotes that enter the host during the insect's next blood meal. Trypomastigotes penetrate a variety of host cell types and multiply intracellularly as amastigotes (2). When amastigotes fi ll the host cell, they diff erentiate into BFT, which are released as the cell ruptures. The BFT invade adjacent tissues and/or spread via the lymphatic and circulatory systems to distant sites where they undergo further cycles of intracellular multiplication. In this way, humans maintain a parasitemia infective for vectors, thus completing the transmission cycle. T. cruzi may also be transmitted by other means such as by blood transfusion, laboratory accidents, organ transplantation, and from mother to fetus (3, 4).

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Effects of thromboxane analog U46619 on endothelial damaged canine coronary arteries in vivo

Cited by 8 publications

References 38 publications

A high-throughput in vitro ring assay for vasoactivity using magnetic 3D bioprinting

A high-throughput in vitro ring assay for vasoactivity using magnetic 3D bioprinting

Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection

Thromboxane A₂is a key regulator of pathogenesis duringTrypanosoma cruziinfection

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Effects of thromboxane analog U46619 on endothelial damaged canine coronary arteries in vivo

Cited by 8 publications

References 38 publications

A high-throughput in vitro ring assay for vasoactivity using magnetic 3D bioprinting

A high-throughput in vitro ring assay for vasoactivity using magnetic 3D bioprinting

Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection

Thromboxane A2is a key regulator of pathogenesis duringTrypanosoma cruziinfection

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Thromboxane A₂is a key regulator of pathogenesis duringTrypanosoma cruziinfection