Mechanisms of α‐thrombin, histamine, and bradykinin induced endothelial permeability

Ehringer, William D.; Edwards, Michael J.; Miller, Frederick N.

doi:10.1002/(sici)1097-4652(199606)167:3<562::aid-jcp20>3.3.co;2-k

Cited by 24 publications

(33 citation statements)

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“…4. Of interest, the absolute values of are from 2 to 10 times lower than those reported in cultured cell models with continuous endothelium (8,9,12,18,61).…”

Section: Pathways For Transvascular Macromolecule Exchangementioning

confidence: 80%

Sexual dimorphism in the permeability response of coronary microvessels to adenosine

Huxley

Wang

Whitt

2005

American Journal of Physiology-Heart and Circulatory Physiology

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Gender influences volume regulation via several mechanisms; whether these include microvascular exchange, especially in the heart, is not known. In response to adenosine (Ado), permeability (P s )to protein of coronary arterioles of female pigs decreases acutely. Whether Ado induces similar P s changes in arterioles from males or whether equivalent responses occur in coronary venules of either sex has not been determined. Hypotheses that 1) basal P s properties and 2) P s responses to vasoactive stimuli are sex independent were evaluated from measures of P s to two hydrophilic proteins, α-lactalbumin and porcine serum albumin (PSA), in arterioles and venules isolated from hearts of adult male and female pigs. Consistent with hypothesis 1, basal P s values of both microvessel types were independent of sex. Contrary to hypothesis 2, P s responses to Ado varied with sex, protein, and vessel type. Confirming earlier studies, Ado induced a ~20% decrease in P s to both proteins in coronary arterioles from females. In arterioles from males, Ado did not change P s for α-lactalbumin ( , 3 ± 13%) whereas P s for PSA ( ) decreased by 27 ± 8% (P < 0.005). In venules from females, Ado elevated by 44 ± 20% (P < 0.05), whereas in those from males, Ado reduced by 24 ± 5% (P < 0.05). The variety of outcomes is consistent with transvascular protein and protein-carried solute flux being regulated by multiple sex-dependent mechanisms in the heart and provides evidence of differences in exchange homeostasis of males and females in health and, likely, disease.

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“…4. Of interest, the absolute values of are from 2 to 10 times lower than those reported in cultured cell models with continuous endothelium (8,9,12,18,61).…”

Section: Pathways For Transvascular Macromolecule Exchangementioning

confidence: 80%

Sexual dimorphism in the permeability response of coronary microvessels to adenosine

Huxley

Wang

Whitt

2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…The structural organization of vimentin was strongly disrupted in the presence of the calcium channel blocker, and increased concentrations of calcium channel blocker could reduce the levels and assembly of vimentin phosphate. Therefore, we deduced that the inhibition of [Ca 2ϩ ] i rise was involved during the modulation of vimentin morphology by LMWH in HUVECs (Retrosen and Gallin, 1986;Ehringer et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Role of Vimentin in the Inhibitory Effects of Low-Molecular-Weight Heparin on PC-3M Cell Adhesion to, and Migration through, Endothelium

Pan¹,

Lei²,

Teng³

et al. 2011

J Pharmacol Exp Ther

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Low-molecular-weight heparin (LMWH) has been used in cancer patients with venous thromboembolic complications, resulting in a higher survival rate and an inhibitory action on experimental metastasis. In the present study, human umbilical vein endothelial cells (HUVECs) were treated with LMWH for 24 h. We found that the resulting HUVECs could significantly inhibit the highly metastatic human prostate cancer cell line (PC-3M) in terms of its adhesion to the endothelium and migration across the endothelium, according to scanning electron microscopy. We also determined the elevated levels of endothelial intercellular Ca 2ϩ concentration after the adhesion of PC-3M cells to HUVECs was greatly reduced by incubation with LMWH. Using proteomics, we surveyed the global protein changes in HUVECs after LMWH treatment and identified four down-regulated proteins that were possible isoforms of cytoskeletal vimentin intermediate filaments, cartilage-derived Ctype lectin, and serine/threonine protein phosphatase 1␤ (PP-1B). LMWH affected the morphology of vimentin and the expression levels of ␣ v integrin and PP-1B in HUVECs bound to PC-3M cells. Vimentin assists in the adhesion of PC-3M cells, which was confirmed by short interfering RNA experiments. Furthermore, the direct binding of purified vimentin protein with LMWH was detected with surface plasmon resonance methods. However, when we used fluorescence-labeled heparin for 24 h to identify whether this binding occurred within cells, heparin was distributed principally around endothelial cells. Taken together, these findings suggest that the monoincubation of LMWH with HUVECs could inhibit PC-3M cell adhesion to, and migration through, endothelium. LMWH's regulation of vimentin plays a role in the antimetastatic action.

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“…It is a potent endothelium-dependent vasodilator. Permeabilization of the endothelium by bradykinin is accomplished by the formation of intercellular gaps, permitting the passage of macromolecules (Ehringer et al, 1996). The positive effect of bradykinin on permeability changes in the coronary vasculature after adenoviral delivery was also shown (Donahue et al, 1998).…”

Section: Figmentioning

confidence: 99%

Myocardial Gene Transfer: Routes and Devices for Regulation of Transgene Expression by Modulation of Cellular Permeability

Katz

Fargnoli²,

Bridges³

2013

Human Gene Therapy

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Heart diseases are major causes of morbidity and mortality in Western society. Gene therapy approaches are becoming promising therapeutic modalities to improve underlying molecular processes affecting failing cardiomyocytes. Numerous cardiac clinical gene therapy trials have yet to demonstrate strong positive results and advantages over current pharmacotherapy. The success of gene therapy depends largely on the creation of a reliable and efficient delivery method. The establishment of such a system is determined by its ability to overcome the existing biological barriers, including cellular uptake and intracellular trafficking as well as modulation of cellular permeability. In this article, we describe a variety of physical and mechanical methods, based on the transient disruption of the cell membrane, which are applied in nonviral gene transfer. In addition, we focus on the use of different physiological techniques and devices and pharmacological agents to enhance endothelial permeability. Development of these methods will undoubtedly help solve major problems facing gene therapy.

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Mechanisms of α‐thrombin, histamine, and bradykinin induced endothelial permeability

Cited by 24 publications

References 0 publications

Sexual dimorphism in the permeability response of coronary microvessels to adenosine

Sexual dimorphism in the permeability response of coronary microvessels to adenosine

Role of Vimentin in the Inhibitory Effects of Low-Molecular-Weight Heparin on PC-3M Cell Adhesion to, and Migration through, Endothelium

Myocardial Gene Transfer: Routes and Devices for Regulation of Transgene Expression by Modulation of Cellular Permeability

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