Interleukin 1 and lipopolysaccharide induce an inhibitor of tissue-type plasminogen activator in vivo and in cultured endothelial cells.

Abstract

Human IL-1, recombinant murine IL-1 and E. coli LPS were found to be potent inducers of plasminogen activator (PA)-inhibitor activity, both in vivo, in rats, as well as in cultured human endothelial cells. In vivo, LPS rapidly and dose-dependently (0.01-1,000 micrograms/kg) increased plasma PA-inhibitor activity. Infusion of IL-1 into rats resulted in a small but significant increase in PA-inhibitor activity in rat plasma. Likewise, in cultured human umbilical vein endothelial cells, LPS and IL-1 induced increased synthesis of PA-inhibitor. We suggest that the induced rat plasma inhibitor might be of endothelial origin.

Antithrombotic, procoagulant, and fibrinolytic mechanisms in cerebral circulation: implications for brain injury and protection

“…[12] The release of both tPA and PAI-1 by LPS in vivo has also been reported in rats. [33] In vivo studies in rats when contrasted with in vivo studies in nonhuman primates indicated that neither TNF-alpha nor IL-1 is significantly involved in the induction of PAI-1 by LPS. [33] Among other differences, the expression of tPA in cerebral microvessels in nonhuman primates in vivo was found to be limited to some precapillary arterioles and postcapillary venules, [75] whereas in rats and guinea pigs tPA and PAI-1 antigens are expressed in cerebral capillaries in vivo.…”

“…[33] In vivo studies in rats when contrasted with in vivo studies in nonhuman primates indicated that neither TNF-alpha nor IL-1 is significantly involved in the induction of PAI-1 by LPS. [33] Among other differences, the expression of tPA in cerebral microvessels in nonhuman primates in vivo was found to be limited to some precapillary arterioles and postcapillary venules, [75] whereas in rats and guinea pigs tPA and PAI-1 antigens are expressed in cerebral capillaries in vivo. [70,133] It has also been shown recently that tPA and PAI-1 regulation in rat aorta in response to LPS differs from observations in mouse aorta and rat carotid artery.…”

“…[78] It has been suggested that tPA and PAI-1 expression may vary among species, tissues, and with the type of stimulation. [12,33,70,71,75,91,133] The expression of tPA and PAI-1 has recently been shown in bovine [71] and human [107] brain microvascular endothelial cells in vitro.…”

“…For example, coordinated induction of both tPA and PAI-1 has been reported with thrombin or basic fibroblast growth factor (bFGF), whereas histamine, activated protein C, and phorbol ester induce tPA alone, and lipopolysaccharide (LPS), transforming growth factor-ß, interleukin-1 (IL-1), or tumor necrosis factor-alpha (TNF-alpha) induce PAI-1 alone. [33,56,76,[102][103][104][105] It has been shown that human systemic endothelial cells in vitro secrete more tPA when exposed to an arterial level of shear stress [26] and pulsatile stretch, [63] whereas PAI-1 secretion remains unaffected. It has been also demonstrated that tPA secretion and tPA mRNA are significantly upregulated after serial passages in culture, whereas the urokinase-type plasminogen activator gene that is normally not expressed in primary culture, becomes quite active at higher passage numbers.…”

A Comparison Of Il-1β, E2 (Pge2), Pai-2 and Tnf-Α Levels in Gingival Crevicular Fluid (Gcf) and Peri-Implant Crevicular Fluid (Picf) from Groups of Patients with Healthy Teeth, Healthy Implants, Periodontitis and Peri-Implantitis

“…However, IL-1a and IL-1ß may be the principal inflammatoninduced cytokines stimulating bone resorption in periodontitis [8][9][10]. In peri-implant crevicular fluid (PICF), higher levels of IL-1ß have been associated with peri-implantitis [11][12][13][14][15].…”