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Effect of factor XIII on endothelial barrier function.

Noll T, Wozniak G, McCarson K, Hajimohammad A, Metzner HJ, Inserte J, Kummer W, Hehrlein FW, Piper HM - J. Exp. Med. (1999)

Bottom Line: The thrombin-activated plasma factor XIII (1 U/ml) reduced albumin permeability of endothelial monolayers within 20 min by 30 +/- 7% (basal value of 5.9 +/- 0.4 x 10(-6) cm/s), whereas the nonactivated plasma factor XIII had no effect.This study shows that activated factor XIII reduces endothelial permeability.Its effect seems related to a modification of the paracellular passageways in endothelial monolayers.

View Article: PubMed Central - PubMed

Affiliation: Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany. thomas.noll@physiologie.med.uni-giessen.de

ABSTRACT
The effect of factor XIII on endothelial barrier function was studied in a model of cultured monolayers of porcine aortic endothelial cells and saline-perfused rat hearts. The thrombin-activated plasma factor XIII (1 U/ml) reduced albumin permeability of endothelial monolayers within 20 min by 30 +/- 7% (basal value of 5.9 +/- 0.4 x 10(-6) cm/s), whereas the nonactivated plasma factor XIII had no effect. Reduction of permeability to the same extent, i.e., by 34 +/- 9% could be obtained with the thrombin-activated A subunit of factor XIII (1 U/ml), whereas the iodoacetamide-inactivated A subunit as well as the B subunit had no effect on permeability. Endothelial monolayers exposed to the activated factor XIII A exhibited immunoreactive deposition of itself at interfaces of adjacent cells; however, these were not found on exposure to nonactivated factor XIII A or factor XIII B. Hyperpermeability induced by metabolic inhibition (1 mM potassium cyanide plus 1 mM 2-deoxy-D-glucose) was prevented in the presence of the activated factor XIII A. Likewise, the increase in myocardial water content in ischemic-reperfused rat hearts was prevented in its presence. This study shows that activated factor XIII reduces endothelial permeability. It can prevent the loss of endothelial barrier function under conditions of energy depletion. Its effect seems related to a modification of the paracellular passageways in endothelial monolayers.

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Effect of factor XIII on changes of myocardial water content under low-flow ischemia and reperfusion. Rat hearts in Langendorff  mode were perfused for 60 min with normoxic perfusate at 10 ml/min,  followed by 40 min low-flow perfusion at 0.5 ml/min, and 60 min reperfusion with normoxic perfusate at 10 ml/min. Control hearts were perfused up to 160 min with normoxic media at 10 ml/min (•). Perfusate of  low-flow ischemia and reperfusion was supplemented with either nonactivated factor XIII A (▪, 50 μg/ml) or thrombin-activated factor XIII A  (▴, 50 μg/ml = to 5 U/ml). Data are means ± SD of n = 4 separate experiments of independent heart preparations. *P < 0.05 vs. 160 min normoxia; #P < 0.05 vs. activated factor XIII A.
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Figure 11: Effect of factor XIII on changes of myocardial water content under low-flow ischemia and reperfusion. Rat hearts in Langendorff mode were perfused for 60 min with normoxic perfusate at 10 ml/min, followed by 40 min low-flow perfusion at 0.5 ml/min, and 60 min reperfusion with normoxic perfusate at 10 ml/min. Control hearts were perfused up to 160 min with normoxic media at 10 ml/min (•). Perfusate of low-flow ischemia and reperfusion was supplemented with either nonactivated factor XIII A (▪, 50 μg/ml) or thrombin-activated factor XIII A (▴, 50 μg/ml = to 5 U/ml). Data are means ± SD of n = 4 separate experiments of independent heart preparations. *P < 0.05 vs. 160 min normoxia; #P < 0.05 vs. activated factor XIII A.

Mentions: To analyze whether the activated factor XIII A can also affect endothelial barrier function in the coronary system, the isolated perfused heart was used and changes of myocardial water content were determined. Under control conditions, the myocardial water content of the normoxic perfused rat heart was, on average, 430 ml/100 g dry wt over a period of 160 min of observation (Fig. 11). To provoke an increase in vascular permeability, hearts were exposed to a 40-min period of low-flow ischemia followed by a period of 60 min of normoxic reperfusion. Ischemia-reperfusion experiments were performed with addition of either the nonactivated or the activated factor XIII A 5 min before onset of anoxic low-flow perfusion. With the nonactivated factor XIII A, the water content of reperfused hearts rose to 530 ml/100 g dry wt. In the presence of the activated factor XIII A (5 U/ml), myocardial water content remained as it was before reperfusion.


Effect of factor XIII on endothelial barrier function.

Noll T, Wozniak G, McCarson K, Hajimohammad A, Metzner HJ, Inserte J, Kummer W, Hehrlein FW, Piper HM - J. Exp. Med. (1999)

Effect of factor XIII on changes of myocardial water content under low-flow ischemia and reperfusion. Rat hearts in Langendorff  mode were perfused for 60 min with normoxic perfusate at 10 ml/min,  followed by 40 min low-flow perfusion at 0.5 ml/min, and 60 min reperfusion with normoxic perfusate at 10 ml/min. Control hearts were perfused up to 160 min with normoxic media at 10 ml/min (•). Perfusate of  low-flow ischemia and reperfusion was supplemented with either nonactivated factor XIII A (▪, 50 μg/ml) or thrombin-activated factor XIII A  (▴, 50 μg/ml = to 5 U/ml). Data are means ± SD of n = 4 separate experiments of independent heart preparations. *P < 0.05 vs. 160 min normoxia; #P < 0.05 vs. activated factor XIII A.
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Related In: Results  -  Collection

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Figure 11: Effect of factor XIII on changes of myocardial water content under low-flow ischemia and reperfusion. Rat hearts in Langendorff mode were perfused for 60 min with normoxic perfusate at 10 ml/min, followed by 40 min low-flow perfusion at 0.5 ml/min, and 60 min reperfusion with normoxic perfusate at 10 ml/min. Control hearts were perfused up to 160 min with normoxic media at 10 ml/min (•). Perfusate of low-flow ischemia and reperfusion was supplemented with either nonactivated factor XIII A (▪, 50 μg/ml) or thrombin-activated factor XIII A (▴, 50 μg/ml = to 5 U/ml). Data are means ± SD of n = 4 separate experiments of independent heart preparations. *P < 0.05 vs. 160 min normoxia; #P < 0.05 vs. activated factor XIII A.
Mentions: To analyze whether the activated factor XIII A can also affect endothelial barrier function in the coronary system, the isolated perfused heart was used and changes of myocardial water content were determined. Under control conditions, the myocardial water content of the normoxic perfused rat heart was, on average, 430 ml/100 g dry wt over a period of 160 min of observation (Fig. 11). To provoke an increase in vascular permeability, hearts were exposed to a 40-min period of low-flow ischemia followed by a period of 60 min of normoxic reperfusion. Ischemia-reperfusion experiments were performed with addition of either the nonactivated or the activated factor XIII A 5 min before onset of anoxic low-flow perfusion. With the nonactivated factor XIII A, the water content of reperfused hearts rose to 530 ml/100 g dry wt. In the presence of the activated factor XIII A (5 U/ml), myocardial water content remained as it was before reperfusion.

Bottom Line: The thrombin-activated plasma factor XIII (1 U/ml) reduced albumin permeability of endothelial monolayers within 20 min by 30 +/- 7% (basal value of 5.9 +/- 0.4 x 10(-6) cm/s), whereas the nonactivated plasma factor XIII had no effect.This study shows that activated factor XIII reduces endothelial permeability.Its effect seems related to a modification of the paracellular passageways in endothelial monolayers.

View Article: PubMed Central - PubMed

Affiliation: Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany. thomas.noll@physiologie.med.uni-giessen.de

ABSTRACT
The effect of factor XIII on endothelial barrier function was studied in a model of cultured monolayers of porcine aortic endothelial cells and saline-perfused rat hearts. The thrombin-activated plasma factor XIII (1 U/ml) reduced albumin permeability of endothelial monolayers within 20 min by 30 +/- 7% (basal value of 5.9 +/- 0.4 x 10(-6) cm/s), whereas the nonactivated plasma factor XIII had no effect. Reduction of permeability to the same extent, i.e., by 34 +/- 9% could be obtained with the thrombin-activated A subunit of factor XIII (1 U/ml), whereas the iodoacetamide-inactivated A subunit as well as the B subunit had no effect on permeability. Endothelial monolayers exposed to the activated factor XIII A exhibited immunoreactive deposition of itself at interfaces of adjacent cells; however, these were not found on exposure to nonactivated factor XIII A or factor XIII B. Hyperpermeability induced by metabolic inhibition (1 mM potassium cyanide plus 1 mM 2-deoxy-D-glucose) was prevented in the presence of the activated factor XIII A. Likewise, the increase in myocardial water content in ischemic-reperfused rat hearts was prevented in its presence. This study shows that activated factor XIII reduces endothelial permeability. It can prevent the loss of endothelial barrier function under conditions of energy depletion. Its effect seems related to a modification of the paracellular passageways in endothelial monolayers.

Show MeSH
Related in: MedlinePlus