Presentation Title
Effects of tranexamic acid on mitochondrial homeostasis in endothelial cells and leukocytes
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Document Type
Oral Presentation
Faculty Mentor
Igor Prudovsky, PhD
Abstract
Our project focuses on studying the biological effects of Tranexamic Acid (TXA, trans-4-aminomethyl-cyclohexane-1-carboxylic acid), a synthetic analog of the amino acid lysine, widely used for inhibiting fibrinolysis in hemorrhagic trauma patients. The clinical data indicates that the beneficial effects of TXA widely transcend its anti-fibrinolytic activity. The present study aims to analyze the cellular effects of TXA on a biochemical level. The experiments were conducted on neutrophils and endothelial cell cultures. Neutrophils were differentiated from a culture of myelomonocytic leukemia cell line (HL60) treated with retinoic acid. In our studies, immunoblotting and confocal microscopy were used. TXA has been shown previously by our group to have the ability to increase the mitochondrial respiration, decrease the release of mitochondrial DNA, and therefore reduce the effects of the damage suffered by the cells. We have analyzed using endothelial cells and neutrophils the effects of TXA on the expression of structural mitochondrial proteins and transcription factors regulating mitochondrial biogenesis. In addition, we studied the effects of TXA on the levels of mitochondrial pro-apoptotic proteins. Confocal microscopy has been applied to study the morphological changes of mitochondria in TXA-treated cells. The results of our studies indicate that TXA enhances mitochondrial biogenesis.
Victoria Vieira Zucco Presentation Transcript
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Effects of tranexamic acid on mitochondrial homeostasis in endothelial cells and leukocytes
Our project focuses on studying the biological effects of Tranexamic Acid (TXA, trans-4-aminomethyl-cyclohexane-1-carboxylic acid), a synthetic analog of the amino acid lysine, widely used for inhibiting fibrinolysis in hemorrhagic trauma patients. The clinical data indicates that the beneficial effects of TXA widely transcend its anti-fibrinolytic activity. The present study aims to analyze the cellular effects of TXA on a biochemical level. The experiments were conducted on neutrophils and endothelial cell cultures. Neutrophils were differentiated from a culture of myelomonocytic leukemia cell line (HL60) treated with retinoic acid. In our studies, immunoblotting and confocal microscopy were used. TXA has been shown previously by our group to have the ability to increase the mitochondrial respiration, decrease the release of mitochondrial DNA, and therefore reduce the effects of the damage suffered by the cells. We have analyzed using endothelial cells and neutrophils the effects of TXA on the expression of structural mitochondrial proteins and transcription factors regulating mitochondrial biogenesis. In addition, we studied the effects of TXA on the levels of mitochondrial pro-apoptotic proteins. Confocal microscopy has been applied to study the morphological changes of mitochondria in TXA-treated cells. The results of our studies indicate that TXA enhances mitochondrial biogenesis.
