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22 results on '"Arce, Maximiliano"'

1. Coronary Artery Disease Risk Variant Dampens the Expression of CALCRL by Reducing HSF Binding to Shear Stress Responsive Enhancer in Endothelial Cells In Vitro

Author

Selvarajan, Ilakya, Kiema, Miika, Huang, Ru-Ting, Li, Jin, Zhu, Jiayu, Pölönen, Petri, Örd, Tiit, Õunap, Kadri, Godiwala, Mehvash, Golebiewski, Anna Kathryn, Ravindran, Aarthi, Mäklin, Kiira, Toropainen, Anu, Stolze, Lindsey K., Arce, Maximiliano, Magnusson, Peetra U., White, Stephen, Romanoski, Casey E., Heinäniemi, Merja, Laakkonen, Johanna P., Fang, Yun, and Kaikkonen, Minna U.

Published
2024
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2. Immunothrombosis and vascular heterogeneity in cerebral cavernous malformation

Author

Globisch, Maria A., Onyeogaziri, Favour C., Jauhiainen, Suvi, Yau, Anthony C.Y., Orsenigo, Fabrizio, Conze, Lei L., Arce, Maximiliano, Corada, Monica, Smith, Ross O., Rorsman, Charlotte, Sundell, Veronica, Fernando, Dinesh, Daniel, Geoffrey, Mattsson, Oscar, Savander, Henri, Wanders, Alkwin, Rezai Jahromi, Behnam, Laakso, Aki, Niemelä, Mika, Dejana, Elisabetta, and Magnusson, Peetra U.

Published
2022
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4. Propranolol Reduces the Development of Lesions and Rescues Barrier Function in Cerebral Cavernous Malformations: A Preclinical Study

Author

Oldenburg, Joppe, Malinverno, Matteo, Globisch, Maria Ascencion, Maderna, Claudio, Corada, Monica, Orsenigo, Fabrizio, Conze, Lei Liu, Rorsman, Charlotte, Sundell, Veronica, Arce, Maximiliano, Smith, Ross O., Yau, Anthony C.Y., Billström, Gry Hulsart, Mägi, Caroline Öhman, Beznoussenko, Galina V., Mironov, Alexander A., Fernando, Dinesh, Daniel, Geoffrey, Olivari, Davide, Fumagalli, Francesca, Lampugnani, Maria Grazia, Dejana, Elisabetta, and Magnusson, Peetra U.

Published
2021
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5. Slow-Closing Clip for the Treatment of Nonsaccular Vertebrobasilar Aneurysms: A Retrospective Case Series

Author

Rezai Jahromi, Behnam, primary, Dashti, Reza, additional, Rustemi, Oriela, additional, Silva, João M., additional, Srinivasan, Visish M., additional, Tulamo, Riikka, additional, Kozyrev, Danil A., additional, Jauhiainen, Suvi, additional, Magnusson, Peetra U., additional, Arce, Maximiliano, additional, Kaukovalta, Hanna, additional, Schwartz, Christoph, additional, Numminen, Jussi, additional, Sarpaneva, Stepan, additional, Hirvelä, Valdemar, additional, Lawton, Michael T., additional, Tanikawa, Rokuya, additional, Niemelä, Mika, additional, and Hernesniemi, Juha, additional

Published
2022
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7. Dysregulated Hemostasis and Immunothrombosis in Cerebral Cavernous Malformations

Author

Globisch, Maria Ascencion, Onyeogaziri, Favour, Smith, Ross O., Arce, Maximiliano, Magnusson, Peetra, Globisch, Maria Ascencion, Onyeogaziri, Favour, Smith, Ross O., Arce, Maximiliano, and Magnusson, Peetra

Abstract

Cerebral cavernous malformation (CCM) is a neurovascular disease that affects 0.5% of the general population. For a long time, CCM research focused on genetic mutations, endothelial junctions and proliferation, but recently, transcriptome and proteome studies have revealed that the hemostatic system and neuroinflammation play a crucial role in the development and severity of cavernomas, with some of these publications coming from our group. The aim of this review is to give an overview of the latest molecular insights into the interaction between CCM-deficient endothelial cells with blood components and the neurovascular unit. Specifically, we underscore how endothelial dysfunction can result in dysregulated hemostasis, bleeding, hypoxia and neurological symptoms. We conducted a thorough review of the literature and found a field that is increasingly poised to regard CCM as a hemostatic disease, which may have implications for therapy.

Published
2022
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8. Slow-Closing Clip for the Treatment of Nonsaccular Vertebrobasilar Aneurysms : A Retrospective Case Series

Author

Rezai Jahromi, Behnam, Dashti, Reza, Rustemi, Oriela, Silva, João M., Srinivasan, Visish M., Tulamo, Riikka, Kozyrev, Danil A., Jauhiainen, Suvi, Magnusson, Peetra U., Arce, Maximiliano, Kaukovalta, Hanna, Schwartz, Christoph, Numminen, Jussi, Sarpaneva, Stepan, Hirvelä, Valdemar, Lawton, Michael T., Tanikawa, Rokuya, Niemelä, Mika, Hernesniemi, Juha, Rezai Jahromi, Behnam, Dashti, Reza, Rustemi, Oriela, Silva, João M., Srinivasan, Visish M., Tulamo, Riikka, Kozyrev, Danil A., Jauhiainen, Suvi, Magnusson, Peetra U., Arce, Maximiliano, Kaukovalta, Hanna, Schwartz, Christoph, Numminen, Jussi, Sarpaneva, Stepan, Hirvelä, Valdemar, Lawton, Michael T., Tanikawa, Rokuya, Niemelä, Mika, and Hernesniemi, Juha

Abstract

Objective Vertebrobasilar artery nonsaccular aneurysms (VBANSAs) are associated with a 13% annual mortality. Revascularization and flow diversion are life-saving options in select cases; technical failures and rapid hemodynamic changes may contribute to unwanted outcomes. We describe a technique and report clinical outcomes of patients treated with an experimental slow-closing clip (SCC). Methods An experimental SCC was created to gradually close the parent artery of aneurysms. Clinical, radiographic, and outcome data from patients with VBANSAs who underwent experimental treatment with the SCC were retrospectively analyzed. Results Among 10 patients (7 men; mean age, 49.5 years; range, 18–73 years), 6 presented with mass effect symptoms, 1 with ischemic stroke, 2 with subarachnoid hemorrhage, and 1 with hydrocephalus. Five patients underwent revascularization plus SCC application, and 5 were treated with SCC alone. The mean follow-up was 6.7 years. The expected mortality among patients with unruptured VBANSAs with previous treatment options in this period was 52.7%, whereas the observed rate was 20%. Four patients died within 12 months after treatment. Causes of death were brainstem ischemic stroke, poor-grade subarachnoid hemorrhage, poor clinical presentation, and unknown. Six patients were alive at last follow-up, with unchanged or improved modified Rankin Scale scores. Mortality was associated with posterior-projecting aneurysms and late-stage treatment. Conclusions In this small case series, use of SCC overcame the natural history of VBANSAs when treatment timing and aneurysm anatomy were suitable. The SCC potentially favors aneurysm thrombosis and collateral reactivation. More studies are necessary to better develop the SCC.

Published
2022
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9. Immunothrombosis and vascular heterogeneity in cerebral cavernous malformation

Author

Globisch, Maria Ascencion, Onyeogaziri, Favour Chinyere, Jauhiainen, Suvi, Yau, Anthony C Y, Orsenigo, Fabrizio, Conze, Lei Liu, Arce, Maximiliano, Corada, Monica, Smith, Ross O, Rorsman, Charlotte, Sundell, Veronica, Fernando, Dinesh, Daniel, Geoffrey, Mattsson, Oscar, Savander, Henri S, Wanders, Alkwin, Jahromi, Behnam Rezai, Laakso, Aki, Niemelä, Mika, Dejana, Elisabetta, and Magnusson, Peetra Ulrica

Subjects
Hemangioma, Cavernous, Central Nervous System, Thromboinflammation, Neurologi, Endothelial Cells, Hematology, Mice, Neurology, von Willebrand Factor, Humans, Animals, Hematologi, Apoptosis Regulatory Proteins, Hypoxia, Cell and Molecular Biology
Abstract

Cerebral cavernous malformation (CCM) is a neurovascular disease that results in various neurological symptoms. Thrombi have been reported in surgically resected CCM patient biopsies, but the molecular signatures of these thrombi remain elusive. Here, we investigated the kinetics of thrombi formation in CCM and how thrombi affect the vasculature and contribute to cerebral hypoxia. We used RNA sequencing to investigate the transcriptome of mouse brain endothelial cells with an inducible endothelial-specific Ccm3 knock-out (Ccm3-iECKO). We found that Ccm3-deficient brain endothelial cells had a higher expression of genes related to the coagulation cascade and hypoxia when compared with wild-type brain endothelial cells. Immunofluorescent assays identified key molecular signatures of thrombi such as fibrin, von Willebrand factor, and activated platelets in Ccm3-iECKO mice and human CCM biopsies. Notably, we identified polyhedrocytes in Ccm3-iECKO mice and human CCM biopsies and report it for the first time. We also found that the parenchyma surrounding CCM lesions is hypoxic and that more thrombi correlate with higher levels of hypoxia. We created an in vitro model to study CCM pathology and found that human brain endothelial cells deficient for CCM3 expressed elevated levels of plasminogen activator inhibitor-1 and had a redistribution of von Willebrand factor. With transcriptomics, comprehensive imaging, and an in vitro CCM preclinical model, this study provides experimental evidence that genes and proteins related to the coagulation cascade affect the brain vasculature and promote neurological side effects such as hypoxia in CCMs. This study supports the concept that antithrombotic therapy may be beneficial for patients with CCM.

Published
2022

10. TBD (coagulation factor X in cancer)

Author

Arce, Maximiliano, Owen, Gareth, Quest, Andrew, and Pontificia Universidad Católica de Chile

Abstract

FONDAP FONDAP ACCDiS

Published
2019

11. Coagulation Factor Xa Promotes Solid Tumor Growth, Experimental Metastasis and Endothelial Cell Activation

Author

Arce, Maximiliano, Pinto, Mauricio P., Galleguillos, Macarena, Munoz, Catalina, Lange, Soledad, Ramirez, Carolina, Erices, Rafaela, Gonzalez, Pamela, Velasquez, Ethel, Tempio, Fabian, Lopez, Mercedes N., Salazar-Onfray, Flavio, Cautivo, Kelly, Kalergis, Alexis M., Cruz, Sebastian, Lladser, Alvaro, Lobos-Gonzalez, Lorena, Valenzuela, Guillermo, Olivares, Nixa, Saez, Claudia, Koning, Tania, Sanchez, Fabiola A., Fuenzalida, Patricia, Godoy, Alejandro, Contreras Orellana, Pamela, Leyton, Lisette, Lugano, Roberta, Dimberg, Anna, Quest, Andrew F. G., Owen, Gareth, I, Arce, Maximiliano, Pinto, Mauricio P., Galleguillos, Macarena, Munoz, Catalina, Lange, Soledad, Ramirez, Carolina, Erices, Rafaela, Gonzalez, Pamela, Velasquez, Ethel, Tempio, Fabian, Lopez, Mercedes N., Salazar-Onfray, Flavio, Cautivo, Kelly, Kalergis, Alexis M., Cruz, Sebastian, Lladser, Alvaro, Lobos-Gonzalez, Lorena, Valenzuela, Guillermo, Olivares, Nixa, Saez, Claudia, Koning, Tania, Sanchez, Fabiola A., Fuenzalida, Patricia, Godoy, Alejandro, Contreras Orellana, Pamela, Leyton, Lisette, Lugano, Roberta, Dimberg, Anna, Quest, Andrew F. G., and Owen, Gareth, I

Abstract

Hypercoagulable state is linked to cancer progression; however, the precise role of the coagulation cascade is poorly described. Herein, we examined the contribution of a hypercoagulative state through the administration of intravenous Coagulation Factor Xa (FXa), on the growth of solid human tumors and the experimental metastasis of the B16F10 melanoma in mouse models. FXa increased solid tumor volume and lung, liver, kidney and lymph node metastasis of tail-vein injected B16F10 cells. Concentrating on the metastasis model, upon coadministration of the anticoagulant Dalteparin, lung metastasis was significantly reduced, and no metastasis was observed in other organs. FXa did not directly alter proliferation, migration or invasion of cancer cells in vitro. Alternatively, FXa upon endothelial cells promoted cytoskeleton contraction, disrupted membrane VE-Cadherin pattern, heightened endothelial-hyperpermeability, increased inflammatory adhesion molecules and enhanced B16F10 adhesion under flow conditions. Microarray analysis of endothelial cells treated with FXa demonstrated elevated expression of inflammatory transcripts. Accordingly, FXa treatment increased immune cell infiltration in mouse lungs, an effect reduced by dalteparin. Taken together, our results suggest that FXa increases B16F10 metastasis via endothelial cell activation and enhanced cancer cell-endothelium adhesion advocating that the coagulation system is not merely a bystander in the process of cancer metastasis.

Published
2019
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12. Coagulation Factor Xa Promotes Solid Tumor Growth, Experimental Metastasis and Endothelial Cell Activation

Author

Arce, Maximiliano, primary, Pinto, Mauricio P., additional, Galleguillos, Macarena, additional, Muñoz, Catalina, additional, Lange, Soledad, additional, Ramirez, Carolina, additional, Erices, Rafaela, additional, Gonzalez, Pamela, additional, Velasquez, Ethel, additional, Tempio, Fabián, additional, Lopez, Mercedes N., additional, Salazar-Onfray, Flavio, additional, Cautivo, Kelly, additional, Kalergis, Alexis M., additional, Cruz, Sebastián, additional, Lladser, Álvaro, additional, Lobos-González, Lorena, additional, Valenzuela, Guillermo, additional, Olivares, Nixa, additional, Sáez, Claudia, additional, Koning, Tania, additional, Sánchez, Fabiola A., additional, Fuenzalida, Patricia, additional, Godoy, Alejandro, additional, Contreras Orellana, Pamela, additional, Leyton, Lisette, additional, Lugano, Roberta, additional, Dimberg, Anna, additional, Quest, Andrew F.G., additional, and Owen, Gareth I., additional

Published
2019
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17. Independent anti-angiogenic capacities of coagulationfactors x and xa

Author

Lange, Soledad, Gonzalez, Ibeth, Pinto, Mauricio P., Arce, Maximiliano, Valenzuela, Rodrigo, Aranda, Evelyn, Elliot, Matias, Alvarez, Marjorie, Henriquez, Soledad, Velasquez, Ethel V., Orge, Felipe, Oliva, Barbara, Gonzalez, Pamela, Villalon, Manuel, Cautivo, Kelly M., Kalergis, Alexis M., Pereira, Karla, Mendoza, Camila, Saez, Claudia, Kato, Sumie, Cuello, Mauricio A., Parborell, Fernanda, Irusta, Griselda, Palma, Veronica, Allende, Miguel L., and Owen, Gareth I.

Published
2014

18. Independent anti-angiogenic capacities of coagulation factors x and xa

Author

Lange, Soledad, González, Ibeth, Pinto, Mauricio P, Arce, Maximiliano, Valenzuela, Rodrigo, Aranda, Evelyn, Elliot, Matias, Álvarez, Marjorie, Henríquez, Soledad, Velasquez, Ethel V, Orge, Felipe, Oliva, Bárbara, González, Pamela, Villalon, Manuel, and Cautiv

Abstract

Knockout models have shown that the coagulation system has a role in vascular development and angiogenesis. Herein, we report for the first time that zymogen FX and its active form (FXa) possess anti-angiogenic properties. Both the recombinant FX and FXa

Published
2014

19. Independent anti-angiogenic capacities of coagulation factors X and Xa

Author

Lange, Soledad, Gonzalez, Ibeth, Pinto, Mauricio P., Arce, Maximiliano, Valenzuela, Rodrigo, Aranda, Evelyn, Elliot, Matias, Alvarez, Marjorie, Henriquez, Soledad, Velazquez, Ethel, Orge, Felipe, Oliva, Bárbara, Gonzalez, Pamela, Villalon, Manuel, Cautivo, Kelly M., Kalergis, Alexis M., Pereira, Karla, Mendoza, Camila, Saez, Claudia, Kato, Sumie, Cuello, Mauricio, Parborell, Maria Fernanda Agustina, Irusta, Griselda, Palma, Verónica, Allende, Miguel L., and Owen, Gareth I.

Subjects
FXa, CIENCIAS MÉDICAS Y DE LA SALUD, Neovascularization, Pathologic, ANGIOGENESIS INHIBITORS, Cell Cycle, COAGULATION, Neovascularization, Physiologic, Patología, Angiogenesis Inhibitors, Chick Embryo, Helminth Proteins, Ciencias Biológicas, Medicina Básica, Biología Celular, Microbiología, Cell Movement, Cell Line, Tumor, Factor X, Factor Xa, Human Umbilical Vein Endothelial Cells, Animals, Humans, Receptor, PAR-1, FX, CIENCIAS NATURALES Y EXACTAS, Zebrafish
Abstract

Knockout models have shown that the coagulation system has a role in vascular development and angiogenesis. Herein, we report for the first time that zymogen FX and its active form (FXa) possess anti-angiogenic properties. Both the recombinant FX and FXa inhibit angiogenesis in vitro using endothelial EA.hy926 and human umbilical cord vascular endothelial cells (HUVEC). This effect is dependent on the Gla domain of FX. We demonstrate that FX and FXa use different mechanisms: the use of Rivaroxaban (RX) a specific inhibitor of FXa attenuated its anti-angiogenic properties but did not modify the anti-angiogenic effect of FX. Furthermore, only the anti-angiogenic activity of FXa is PAR-1dependent. Using in vivo models, we show that FX and FXa are anti-angiogenic in the zebrafish intersegmental vasculature (ISV) formation and in the chick embryo chorioallantoic membrane (CAM) assays. Our results provide further evidence for the non-hemostatic functions of FX and FXa and demonstrate for the first time a biological role for the zymogen FX. Fil: Lange, Soledad. Pontificia Universidad Católica de Chile; Chile Fil: Gonzalez, Ibeth. Pontificia Universidad Católica de Chile; Chile Fil: Pinto, Mauricio P.. Pontificia Universidad Católica de Chile; Chile Fil: Arce, Maximiliano. Pontificia Universidad Católica de Chile; Chile Fil: Valenzuela, Rodrigo. Pontificia Universidad Católica de Chile; Chile Fil: Aranda, Evelyn. Pontificia Universidad Católica de Chile; Chile Fil: Elliot, Matias. Universidad de Chile. Facultad de Ciencias; Chile Fil: Alvarez, Marjorie. Universidad de Chile. Facultad de Ciencias; Chile Fil: Henriquez, Soledad. Pontificia Universidad Católica de Chile; Chile Fil: Velazquez, Ethel. Pontificia Universidad Católica de Chile; Chile Fil: Orge, Felipe. Pontificia Universidad Católica de Chile; Chile Fil: Oliva, Bárbara. Pontificia Universidad Católica de Chile; Chile Fil: Gonzalez, Pamela. Pontificia Universidad Católica de Chile; Chile Fil: Villalon, Manuel. Pontificia Universidad Católica de Chile; Chile Fil: Cautivo, Kelly M.. Pontificia Universidad Católica de Chile; Chile Fil: Kalergis, Alexis M.. Pontificia Universidad Católica de Chile; Chile Fil: Pereira, Karla. Pontificia Universidad Católica de Chile; Chile Fil: Mendoza, Camila. Pontificia Universidad Católica de Chile; Chile Fil: Saez, Claudia. Pontificia Universidad Católica de Chile; Chile Fil: Kato, Sumie. Pontificia Universidad Católica de Chile; Chile Fil: Cuello, Mauricio. Pontificia Universidad Católica de Chile; Chile Fil: Parborell, Maria Fernanda Agustina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina Fil: Irusta, Griselda. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina Fil: Palma, Verónica. Universidad de Chile. Facultad de Ciencias; Chile Fil: Allende, Miguel L.. Universidad de Chile. Facultad de Ciencias; Chile Fil: Owen, Gareth I.. Pontificia Universidad Católica de Chile; Chile. Biomedical Research Consortium Chile; Chile

Published
2013

21. Independent Anti-Angiogenic Capacities of Coagulation Factors X and Xa

Author

Lange, Soledad, primary, Gonzalez, Ibeth, additional, Pinto, Mauricio P., additional, Arce, Maximiliano, additional, Valenzuela, Rodrigo, additional, Aranda, Evelyn, additional, Elliot, Matias, additional, Alvarez, Marjorie, additional, Henriquez, Soledad, additional, Velasquez, Ethel V., additional, Orge, Felipe, additional, Oliva, Barbara, additional, Gonzalez, Pamela, additional, Villalon, Manuel, additional, Cautivo, Kelly M., additional, Kalergis, Alexis M., additional, Pereira, Karla, additional, Mendoza, Camila, additional, Saez, Claudia, additional, Kato, Sumie, additional, Cuello, Mauricio A., additional, Parborell, Fernanda, additional, Irusta, Griselda, additional, Palma, Veronica, additional, Allende, Miguel L., additional, and Owen, Gareth I., additional

Published
2014
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22. Propranolol Reduces the Development of Lesions and Rescues Barrier Function in Cerebral Cavernous Malformations

Author

Oldenburg, Joppe, Malinverno, Matteo, Globisch, Maria Ascencion, Maderna, Claudio, Corada, Monica, Orsenigo, Fabrizio, Conze, Lei Liu, Rorsman, Charlotte, Sundell, Veronica, Arce, Maximiliano, Smith, Ross O., Yau, Anthony C.Y., Billström, Gry Hulsart, Mägi, Caroline Öhman, Beznoussenko, Galina V., Mironov, Alexander A., Fernando, Dinesh, Daniel, Geoffrey, Olivari, Davide, Fumagalli, Francesca, Lampugnani, Maria Grazia, Dejana, Elisabetta, and Magnusson, Peetra U.

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