Search

Your search keyword '"Chadjichristos, Christos E."' showing total 157 results
Start Over Author "Chadjichristos, Christos E." Publication Year Range Last 50 years
157 results on '"Chadjichristos, Christos E."'

4. Galectin-3 in Kidney Diseases: From an Old Protein to a New Therapeutic Target

Author

Boutin, Louis, Dépret, François, Gayat, Etienne, Legrand, Matthieu, and Chadjichristos, Christos E

Subjects
Biochemistry and Cell Biology, Biological Sciences, Biotechnology, Kidney Disease, Renal and urogenital, Fibrosis, Galectin 3, Humans, Kidney, Kidney Diseases, Signal Transduction, galectin-3, kidney disease, lectins, Other Chemical Sciences, Genetics, Other Biological Sciences, Chemical Physics, Biochemistry and cell biology, Microbiology, Medicinal and biomolecular chemistry
Abstract

Galectin-3 (Gal-3) is a 30KDa lectin implicated in multiple pathophysiology pathways including renal damage and fibrosis. Gal-3 binds β-galactoside through its carbohydrate-recognition domain. From intra-cellular to extra-cellular localization, Gal-3 has multiple roles including transduction signal pathway, cell-to-cell adhesion, cell to extracellular matrix adhesion, and immunological chemoattractant protein. Moreover, Gal-3 has also been linked to kidney disease in both preclinical models and clinical studies. Gal-3 inhibition appears to improve renal disease in several pathological conditions, thus justifying the development of multiple drug inhibitors. This review aims to summarize the latest literature regarding Gal-3 in renal pathophysiology, from its role as a biomarker to its potential as a therapeutic agent.

Published
2022

6. Acute Kidney Injury Induces Remote Cardiac Damage and Dysfunction Through the Galectin-3 Pathway.

Author

Prud'homme, Mathilde, Coutrot, Maxime, Michel, Thibault, Boutin, Louis, Genest, Magali, Poirier, Françoise, Launay, Jean-Marie, Kane, Bocar, Kinugasa, Satoshi, Prakoura, Niki, Vandermeersch, Sophie, Cohen-Solal, Alain, Delcayre, Claude, Samuel, Jane-Lise, Mehta, Ravindra, Gayat, Etienne, Mebazaa, Alexandre, Chadjichristos, Christos E, and Legrand, Matthieu

Subjects
AKI, acute kidney injury, BM, bone marrow, BUN, blood urea nitrogen, Cr, creatinine, Gal-3, galectin-3, ICAM, intercellular adhesion molecule, ICU, intensive care unit, IL, interleukin, IR, ischemia-reperfusion, KDIGO, Kidney Disease Improving Global Outcome, KO, knock-out, MCP, modified citrus pectin, NT-proBNP, N-terminal-pro-brain natriuretic peptide, TGF, transforming growth factor, TNF, tumor necrosis factor, UUO, unilateral ureteral obstruction, WT, wild type, eGFR, estimated glomerular filtration rate, fibrosis, heart failure, inflammation, macrophages, renal failure, AKI, acute kidney injury, BM, bone marrow, BUN, blood urea nitrogen, Cr, creatinine, Gal-3, galectin-3, ICAM, intercellular adhesion molecule, ICU, intensive care unit, IL, interleukin, IR, ischemia-reperfusion, KDIGO, Kidney Disease Improving Global Outcome, KO, knock-out, MCP, modified citrus pectin, NT-proBNP, N-terminal-pro-brain natriuretic peptide, TGF, transforming growth factor, TNF, tumor necrosis factor, UUO, unilateral ureteral obstruction, WT, wild type, eGFR, estimated glomerular filtration rate, Cardiorespiratory Medicine and Haematology, Clinical Sciences
Abstract

Acute kidney injury is associated with increased risk of heart failure and mortality. This study demonstrates that acute kidney injury induces remote cardiac dysfunction, damage, injury, and fibrosis via a galectin-3 (Gal-3) dependent pathway. Gal-3 originates from bone marrow-derived immune cells. Cardiac damage could be prevented by blocking this pathway.

Published
2019

7. Acute Kidney Injury Induces Remote Cardiac Damage and Dysfunction Through the Galectin-3 Pathway

Author

Prud’homme, Mathilde, Coutrot, Maxime, Michel, Thibault, Boutin, Louis, Genest, Magali, Poirier, Françoise, Launay, Jean-Marie, Kane, Bocar, Kinugasa, Satoshi, Prakoura, Niki, Vandermeersch, Sophie, Cohen-Solal, Alain, Delcayre, Claude, Samuel, Jane-Lise, Mehta, Ravindra, Gayat, Etienne, Mebazaa, Alexandre, Chadjichristos, Christos E, and Legrand, Matthieu

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Prevention, Cardiovascular, Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Renal and urogenital, Good Health and Well Being, fibrosis, heart failure, inflammation, macrophages, renal failure, AKI, acute kidney injury, BM, bone marrow, BUN, blood urea nitrogen, Cr, creatinine, Gal-3, galectin-3, ICAM, intercellular adhesion molecule, ICU, intensive care unit, IL, interleukin, IR, ischemia-reperfusion, KDIGO, Kidney Disease Improving Global Outcome, KO, knock-out, MCP, modified citrus pectin, NT-proBNP, N-terminal-pro-brain natriuretic peptide, TGF, transforming growth factor, TNF, tumor necrosis factor, UUO, unilateral ureteral obstruction, WT, wild type, eGFR, estimated glomerular filtration rate, Cardiorespiratory Medicine and Haematology, Cardiovascular medicine and haematology
Abstract

Acute kidney injury is associated with increased risk of heart failure and mortality. This study demonstrates that acute kidney injury induces remote cardiac dysfunction, damage, injury, and fibrosis via a galectin-3 (Gal-3) dependent pathway. Gal-3 originates from bone marrow-derived immune cells. Cardiac damage could be prevented by blocking this pathway.

Published
2019

9. Super‐resolved highly multiplexed immunofluorescence imaging for precise protein localization and podocyte ultrastructure.

Author

Siegerist, Florian, Kitzel, Svenja, Telli, Nihal, Dikou, Juan Saydou, Drenić, Vedran, Chadjichristos, Christos E., Chatziantoniou, Christos, and Endlich, Nicole

Subjects
OPTICAL resolution, OPTICAL limiting, MICROSCOPES, IMMUNOFLUORESCENCE, MICROSCOPY
Abstract

Deep insights into the complex cellular and molecular changes occurring during (patho‐)physiological conditions are essential for understanding the interactions and regulation of proteins. This understanding is crucial for research and diagnostics. However, the effectiveness of conventional immunofluorescence and light microscope, tools for visualizing the spatial distribution of cells or proteins, are limited both in resolution and multiplexity in complex tissues. This is mainly due to challenges such as the spectral overlap of fluorophore wavelengths, a limited range of antibody types, the inherent variability of samples and the optical resolution limit. The herein demonstrated combination of multiplex immunofluorescence imaging and super resolution microscopy offers a solution to these limitations by enabling the identification of different cell types and precise subcellular localization of proteins in tissue sections. In this study, we demonstrate the cyclic staining and de‐staining of paraffin kidney sections, making it suitable for routine use and compatible with super‐resolution microscopy for podocyte ultrastructural studies. We have further developed a computerized workflow for data processing which is accessible through available reagents and open‐access code. As a proof of principle, we identified CDH2 as a marker for cellular lesions of sclerotic glomeruli in the nephrotoxic serum nephritis mouse model and cross‐validated this finding with a human Nephroseq dataset indicating its translatability. In summary, our work represents an advance in multiplex imaging, which is crucial for understanding the localization of numerous proteins in a single FFPE kidney section and the compatibility with super‐resolution microscopy to study ultrastructural changes of podocytes. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

16. The Angiogenesis Inhibitor Isthmin-1 (ISM1) Is Overexpressed in Experimental Models of Glomerulopathy and Impairs the Viability of Podocytes

Author

Sahiri, Virgilia, primary, Caron, Jonathan, additional, Roger, Elena, additional, Desterke, Christophe, additional, Ghachem, Khalil, additional, Mohamadou, Inna, additional, Serre, Justine, additional, Prakoura, Niki, additional, Fellahi, Soraya, additional, Placier, Sandrine, additional, Adriouch, Sahil, additional, Zhang, Lu, additional, Chadjichristos, Christos E., additional, Chatziantoniou, Christos, additional, Lorenzo, Hans Kristian, additional, and Boffa, Jean-Jacques, additional

Published
2023
Full Text
View/download PDF

19. List of Contributors

Author

Abecassis, Michael, primary, Abed, Ahmed, additional, Abelli, Massimo, additional, Ahmad, Sarwat, additional, Alessiani, Mario, additional, Alsharidi, Aynaa, additional, Altruda, Fiorella, additional, Amorese, Gabriella, additional, Angeletti, Andrea, additional, Angelico, Mario, additional, Angelico, Roberta, additional, Angelotti, Maria L., additional, Applegate, Robert J., additional, Atala, Anthony, additional, Attanasio, Chiara, additional, Axelrod, David, additional, Bababekov, Yanik, additional, Basu, Joydeep, additional, Becherucci, Francesca, additional, Belford, P. Matthew, additional, Benedetti, Enrico, additional, Benedetti, Valentina, additional, Benigni, Ariela, additional, Bertram, Timothy A., additional, Bestard, Oriol, additional, Blake, Joshua, additional, Boggi, Ugo, additional, Brasile, Lauren, additional, Bromberg, Jonathan S., additional, Brouard, Sophie, additional, Brovold, Matthew, additional, Burke, George W., additional, Busic, Mirela, additional, Butt, Zeeshan, additional, Caddeo, Silvia, additional, Calzone, Stefano, additional, Campistol, Josep M., additional, Carmagnola, Irene, additional, Carty, Fiona, additional, Castanares-Zapatero, Diego, additional, Chadjichristos, Christos E., additional, Chambers, Brooke E., additional, Chandran, Sindhu, additional, Chatziantoniou, Christos, additional, Chen, Ashton, additional, Chen, Linda, additional, Chen, Xiwu, additional, Chiono, Valeria, additional, Chiusa, Manuel, additional, Ciancio, Gaetano, additional, Ciardelli, Gianluca, additional, Coletti, Gino, additional, Coll, Elisabeth, additional, Collienne, Christine, additional, Colvin, Robert B., additional, Cortinovis, Monica, additional, Cosimi, A. Benedict, additional, Cravedi, Paolo, additional, D’Amico, Giuseppe, additional, Da Sacco, Stefano, additional, Danger, Richard, additional, Dantal, Jacques, additional, Davidson, Alan J., additional, De Chiara, Letizia, additional, De Fijter, Johannes W., additional, de la Rosa, Gloria, additional, Delmonico, Francis L., additional, Deng, Junhong, additional, Deurdulian, Corinne, additional, Dhal, Abritee, additional, Dionigi, Paolo, additional, Domínguez-Gil, Beatriz, additional, Drozdzik, Marek, additional, Dussaule, Jean-Claude, additional, Edgar, Lauren, additional, Egidi, Maria Francesca, additional, El Hennawy, Hany, additional, English, Karen, additional, Everly, Matthew J., additional, Fagoonee, Sharmila, additional, Famulari, Elvira Smeralda, additional, Farney, Alan C., additional, Figliuzzi, Marina, additional, Framarino-dei-Malatesta, Marialuisa, additional, Fumo, David E., additional, Gagliardini, Elena, additional, Gallon, Lorenzo, additional, Gandhi, Sanjay K., additional, Gautreaux, Michael D., additional, Geraedts, Anna, additional, Giannese, Domenico, additional, Giulianotti, Pier C., additional, Goligorsky, Michael S., additional, Griesemar, Adam, additional, Grinyó, Josep M., additional, Gruessner, Angelika C., additional, Gruessner, Rainer W.G., additional, He, Bulang, additional, Heher, Eliot, additional, Ho, Bing, additional, Hosgood, Sarah A., additional, Hotta, Kiyohiko, additional, Humar, Atul, additional, Humes, H. David, additional, Iaria, Giuseppe, additional, Imberti, Barbara, additional, Izpisua Belmonte, Juan Carlos, additional, Jochmans, Ina, additional, Katari, Ravi, additional, Kavvadas, Panagiotis, additional, Kawai, Tatsuo, additional, Kengla, Carlos, additional, Keys, Tristan, additional, Kidiyoor, Amritha, additional, Kidokoro, Kengo, additional, Kumar, Deepali, additional, Kutcher, Michael A., additional, Lai, Quirino, additional, Laterre, Pierre-François, additional, Lebbé, Céleste, additional, Legendre, Christophe, additional, Lennon, Rachel, additional, Li, Peng, additional, Lin, Jen-Jar, additional, Little, Melissa H., additional, Lu, Xiongbing, additional, Ludlow, John W., additional, Mahíllo, Beatriz, additional, Masereeuw, Rosalinde, additional, Matesanz, Rafael, additional, Matovinovic, Mirjana S., additional, Mazzinghi, Benedetta, additional, Mbiandjeu Toya, Serge Cedrick, additional, McEwen, Scott, additional, Melandro, Fabio, additional, Melchiorri, Loredana, additional, Menon, Madhav C., additional, Mirzazadeh, Majid, additional, Montag, Samantha, additional, Montgomery, Robert A., additional, Montiel, Virginie, additional, Montserrat, Nuria, additional, Morigi, Marina, additional, Morrill, Christian C., additional, Mourad, Michel, additional, Murphy, Sean V., additional, Murray, Patricia, additional, Nardo, Tiziana, additional, Netti, Paolo A., additional, Nguyen, Mark, additional, Nicholson, Michael L., additional, O’Callaghan, John M., additional, Ohler, Linda, additional, Orlando, Giuseppe, additional, Osafune, Kenji, additional, Oura, Tetsu, additional, Peired, Anna, additional, Peloso, Andrea, additional, Peng, Zhenzhen, additional, Perico, Norberto, additional, Perin, Laura, additional, Perrone, Vittorio, additional, Persad, Paul, additional, Peti-Peterdi, János, additional, Petrosyan, Astgik, additional, Pietrabissa, Andrea, additional, Pino, Christopher J., additional, Pirenne, Jacques, additional, Pisani, Francesco, additional, Ploeg, Rutger J., additional, Porrini, Esteban, additional, Pozzi, Ambra, additional, Pugliese, Alberto, additional, Pugliese, Luigi, additional, Rabelink, Ton J., additional, Rampino, Teresa, additional, Rees, Michael A., additional, Reinders, Marlies E.J., additional, Remuzzi, Andrea, additional, Remuzzi, Giuseppe, additional, Riquier-Brison, Anne, additional, Roca, Raquel G., additional, Rogers, Jeffrey, additional, Romagnani, Paola, additional, Rosales, Ivy A., additional, Rosenblum, Norman D., additional, Rota, Cinzia, additional, Ruggenenti, Piero, additional, Ruini, Francesca, additional, Sageshima, Junichiro, additional, El Salem, Fadi, additional, Sandal, Shaifali, additional, Sander, Veronika, additional, Santeramo, Ilaria, additional, Santos, Renato M., additional, Sarwal, Minnie, additional, Shah, Jigesh, additional, Shetty, Aneesha A., additional, Silengo, Lorenzo, additional, Siskind, Eric, additional, Skaro, Anton, additional, Snanoudj, Renaud, additional, Soker, Shay, additional, South, Andrew M., additional, Spasovski, Goce, additional, Stratta, Robert J., additional, Strom, Charles, additional, Stubenitsky, Bart, additional, Tamburrini, Riccardo, additional, Tang, Qizhi, additional, Tantissattamo, Ekamol, additional, Tasaki, Masayuki, additional, Tchelepi, Hisham, additional, Ticozzelli, Elena, additional, Traitanon, Opas, additional, Trillini, Matias, additional, Tzvetanov, Ivo, additional, Valentín, María O., additional, Vincenti, Flavio, additional, Vistoli, Fabio, additional, Vriend, Jelle, additional, Walker, Stephen J., additional, Wertheim, Jason A., additional, Williams, David F., additional, Wilm, Bettina, additional, Wilmer, Martijn J., additional, Wingert, Rebecca A., additional, Wittebole, Xavier, additional, Xia, Yun, additional, Xinaris, Christodoulos, additional, Yamada, Kazuhiko, additional, Yokoo, Takashi, additional, Yokote, Shinya, additional, Zandvliet, Maarten L., additional, Zent, Roy, additional, Zhang, Yuanyuan, additional, Zhao, David X., additional, Zhao, Lihui, additional, and Zhao, Susan Y., additional

Published
2017
Full Text
View/download PDF

20. Reversibility of Renal Fibrosis

Author

Chadjichristos, Christos E., primary, Kavvadas, Panagiotis, additional, Dussaule, Jean-Claude, additional, Abed, Ahmed, additional, and Chatziantoniou, Christos, additional

Published
2017
Full Text
View/download PDF

21. Deletion of Notch3 Impairs Contractility of Renal Resistance Vessels Due to Deficient Ca2+ Entry

Author

Helle, Frank, Hultström, Michael, Kavvadas, Panagiotis, Iversen, Bjarne, Chadjichristos, Christos E., Chatziantoniou, Christos, Helle, Frank, Hultström, Michael, Kavvadas, Panagiotis, Iversen, Bjarne, Chadjichristos, Christos E., and Chatziantoniou, Christos

Abstract

Notch3 plays an important role in the differentiation and development of vascular smooth muscle cells. Mice lacking Notch3 show deficient renal autoregulation. The aim of the study was to investigate the mechanisms involved in the Notch3-mediated control of renal vascular response. To this end, renal resistance vessels (afferent arterioles) were isolated from Notch3(-/-) and wild-type littermates (WT) and stimulated with angiotensin II (ANG II). Contractions and intracellular Ca2+ concentrations were blunted in Notch3(-/-) vessels. ANG II responses in precapillary muscle arterioles were similar between the WT and Notch3(-/-) mice, suggesting a focal action of Notch3 in renal vasculature. Abolishing stored Ca2+ with thapsigargin reduced Ca2+ responses in the renal vessels of the two strains, signifying intact intracellular Ca2+ mobilization in Notch3(-/-). EGTA (Ca2+ chelating agent), nifedipine (L-type channel-blocker), or mibefradil (T-type channel-blocker) strongly reduced contraction and Ca2+ responses in WT mice but had no effect in Notch3(-/-) mice, indicating defective Ca2+ entry. Notch3(-/-) vessels responded normally to KCl-induced depolarization, which activates L-type channels directly. Differential transcriptomic analysis showed a major down-regulation of Cacna1h gene expression, coding for the alpha(1H) subunit of the T-type Ca2+ channel, in Notch3(-/-) vessels. In conclusion, renal resistance vessels from Notch3(-/-) mice display altered vascular reactivity to ANG II due to deficient Ca2+-entry. Consequently, Notch3 is essential for proper excitation-contraction coupling and vascular-tone regulation in the kidney.

Published
2022
Full Text
View/download PDF

24. Connexin 43: A target for the treatment of inflammation in secondary complications of the kidney and eye in diabetes

Author

Cliff, Chelsy L, Williams, Bethany, Chadjichristos, Christos E, Mouritzen, Ulrik, Squires, Paul E, and Hills, Claire E

Subjects
B210 Pharmacology, C130 Cell Biology, A100 Pre-clinical Medicine, B120 Physiology
Abstract

Of increasing prevalence, diabetes is characterised by elevated blood glucose and chronic inflammation that precedes the onset of multiple secondary complications, including those of the kidney and the eye. As the leading cause of end stage renal disease and blindness in the working population, more than ever is there a demand to develop clinical interventions which can both delay and prevent disease progression. Connexins are membrane bound proteins that can form pores (hemichannels) in the cell membrane. Gated by cellular stress and injury, they open under patho- physiological conditions and in doing so release ‘danger signals’ including adenosine triphosphate into the extracellular environment. Linked to sterile inflammation via activation of the nod-like receptor protein 3 inflammasome, targeting aberrant hemichannel activity and the release of these danger signals has met with favourable outcomes in multiple models of disease, including secondary complications of diabetes. In this review, we provide a comprehensive update on those studies which document a role for aberrant connexin hemichannel activity in the pathogenesis of both diabetic eye and kidney disease, ahead of evaluating the efficacy of blocking connexin-43 specific hemichannels in these target tissues on tissue health and function.

Published
2022

28. Deletion of Notch3 Impairs Contractility of Renal Resistance Vessels Due to Deficient Ca 2+ Entry.

Author

Helle, Frank, Hultström, Michael, Kavvadas, Panagiotis, Iversen, Bjarne, Chadjichristos, Christos E., and Chatziantoniou, Christos

Subjects
CALCIUM channels, VASCULAR smooth muscle, ANGIOTENSIN II, CHELATING agents, RENAL veins, MUSCLE cells
Abstract

Notch3 plays an important role in the differentiation and development of vascular smooth muscle cells. Mice lacking Notch3 show deficient renal autoregulation. The aim of the study was to investigate the mechanisms involved in the Notch3-mediated control of renal vascular response. To this end, renal resistance vessels (afferent arterioles) were isolated from Notch3−/− and wild-type littermates (WT) and stimulated with angiotensin II (ANG II). Contractions and intracellular Ca2+ concentrations were blunted in Notch3−/− vessels. ANG II responses in precapillary muscle arterioles were similar between the WT and Notch3−/− mice, suggesting a focal action of Notch3 in renal vasculature. Abolishing stored Ca2+ with thapsigargin reduced Ca2+ responses in the renal vessels of the two strains, signifying intact intracellular Ca2+ mobilization in Notch3−/−. EGTA (Ca2+ chelating agent), nifedipine (L-type channel-blocker), or mibefradil (T-type channel-blocker) strongly reduced contraction and Ca2+ responses in WT mice but had no effect in Notch3−/− mice, indicating defective Ca2+ entry. Notch3−/− vessels responded normally to KCl-induced depolarization, which activates L-type channels directly. Differential transcriptomic analysis showed a major down-regulation of Cacna1h gene expression, coding for the α1H subunit of the T-type Ca2+ channel, in Notch3−/− vessels. In conclusion, renal resistance vessels from Notch3−/− mice display altered vascular reactivity to ANG II due to deficient Ca2+-entry. Consequently, Notch3 is essential for proper excitation–contraction coupling and vascular-tone regulation in the kidney. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

34. MiR‐21 is up‐regulated in urinary exosomes of chronic kidney disease patients and after glomerular injury

Author

Lange, Tim, primary, Artelt, Nadine, additional, Kindt, Frances, additional, Stracke, Sylvia, additional, Rettig, Rainer, additional, Lendeckel, Uwe, additional, Chadjichristos, Christos E., additional, Kavvadas, Panagiotis, additional, Chatziantoniou, Christos, additional, Endlich, Karlhans, additional, and Endlich, Nicole, additional

Published
2019
Full Text
View/download PDF

37. The Role of Palladin in Podocytes

Author

Artelt, Nadine, primary, Ludwig, Tim A., additional, Rogge, Henrik, additional, Kavvadas, Panagiotis, additional, Siegerist, Florian, additional, Blumenthal, Antje, additional, van den Brandt, Jens, additional, Otey, Carol A., additional, Bang, Marie-Louise, additional, Amann, Kerstin, additional, Chadjichristos, Christos E., additional, Chatziantoniou, Christos, additional, Endlich, Karlhans, additional, and Endlich, Nicole, additional

Published
2018
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results