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Your search keyword '"Batourina, Ekatherina"' showing total 27 results
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27 results on '"Batourina, Ekatherina"'

1. Rosiglitazone and trametinib exhibit potent anti-tumor activity in a mouse model of muscle invasive bladder cancer

Author

Plumber, Sakina A., Tate, Tiffany, Al-Ahmadie, Hikmat, Chen, Xiao, Choi, Woonyoung, Basar, Merve, Lu, Chao, Viny, Aaron, Batourina, Ekatherina, Li, Jiaqi, Gretarsson, Kristjan, Alija, Besmira, Molotkov, Andrei, Wiessner, Gregory, Lee, Byron Hing Lung, McKiernan, James, McConkey, David J., Dinney, Colin, Czerniak, Bogdan, and Mendelsohn, Cathy Lee

Published
2024
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4. Retinoid Signaling in Progenitors Controls Specification and Regeneration of the Urothelium

Author

Gandhi, Devangini, Molotkov, Andrei, Batourina, Ekatherina, Schneider, Kerry, Dan, Hanbin, Reiley, Maia, Laufer, Ed, Metzger, Daniel, Liang, Fengxia, Liao, Yi, Sun, Tung-Tien, Aronow, Bruce, Rosen, Roni, Mauney, Josh, Adam, Rosalyn, Rosselot, Carolina, Van Batavia, Jason, McMahon, Andrew, McMahon, Jill, Guo, Jin-Jin, and Mendelsohn, Cathy

Subjects
Stem Cell Research, Urologic Diseases, Regenerative Medicine, Stem Cell Research - Nonembryonic - Non-Human, Animals, Biological Transport, Cell Differentiation, Epithelium, Gene Expression Regulation, Developmental, Humans, Keratin-5, Mice, Regeneration, Stem Cells, Urinary Tract, Uroplakins, Urothelium, Wound Healing, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

The urothelium is a multilayered epithelium that serves as a barrier between the urinary tract and blood, preventing the exchange of water and toxic substances. It consists of superficial cells specialized for synthesis and transport of uroplakins that assemble into a tough apical plaque, one or more layers of intermediate cells, and keratin 5-expressing basal cells (K5-BCs), which are considered to be progenitors in the urothelium and other specialized epithelia. Fate mapping, however, reveals that intermediate cells rather than K5-BCs are progenitors in the adult regenerating urothelium, that P cells, a transient population, are progenitors in the embryo, and that retinoids are critical in P cells and intermediate cells, respectively, for their specification during development and regeneration. These observations have important implications for tissue engineering and repair and, ultimately, may lead to treatments that prevent loss of the urothelial barrier, a major cause of voiding dysfunction and bladder pain syndrome.

Published
2013

5. Combined Mek inhibition and Pparg activation Eradicates Muscle Invasive Bladder cancer in a Mouse Model of BBN-induced Carcinogenesis

Author

Tate, Tiffany, primary, Plumber, Sakina Assiz, additional, Al-Ahmadie, Hikmat, additional, Chen, Xiaoi, additional, Choi, Woonyoung, additional, Lu, Chao, additional, Viny, Aaron D, additional, Batourina, Ekatherina, additional, Gretarsson, Kristjian, additional, Alija, Besmira, additional, Molotkov, Andrei, additional, Wiessner, Gregory, additional, Mckiernan, James M, additional, McConkey, David J, additional, Dinney, Colin, additional, Czerniak, Bogdan, additional, and Mendelsohn, Cathy Lee, additional

Published
2023
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12. An illustrated anatomical ontology of the developing mouse lower urogenital tract

Author

Georgas, Kylie M., primary, Armstrong, Jane, additional, Keast, Janet R., additional, Larkins, Christine E., additional, McHugh, Kirk M., additional, Southard-Smith, E. Michelle, additional, Cohn, Martin J., additional, Batourina, Ekatherina, additional, Dan, Hanbin, additional, Schneider, Kerry, additional, Buehler, Dennis P., additional, Wiese, Carrie B., additional, Brennan, Jane, additional, Davies, Jamie A., additional, Harding, Simon D., additional, Baldock, Richard A., additional, Little, Melissa H., additional, Vezina, Chad M., additional, and Mendelsohn, Cathy, additional

Published
2015
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14. Stromal Protein Ecm1 Regulates Ureteric Bud Patterning and Branching

Author

Paroly, Suneeta S., primary, Wang, Fengwei, additional, Spraggon, Lee, additional, Merregaert, Joseph, additional, Batourina, Ekatherina, additional, Tycko, Benjamin, additional, Schmidt-Ott, Kai M., additional, Grimmond, Sean, additional, Little, Melissa, additional, and Mendelsohn, Cathy, additional

Published
2013
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16. Non-cell-autonomous retinoid signaling is crucial for renal development

Author

Rosselot, Carolina, primary, Spraggon, Lee, additional, Chia, Ian, additional, Batourina, Ekatherina, additional, Riccio, Paul, additional, Lu, Benson, additional, Niederreither, Karen, additional, Dolle, Pascal, additional, Duester, Gregg, additional, Chambon, Pierre, additional, Costantini, Frank, additional, Gilbert, Thierry, additional, Molotkov, Andrei, additional, and Mendelsohn, Cathy, additional

Published
2010
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19. Apoptosis induced by vitamin A signaling is crucial for connecting the ureters to the bladder

Author

Batourina, Ekatherina, primary, Tsai, Sheaumei, additional, Lambert, Sarah, additional, Sprenkle, Preston, additional, Viana, Renata, additional, Dutta, Sonia, additional, Hensle, Terry, additional, Wang, Fengwei, additional, Niederreither, Karen, additional, McMahon, Andrew P, additional, Carroll, Thomas J, additional, and Mendelsohn, Cathy L, additional

Published
2005
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21. 1717: The Bladder Trigone is not a Wolffian Duct Remnant

Author

Sprenkle, Preston C., primary, Batourina, Ekatherina, additional, Tsai, Sheaumei, additional, Lambert, Sarah M., additional, Paragas, Neal, additional, Glassberg, Kenneth I., additional, Hensle, Terry W., additional, and Mendelsohn, Cathy L., additional

Published
2004
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24. Vitamin A controls epithelial/mesenchymal interactions through Ret expression.

Author

Batourina, Ekatherina, Gim, Suzanna, Bello, Natalie, Shy, Michael, Clagett-Dame, Margaret, Srinivas, Shankar, Costantini, Frank, and Mendelsohn, Cathy

Subjects
*KIDNEYS, *VITAMIN A, *GENE expression
Abstract

Mutations or rearrangements in the gene encoding the receptor tyrosine kinase RET result in Hirschsprung disease, cancer and renal malformations. The standard model of renal development involves reciprocal signaling between the ureteric bud epithelium, inducing metanephric mesenchyme to differentiate into nephrons, and metanephric mesenchyme, inducing the ureteric bud to grow and branch. RET and GDNF (a RET ligand) are essential mediators of these epithelial?mesenchymal interactions. Vitamin A deficiency has been associated with widespread embryonic abnormalities, including renal malformations. The vitamin A signal is transduced by nuclear retinoic acid receptors (RARs). We previously showed that two RAR genes, Rara and Rarb2, were colocalized in stromal mesenchyme, a third renal cell type, where their deletion led to altered stromal cell patterning, impaired ureteric bud growth and downregulation of Ret in the ureteric bud. Here we demonstrate that forced expression of Ret in mice deficient for both Rara and Rarb2 (Rara-/-Rarb2-/-) genetically rescues renal development, restoring ureteric bud growth and stromal cell patterning. Our studies indicate the presence of a new reciprocal signaling loop between the ureteric bud epithelium and the stromal mesenchyme, dependent on Ret and vitamin A. In the first part of the loop, vitamin-A?dependent signals secreted by stromal cells control Ret expression in the ureteric bud. In the second part of the loop, ureteric bud signals dependent on Ret control stromal cell patterning. [ABSTRACT FROM AUTHOR]

Published
2001
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25. Stromal cells mediate retinoid-dependent functions essential for renal development

Author

Mendelsohn, Cathy, Batourina, Ekatherina, Fung, Suquin, Gilbert, Thierry, and Dodd, Jane

Abstract

The essential role of vitamin A and its metabolites, retinoids, in kidney development has been demonstrated in vitamin A deficiency and gene targeting studies. Retinoids signal via nuclear transcription factors belonging to the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families. Inactivation of RARα and RARβ2 receptors together, but not singly, resulted in renal malformations, suggesting that within a given renal cell type, their concerted function is required for renal morphogenesis. At birth, RARαβ2−mutants displayed small kidneys, containing few ureteric bud branches, reduced numbers of nephrons and lacking the nephrogenic zone where new nephrons are continuously added. These observations have prompted us to investigate the role of RARα and RARβ2 in renal development in detail. We have found that within the embryonic kidney, RARα and RARβ2 are colocalized in stromal cells, but not in other renal cell types, suggesting that stromal cells mediate retinoid-dependent functions essential for renal development. Analysis of RARαβ2− mutant kidneys at embryonic stages revealed that nephrons were formed and revealed no changes in the intensity or distribution of molecular markers specific for different metanephric mesenchymal cell types. In contrast the development of the collecting duct system was greatly impaired in RARαβ2− mutant kidneys. Fewer ureteric bud branches were present, and ureteric bud ends were positioned abnormally, at a distance from the renal capsule. Analysis of genes important for ureteric bud morphogenesis revealed that the proto-oncogene c-ret was downregulated. Our results suggest that RARα and RARβ2 are required for generating stromal cell signals that maintain c-ret expression in the embryonic kidney. Since c-ret signaling is required for ureteric bud morphogenesis, loss of c-ret expression is a likely cause of impaired ureteric bud branching in RARαβ2− mutants.

Published
1999
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26. Polyploid Superficial Cells that Maintain the Urothelial Barrier Are Produced via Incomplete Cytokinesis and Endoreplication

Author

Wang, Jia, Batourina, Ekatherina, Schneider, Kerry, Souza, Spenser, Swayne, Theresa C., Liu, Chang, George, Christopher D., Tate, Tiffany, Dan, Hanbin, Wiessner, Gregory, Zhuravlev, Yelena, Canman, Julie, Mysorekar, Indira U., and Mendelsohn, Cathy Lee

Subjects
Polyploidy, Epithelium--Physiology, Molecular biology, Urology, Pathology, Cytokines--Immunology, 3. Good health
Abstract

The urothelium is an epithelia barrier lined by a luminal layer of binucleated, octoploid, superficial cells. Superficial cells are critical for production and transport of uroplakins, a family of proteins that assemble into a waterproof crystalline plaque that helps protect against infection and toxic substances. Adult urothelium is nearly quiescent, but rapidly regenerates in response to injury. Yet the mechanism by which binucleated, polyploid, superficial cells are produced remains unclear. Here, we show that superficial cells are likely to be derived from a population of binucleated intermediate cells, which are produced from mononucleated intermediate cells via incomplete cytokinesis. We show that binucleated intermediate and superficial cells increase DNA content via endoreplication, passing through S phase without entering mitosis. The urothelium can be permanently damaged by repetitive or chronic injury or disease. Identification of the mechanism by which superficial cells are produced may be important for developing strategies for urothelial repair.

27. Combined Mek inhibition and Pparg activation Eradicates Muscle Invasive Bladder cancer in a Mouse Model of BBN-induced Carcinogenesis.

Author

Tate T, Plumber SA, Al-Ahmadie H, Chen X, Choi W, Lu C, Viny A, Batourina E, Gartensson K, Alija B, Molotkov A, Wiessner G, McKiernan J, McConkey D, Dinney C, Czerniak B, and Mendelsohn CL

Abstract

Bladder cancers (BCs) can be divided into 2 major subgroups displaying distinct clinical behaviors and mutational profiles: basal/squamous (BASQ) tumors that tend to be muscle invasive, and luminal/papillary (LP) tumors that are exophytic and tend to be non-invasive. Pparg is a likely driver of LP BC and has been suggested to act as a tumor suppressor in BASQ tumors, where it is likely suppressed by MEK-dependent phosphorylation. Here we tested the effects of rosiglitazone, a Pparg agonist, in a mouse model of BBN-induced muscle invasive BC. Rosiglitazone activated Pparg signaling in suprabasal epithelial layers of tumors but not in basal-most layers containing highly proliferative invasive cells, reducing proliferation but not affecting tumor survival. Addition of trametinib, a MEK inhibitor, induced Pparg signaling throughout all tumor layers, and eradicated 91% of tumors within 7-days of treatment. The 2-drug combination also activated a luminal differentiation program, reversing squamous metaplasia in the urothelium of tumor-bearing mice. Paired ATAC-RNA-seq analysis revealed that tumor apoptosis was most likely linked to down-regulation of Bcl-2 and other pro-survival genes, while the shift from BASQ to luminal differentiation was associated with activation of the retinoic acid pathway and upregulation of Kdm6a, a lysine demethylase that facilitates retinoid-signaling. Our data suggest that rosiglitazone, trametinib, and retinoids, which are all FDA approved, may be clinically active in BASQ tumors in patients. That muscle invasive tumors are populated by basal and suprabasal cell types with different responsiveness to PPARG agonists will be an important consideration when designing new treatments.

Published
2023
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