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27 results on '"Sweat, Yan"'

2. The enzyme glutamate-cysteine ligase (GCL) is a target for ferroptosis induction in cancer

Author

Eaton, John K, primary, Chatterji, Priya, additional, Furst, Laura, additional, Basak, Sneha, additional, Patel, Ayesha M, additional, Sweat, Yan Y, additional, Cai, Luke L, additional, Dave, Krishna, additional, Victoria, Rachelle A, additional, Pizzi, Elizabeth, additional, Noorbakhsh, Javad, additional, Tian, Gaochao, additional, Roth, Jennifer A S, additional, Hynes, John, additional, Xing, Gang, additional, Wawer, Mathias J, additional, and Viswanathan, Vasanthi S, additional

Published
2024
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3. Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis

Author

Oami, Takehiko, primary, Abtahi, Shabnam, additional, Shimazui, Takashi, additional, Chen, Ching-Wen, additional, Sweat, Yan Y., additional, Liang, Zhe, additional, Burd, Eileen M., additional, Farris, Alton B., additional, Roland, Joe T., additional, Tsukita, Sachiko, additional, Ford, Mandy L., additional, Turner, Jerrold R., additional, and Coopersmith, Craig M., additional

Published
2024
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4. Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis.

Author

Takehiko Oami, Shabnam Abtahi, Takashi Shimazui, Ching-Wen Chen, Sweat, Yan Y., Zhe Liang, Burd, Eileen M., Farris, Alton B., Roland, Joe T., Sachiko Tsukita, Ford, Mandy L., Turner, Jerrold R., and Coopersmith, Craig M.

Subjects
INTESTINAL barrier function, SEPSIS, DYSBIOSIS, TIGHT junctions, ASCITIC fluids, DENDRITIC cells
Abstract

Intestinal epithelial expression of the tight junction protein claudin-2, which forms paracellular cation and water channels, is precisely regulated during development and in disease. Here, we show that small intestinal epithelial claudin-2 expression is selectively upregulated in septic patients. Similar changes occurred in septic mice, where claudin-2 upregulation coincided with increased flux across the paracellular pore pathway. In order to define the significance of these changes, sepsis was induced in claudin-2 knockout (KO) and wild-type (WT) mice. Sepsis-induced increases in pore pathway permeability were prevented by claudin-2 KO. Moreover, claudin-2 deletion reduced interleukin-17 production and T cell activation and limited intestinal damage. These effects were associated with reduced numbers of neutrophils, macrophages, dendritic cells, and bacteria within the peritoneal fluid of septic claudin-2 KO mice. Most strikingly, claudin-2 deletion dramatically enhanced survival in sepsis. Finally, the microbial changes induced by sepsis were less pathogenic in claudin-2 KO mice as survival of healthy WT mice injected with cecal slurry collected from WT mice 24 h after sepsis was far worse than that of healthy WT mice injected with cecal slurry collected from claudin-2 KO mice 24 h after sepsis. Claudin-2 upregulation and increased pore pathway permeability are, therefore, key intermediates that contribute to development of dysbiosis, intestinal damage, inflammation, ineffective pathogen control, and increased mortality in sepsis. The striking impact of claudin-2 deletion on progression of the lethal cascade activated during sepsis suggests that claudin-2 may be an attractive therapeutic target in septic patients. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Serine 408 phosphorylation is a molecular switch that regulates structure and function of the occludin α-helical bundle

Author

Srivastava, Atul K., primary, Venkata, Bharat Somireddy, additional, Sweat, Yan Y., additional, Rizzo, Heather R., additional, Jean-François, Léa, additional, Zuo, Li, additional, Kurgan, Kathleen W., additional, Moore, Patrick, additional, Shashikanth, Nitesh, additional, Smok, Izabela, additional, Sachleben, Joseph R., additional, Turner, Jerrold R., additional, and Meredith, Stephen C., additional

Published
2022
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7. Tacrolimus-binding protein FKBP8 directs myosin light chain kinase-dependent barrier regulation and is a potential therapeutic target in Crohn's disease.

Author

Li Zuo, Wei-Ting Kuo, Feng Cao, Chanez-Paredes, Sandra D., Zeve, Daniel, Mannam, Prabhath, Jean-François, Léa, Day, Anne, Graham, W. Vallen, Sweat, Yan Y., Shashikanth, Nitesh, Breault, David T., and Turner, Jerrold R.

Subjects
CROHN'S disease, MYOSIN, MYOSIN light chain kinase, CYSTIC fibrosis transmembrane conductance regulator
Published
2023
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8. Tacrolimus-binding protein FKBP8 directs myosin light chain kinase-dependent barrier regulation and is a potential therapeutic target in Crohn’s disease

Author

Zuo, Li, primary, Kuo, Wei-Ting, additional, Cao, Feng, additional, Chanez-Paredes, Sandra D, additional, Zeve, Daniel, additional, Mannam, Prabhath, additional, Jean-François, Léa, additional, Day, Anne, additional, Vallen Graham, W, additional, Sweat, Yan Y, additional, Shashikanth, Nitesh, additional, Breault, David T, additional, and Turner, Jerrold R, additional

Published
2022
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11. Tacrolimus-binding protein FKBP8 directs myosin light chain kinase-dependent barrier regulation and is a potential therapeutic target in Crohn’s disease

Author

Zuo, Li, Kuo, Wei-Ting, Cao, Feng, Chanez-Paredes, Sandra D, Zeve, Daniel, Mannam, Prabhath, Jean-Francois, Léa, Day, Anne, Vallen Graham, W, Sweat, Yan Y, Shashikanth, Nitesh, Breault, David T, and Turner, Jerrold R

Abstract

ObjectiveIntestinal barrier loss is a Crohn’s disease (CD) risk factor. This may be related to increased expression and enzymatic activation of myosin light chain kinase 1 (MLCK1), which increases intestinal paracellular permeability and correlates with CD severity. Moreover, preclinical studies have shown that MLCK1 recruitment to cell junctions is required for tumour necrosis factor (TNF)-induced barrier loss as well as experimental inflammatory bowel disease progression. We sought to define mechanisms of MLCK1 recruitment and to target this process pharmacologically.DesignProtein interactions between FK506 binding protein 8 (FKBP8) and MLCK1 were assessed in vitro. Transgenic and knockout intestinal epithelial cell lines, human intestinal organoids, and mice were used as preclinical models. Discoveries were validated in biopsies from patients with CD and control subjects.ResultsMLCK1 interacted specifically with the tacrolimus-binding FKBP8 PPI domain. Knockout or dominant negative FKBP8 expression prevented TNF-induced MLCK1 recruitment and barrier loss in vitro. MLCK1-FKBP8 binding was blocked by tacrolimus, which reversed TNF-induced MLCK1-FKBP8 interactions, MLCK1 recruitment and barrier loss in vitro and in vivo. Biopsies of patient with CD demonstrated increased numbers of MLCK1-FKBP8 interactions at intercellular junctions relative to control subjects.ConclusionBinding to FKBP8, which can be blocked by tacrolimus, is required for MLCK1 recruitment to intercellular junctions and downstream events leading to immune-mediated barrier loss. The observed increases in MLCK1 activity, MLCK1 localisation at cell junctions and perijunctional MLCK1-FKBP8 interactions in CD suggest that targeting this process may be therapeutic in human disease. These new insights into mechanisms of disease-associated barrier loss provide a critical foundation for therapeutic exploitation of FKBP8-MLCK1 interactions.

Published
2023
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13. Gene-environment interaction in molar-incisor hypomineralization

Author

Bezamat, Mariana, primary, Souza, Juliana F., additional, Silva, Fernanda M. F., additional, Corrêa, Emilly G., additional, Fatturi, Aluhe L., additional, Brancher, João A., additional, Carvalho, Flávia M., additional, Cavallari, Tayla, additional, Bertolazo, Laís, additional, Machado-Souza, Cleber, additional, Koruyucu, Mine, additional, Bayram, Merve, additional, Racic, Andrea, additional, Harrison, Benjamin M., additional, Sweat, Yan Y., additional, Letra, Ariadne, additional, Studen-Pavlovich, Deborah, additional, Seymen, Figen, additional, Amendt, Brad, additional, Werneck, Renata I., additional, Costa, Marcelo C., additional, Modesto, Adriana, additional, and Vieira, Alexandre R., additional

Published
2021
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16. Six2 regulates Pax9 expression, palatogenesis and craniofacial bone formation

Author

Sweat, Yan Yan, primary, Sweat, Mason, additional, Mansaray, Maurisa, additional, Cao, Huojun, additional, Eliason, Steven, additional, Adeyemo, Waisu L., additional, Gowans, Lord J.J., additional, Eshete, Mekonen A., additional, Anand, Deepti, additional, Chalkley, Camille, additional, Saadi, Irfan, additional, Lachke, Salil A., additional, Butali, Azeez, additional, and Amendt, Brad A., additional

Published
2020
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20. The miR‐200family is required for ectodermal organ development through the regulation of the epithelial stem cell niche

Author

Sweat, Mason, Sweat, Yan, Yu, Wenjie, Su, Dan, Leonard, Riley J., Eliason, Steven L., and Amendt, Brad A.

Abstract

The murine lower incisor ectodermal organ contains a single epithelial stem cell (SC) niche that provides epithelial progenitor cells to the continuously growing rodent incisor. The dental stem cell niche gives rise to several cell types and we demonstrate that the miR‐200family regulates these cell fates. The miR‐200family is highly enriched in the differentiated dental epithelium and absent in the stem cell niche. In this study, we inhibited the miR‐200family in developing murine embryos using new technology, resulting in an expanded epithelial stem cell niche and lack of cell differentiation. Inhibition of individual miRs within the miR‐200cluster resulted in differential developmental and cell morphology defects. miR‐200inhibition increased the expression of dental epithelial stem cell markers, expanded the stem cell niche and decreased progenitor cell differentiation. RNA‐seq. identified miR‐200regulatory pathways involved in cell differentiation and compartmentalization of the stem cell niche. The miR‐200family regulates signaling pathways required for cell differentiation and cell cycle progression. The inhibition of miR‐200decreased the size of the lower incisor due to increased autophagy and cell death. New miR‐200targets demonstrate gene networks and pathways controlling cell differentiation and maintenance of the stem cell niche. This is the first report demonstrating how the miR‐200family is required for in vivo progenitor cell proliferation and differentiation. The LaCL stem cell niche does not express miR‐200, which regulates Sox2 expression. Progenitor cells exiting the stem cell niche start expressing miR‐200 to promote differentiation and the specification of cell fates for mature tooth development. miR‐200 therefore acts to compartmentalize the stem cell niche

Published
2021
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22. FoxO6 regulates Hippo signaling and growth of the craniofacial complex

Author

Sun, Zhao, primary, da Fontoura, Clarissa S. G., additional, Moreno, Myriam, additional, Holton, Nathan E., additional, Sweat, Mason, additional, Sweat, Yan, additional, Lee, Myoung Keun, additional, Arbon, Jed, additional, Bidlack, Felicitas B., additional, Thedens, Daniel R., additional, Nopoulos, Peggy, additional, Cao, Huojun, additional, Eliason, Steven, additional, Weinberg, Seth M., additional, Martin, James F., additional, Moreno-Uribe, Lina, additional, and Amendt, Brad A., additional

Published
2018
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26. miR-17 acts as a tumor suppressor by negatively regulating the miR-17-92 cluster.

Author

Sweat Y, Ries RJ, Sweat M, Su D, Shao F, Eliason S, and Amendt BA

Abstract

Anaplastic thyroid cancer (ATC) is an aggressive, highly metastatic cancer that expresses high levels of the microRNA ( miR)-17-92 cluster. We employ an miR inhibitor system to study the function of the different miRs within the miR-17-92 cluster based on seed sequence homology in the ATC SW579 cell line. While three of the four miR-17-92 families were oncogenic, we uncovered a novel role for miR-17 as a tumor suppressor in vitro and in vivo . Surprisingly, miR-17 inhibition increased expression of the miR-17-92 cluster and significantly increased the levels of the miR-18a and miR-19a mature miRs. miR-17 inhibition increased expression of the cell cycle activator CCND2, associated with increased cell proliferation and tumor growth in transplanted SW579 cells in xenograft mice. miR-17 regulates MYCN and c-MYC expression in SW579 cells, and the inhibition of miR-17 increased MYCN and c-MYC expression, which increased pri-miR-17-92 transcripts. Thus, inhibition of miR-17 activated the expression of the oncogenic miRs, miR-18a and miR-19a . While many cancers express high levels of miR-17 , linking it with tumorigenesis, we demonstrate that miR-17 inhibition does not inhibit thyroid tumor growth in SW579 and MDA-T32 ATC cells but increases expression of the other miR-17-92 family members and genes to induce cancer progression., Competing Interests: B.A.A. is the owner and Chief Scientific Officer of NaturemiRI, and PMIS microRNA inhibitors., (© 2021 The Author(s).)

Published
2021
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27. Pitx2-Sox2-Lef1 interactions specify progenitor oral/dental epithelial cell signaling centers.

Author

Yu W, Sun Z, Sweat Y, Sweat M, Venugopalan SR, Eliason S, Cao H, Paine ML, and Amendt BA

Subjects
Adaptor Proteins, Signal Transducing genetics, Adaptor Proteins, Signal Transducing metabolism, Animals, Cell Cycle Proteins genetics, Cell Cycle Proteins metabolism, Cell Differentiation, Cell Proliferation, Dental Enamel metabolism, Embryo, Mammalian metabolism, Epithelial Cells cytology, Gene Expression Regulation, Developmental, Hedgehog Proteins metabolism, Homeodomain Proteins genetics, Lymphoid Enhancer-Binding Factor 1 genetics, Mice, Mice, Knockout, Odontogenesis, SOXB1 Transcription Factors genetics, Stem Cell Niche, Stem Cells cytology, Stem Cells metabolism, Tooth cytology, Tooth growth & development, Tooth metabolism, Transcription Factors deficiency, Transcription Factors genetics, YAP-Signaling Proteins, Homeobox Protein PITX2, Epithelial Cells metabolism, Homeodomain Proteins metabolism, Lymphoid Enhancer-Binding Factor 1 metabolism, SOXB1 Transcription Factors metabolism, Signal Transduction, Transcription Factors metabolism
Abstract

Epithelial signaling centers control epithelial invagination and organ development, but how these centers are specified remains unclear. We report that Pitx2 (the first transcriptional marker for tooth development) controls the embryonic formation and patterning of epithelial signaling centers during incisor development. We demonstrate using Krt14 Cre / Pitx2 flox/flox ( Pitx2 cKO ) and Rosa26 CreERT /Pitx2 flox/flox mice that loss of Pitx2 delays epithelial invagination, and decreases progenitor cell proliferation and dental epithelium cell differentiation. Developmentally, Pitx2 regulates formation of the Sox2 + labial cervical loop (LaCL) stem cell niche in concert with two signaling centers: the initiation knot and enamel knot. The loss of Pitx2 disrupted the patterning of these two signaling centers, resulting in tooth arrest at E14.5. Mechanistically, Pitx2 transcriptional activity and DNA binding is inhibited by Sox2, and this interaction controls gene expression in specific Sox2 and Pitx2 co-expression progenitor cell domains. We demonstrate new transcriptional mechanisms regulating signaling centers by Pitx2 , Sox2 , Lef1 and Irx1 ., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

Published
2020
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