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4. Knockdown of vimentin reduces mesenchymal phenotype of cholangiocytes in the Mdr2−/− mouse model of primary sclerosing cholangitis (PSC)

Author

Zhou, Tianhao, Kyritsi, Konstantina, Wu, Nan, Francis, Heather, Yang, Zhihong, Chen, Lixian, O'Brien, April, Kennedy, Lindsey, Ceci, Ludovica, Meadows, Vik, Kusumanchi, Praveen, Wu, Chaodong, Baiocchi, Leonardo, Skill, Nicholas J., Saxena, Romil, Sybenga, Amelia, Xie, Linglin, Liangpunsakul, Suthat, Meng, Fanyin, Alpini, Gianfranco, and Glaser, Shannon

Published
2019
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5. Pinealectomy or light exposure exacerbates biliary damage and liver fibrosis in cholestatic rats through decreased melatonin synthesis

Author

Chen, Lixian, Zhou, Tianhao, Wu, Nan, O'Brien, April, Venter, Julie, Ceci, Ludovica, Kyritsi, Konstantina, Onori, Paolo, Gaudio, Eugenio, Sybenga, Amelia, Xie, Linglin, Wu, Chaodong, Fabris, Luca, Invernizzi, Pietro, Zawieja, David, Liangpunsakul, Suthat, Meng, Fanyin, Francis, Heather, Alpini, Gianfranco, Huang, Qiaobing, and Glaser, Shannon

Published
2019
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8. Mainstreaming Countermemory: Tracing Marginalized Narratives Through Media Representations and Community-Engaged Memory Work.

Author

Cochran, Elliott and O'Brien, April L.

Subjects
MEMORY, NARRATIVES, COLLECTIVE memory
Abstract

This article seeks to determine how and why countermemory shifts from being a fringe narrative to being a part of the U.S.'s collective narrative. We establish two complementary-and often interlocking-reasons for this shift: 1) The role of media portrayals in film and series, and 2) The impact of grassroots community-engaged public memory efforts. In the examples we study, media portrayals preceded community-engaged memory work, but these findings must be analyzed in context with the community work as part of larger rhetorical ecologies. In our research, it becomes evident that media representations can initially inspire community interest, helping groups organize and craft memory sites to shift narratives within a larger socio-political context. [ABSTRACT FROM AUTHOR]

Published
2024

12. Lipocalin‐2 Stimulates Proliferation and a Profibrotic Cholangiocyte Phenotype during Cholestasis

Author

O'Brien, April, primary, Stiles, Danaleigh, additional, White, Tori, additional, Lopez, Matthew, additional, Little, Ashleigh, additional, Childs, Jonathan, additional, Douthitt, Ashley, additional, Phan, Thien, additional, Medford, Abigail, additional, Chen, Lixian, additional, Francis, Heather, additional, Alpini, Gianfranco, additional, Chakraborty, Sanjukta, additional, and Glaser, Shannon, additional

Published
2022
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13. FGF1 Signaling Modulates Biliary Injury and Liver Fibrosis in the Mdr2−/− Mouse Model of Primary Sclerosing Cholangitis

Author

O’Brien, April, primary, Zhou, Tianhao, additional, White, Tori, additional, Medford, Abigail, additional, Chen, Lixian, additional, Kyritsi, Konstantina, additional, Wu, Nan, additional, Childs, Jonathan, additional, Stiles, Danaleigh, additional, Ceci, Ludovica, additional, Chakraborty, Sanjukta, additional, Ekser, Burcin, additional, Baiocchi, Leonardo, additional, Carpino, Guido, additional, Gaudio, Eugenio, additional, Wu, Chaodong, additional, Kennedy, Lindsey, additional, Francis, Heather, additional, Alpini, Gianfranco, additional, and Glaser, Shannon, additional

Published
2022
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15. Recent Advances in Intrahepatic Biliary Epithelial Heterogeneity.

Author

Little, Ashleigh, Medford, Abigail, O'Brien, April, Childs, Jonathan, Pan, Sharon, Machado, Jolaine, Chakraborty, Sanjukta, and Glaser, Shannon

Subjects
BILIARY tract, BILE ducts, HETEROGENEITY, LIVER regeneration, LIVER cells
Abstract

Biliary epithelium (i.e., cholangiocytes) is a heterogeneous population of epithelial cells in the liver, which line small and large bile ducts and have individual responses and functions dependent on size and location in the biliary tract. We discuss the recent findings showing that the intrahepatic biliary tree is heterogeneous regarding (1) morphology and function, (2) hormone expression and signaling (3), response to injury, and (4) roles in liver regeneration. This review overviews the significant characteristics and differences of the small and large cholangiocytes. Briefly, it outlines the in vitro and in vivo models used in the heterogeneity evaluation. In conclusion, future studies addressing biliary heterogeneity's role in the pathogenesis of liver diseases characterized by ductular reaction may reveal novel therapeutic approaches. [ABSTRACT FROM AUTHOR]

Published
2023
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16. Tumor Lymphatic Interactions Induce CXCR2-CXCL5 Axis and Alter Cellular Metabolism and Lymphangiogenic Pathways to Promote Cholangiocarcinoma

Author

Roy, Sukanya, primary, Kumaravel, Subhashree, additional, Banerjee, Priyanka, additional, White, Tori K., additional, O’Brien, April, additional, Seelig, Catherine, additional, Chauhan, Rahul, additional, Ekser, Burcin, additional, Bayless, Kayla J., additional, Alpini, Gianfranco, additional, Glaser, Shannon S., additional, and Chakraborty, Sanjukta, additional

Published
2021
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18. The Apelin–Apelin Receptor Axis Triggers Cholangiocyte Proliferation and Liver Fibrosis During Mouse Models of Cholestasis

Author

Chen, Lixian, primary, Zhou, Tianhao, additional, White, Tori, additional, O'Brien, April, additional, Chakraborty, Sanjukta, additional, Liangpunsakul, Suthat, additional, Yang, Zhihong, additional, Kennedy, Lindsey, additional, Saxena, Romil, additional, Wu, Chaodong, additional, Meng, Fanyin, additional, Huang, Qiaobing, additional, Francis, Heather, additional, Alpini, Gianfranco, additional, and Glaser, Shannon, additional

Published
2021
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19. Fr382 TUMOR-LYMPHATIC INTERACTIONS IN AN INFLAMED MICROENVIRONMENT ACTIVATES CXCR2-CXCL5-YAP SIGNALING AXIS AND ENHANCES LYMPHANGIOGENESIS AND TUMOR MIGRATION IN CHOLANGIOCARCINOMA

Author

Roy, Sukanya, primary, Kumaravel, Subhashree, additional, White, Tori, additional, O'Brien, April, additional, Seelig, Catherine, additional, Chauhan, Rahul, additional, Ekser, Burcin, additional, Alpini, Gianfranco, additional, Glaser, Shannon S., additional, and Chakraborty, Sanjukta, additional

Published
2021
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20. FGF1 Signaling Modulates Biliary Injury and Liver Fibrosis in the Mdr2−/− Mouse Model of Primary Sclerosing Cholangitis.

Author

O'Brien, April, Zhou, Tianhao, White, Tori, Medford, Abigail, Chen, Lixian, Kyritsi, Konstantina, Wu, Nan, Childs, Jonathan, Stiles, Danaleigh, Ceci, Ludovica, Chakraborty, Sanjukta, Ekser, Burcin, Baiocchi, Leonardo, Carpino, Guido, Gaudio, Eugenio, Wu, Chaodong, Kennedy, Lindsey, Francis, Heather, Alpini, Gianfranco, and Glaser, Shannon

Subjects
CHOLANGITIS, FIBROBLAST growth factor receptors, INTRAHEPATIC bile ducts, FIBROBLAST growth factors, HEPATIC fibrosis, LABORATORY mice, CD20 antigen
Abstract

Fibroblast growth factor 1 (FGF1) belongs to a family of growth factors involved in cellular growth and division. MicroRNA 16 (miR‐16) is a regulator of gene expression, which is dysregulated during liver injury and insult. However, the role of FGF1 in the progression of biliary proliferation, senescence, fibrosis, inflammation, angiogenesis, and its potential interaction with miR‐16, are unknown. In vivo studies were performed in male bile duct–ligated (BDL, 12‐week‐old) mice, multidrug resistance 2 knockout (Mdr2−/−) mice (10‐week‐old), and their corresponding controls, treated with recombinant human FGF1 (rhFGF1), fibroblast growth factor receptor (FGFR) antagonist (AZD4547), or anti‐FGF1 monoclonal antibody (mAb). In vitro, the human cholangiocyte cell line (H69) and human hepatic stellate cells (HSCs) were used to determine the expression of proliferation, fibrosis, angiogenesis, and inflammatory genes following rhFGF1 treatment. PSC patient and control livers were used to evaluate FGF1 and miR‐16 expression. Intrahepatic bile duct mass (IBDM), along with hepatic fibrosis and inflammation, increased in BDL mice treated with rhFGF1, with a corresponding decrease in miR‐16, while treatment with AZD4547 or anti‐FGF1 mAb decreased hepatic fibrosis, IBDM, and inflammation in BDL and Mdr2−/− mice. In vitro, H69 and HSCs treated with rhFGF1 had increased expression of proliferation, fibrosis, and inflammatory markers. PSC samples also showed increased FGF1 and FGFRs with corresponding decreases in miR‐16 compared with healthy controls. Conclusion: Our study demonstrates that suppression of FGF1 and miR‐16 signaling decreases the presence of hepatic fibrosis, biliary proliferation, inflammation, senescence, and angiogenesis. Targeting the FGF1 and miR‐16 axis may provide therapeutic options in treating cholangiopathies such as PSC. [ABSTRACT FROM AUTHOR]

Published
2022
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22. 216 MELATONIN MODULATES STIMULATOR OF INTERFERON GENES (STING) ACTIVATION IN THE MDR2-/-MOUSE MODEL OF PRIMARY SCLEROSING CHOLANGITIS (PSC)

Author

Zhou, Tianhao, primary, Wu, Nan, additional, Chen, Lixian, additional, Ceci, Ludovica, additional, O'Brien, April, additional, White, Tori, additional, Kennedy, Lindsey, additional, Wu, Chaodong, additional, Meng, Fanyin, additional, Francis, Heather L., additional, Alpini, Gianfranco, additional, and Glaser, Shannon S., additional

Published
2020
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23. 454 LONG-TERM ADMINISTRATION OF THE SECRETIN RECEPTOR ANTAGONIST, SCT 5-27, INHIBITS BILIARY SENESCENCE AND LIVER FIBROSIS OF PRIMARY SCLEROSING CHOLANGITIS (PSC) IN THE MDR2-/- MOUSE MODEL.

Author

Wu, Nan, primary, Kennedy, Lindsey, additional, Zhou, Tianhao, additional, Kyritsi, Konstantina, additional, Chen, Lixian, additional, Ceci, Ludovica, additional, Grumbles, Kassidy, additional, Francis, Heather L., additional, Meadows, Vik, additional, Meng, Fanyin, additional, Ekser, Burcin, additional, O'Brien, April, additional, Rivosecchi-Fulton, Jessica, additional, Onori, Paolo, additional, Gaudio, Eugenio, additional, White, Tori, additional, Glaser, Shannon S., additional, and Alpini, Gianfranco, additional

Published
2020
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27. Exclusionary Public Memory Documents: Orientating Historical Marker Texts within a Technical Communication Framework.

Author

O'Brien, April L.

Subjects
*COLLECTIVE memory, *HISTORICAL markers, *COMMUNICATION of technical information, *HISTORICAL source material, *WHITE supremacy
Abstract

This paper theorizes historical marker texts (HMT) as succinct, public facing informational reports that reinforce white supremacy and minimize or erase the memory of Black, Indigenous, and people of color (BIPOC) individuals. In this layered content and discourse analysis, I evaluate the demographics of the commissioners at the local and state level, the instructions for the HMT application, and the text of a selected group of HMTs. [ABSTRACT FROM AUTHOR]

Published
2022
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28. Mission Possible

Author

O'Brien, April C.

Subjects
Eastern State Penitentiary of Pennsylvania, Museums--Membership, social cause mission, mission-change
Abstract

The museum membership field has evolved over the course of the last century by creating more affordable and accessible membership levels and benefit packages. As museums continue to work to expand their reach by addressing social causes and injustices on a national and international scale, the effects of the change on the current membership model is unclear. Membership is often viewed as an administrative function, relying heavily on marketing techniques. This paper explores a case study of one museum in the midst of a mission-change, Eastern State Penitentiary Historic Site. Semi-structured interviews of the institution’s members and non-members revealed an unending curiosity and intrigue of Eastern State’s initiatives and future. Yet interviewees struggled to articulate a clear reason for their intrigue. Interviewees also lacked a direct interest in the museum’s new mission through membership. Instead, traditional motivators to become a member emerged such as association, access and value. In summary, a museum’s mission change might not have a considerable impact on the museum’s members and non-members based on the traditional administrative role membership continues to play in the museum. This paper serves a foundation for all museum membership programs of institutions considering a change in direction or mission.

Published
2020
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30. Modulation of the Tryptophan Hydroxylase 1/Monoamine Oxidase‐A/5‐Hydroxytryptamine/5‐Hydroxytryptamine Receptor 2A/2B/2C Axis Regulates Biliary Proliferation and Liver Fibrosis During Cholestasis

Author

Kyritsi, Konstantina, primary, Chen, Lixian, additional, O’Brien, April, additional, Francis, Heather, additional, Hein, Travis W., additional, Venter, Julie, additional, Wu, Nan, additional, Ceci, Ludovica, additional, Zhou, Tianhao, additional, Zawieja, David, additional, Gashev, Anatoliy A., additional, Meng, Fanyin, additional, Invernizzi, Pietro, additional, Fabris, Luca, additional, Wu, Chaodong, additional, Skill, Nicholas J., additional, Saxena, Romil, additional, Liangpunsakul, Suthat, additional, Alpini, Gianfranco, additional, and Glaser, Shannon S., additional

Published
2019
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31. Mo1428 – Role of the Aanat/Melatonin/Mt1/Mt2/Per-1 Axis in the Regulation of Biliary Damage and Liver Fibrosis in Cholestatic Mice

Author

Ceci, Ludovica, primary, Wu, Nan, additional, Chen, Lixian, additional, O'Brien, April, additional, Zhou, Tianhao, additional, Kennedy, Lindsey, additional, Kyritsi, Konstantina, additional, Gaudio, Eugenio, additional, Venter, Julie, additional, Meng, Fanyin, additional, Onori, Paolo, additional, Francis, Heather L., additional, Glaser, Shannon, additional, and Alpini, Gianfranco, additional

Published
2019
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33. Modulation of the Tryptophan Hydroxylase 1/Monoamine Oxidase‐A/5‐Hydroxytryptamine/5‐Hydroxytryptamine Receptor 2A/2B/2C Axis Regulates Biliary Proliferation and Liver Fibrosis During Cholestasis.

Author

Kyritsi, Konstantina, Chen, Lixian, O'Brien, April, Francis, Heather, Hein, Travis W., Venter, Julie, Wu, Nan, Ceci, Ludovica, Zhou, Tianhao, Zawieja, David, Gashev, Anatoliy A., Meng, Fanyin, Invernizzi, Pietro, Fabris, Luca, Wu, Chaodong, Skill, Nicholas J., Saxena, Romil, Liangpunsakul, Suthat, Alpini, Gianfranco, and Glaser, Shannon S.

Published
2020
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34. α7-nAChR Knockout Mice Decreases Biliary Hyperplasia and Liver Fibrosis in Cholestatic Bile Duct-Ligated Mice

Author

Ehrlich, Laurent, primary, O’Brien, April, additional, Hall, Chad, additional, White, Tori, additional, Chen, Lixian, additional, Wu, Nan, additional, Venter, Julie, additional, Scrushy, Marinda, additional, Mubarak, Muhammad, additional, Meng, Fanyin, additional, Dostal, David, additional, Wu, Chaodong, additional, Lairmore, Terry C., additional, Alpini, Gianfranco, additional, and Glaser, Shannon, additional

Published
2018
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36. Mo1377 - Pinealectomy Exacerbates Biliary Proliferation and Senescence and Liver Fibrosis During Rat Cholestatic Liver Through Decreased Biliary Melatonin Synthesis

Author

Chen, Lixian, primary, White, Tori, additional, Venter, Julie, additional, Ehrlich, Laurent, additional, O'Brien, April, additional, Nguyen, Anh-Vu V., additional, Wu, Nan, additional, Kyritsi, Konstantina, additional, Han, Yuyan, additional, Huang, Qiaobing, additional, Meng, Fanyin, additional, Alpini, Gianfranco, additional, Zhou, Tianhao, additional, and Glaser, Shannon, additional

Published
2018
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46. Role of Non-Coding RNAs in the Progression of Liver Cancer: Evidence from Experimental Models.

Author

O'Brien, April, Zhou, Tianhao, Tan, Christopher, Alpini, Gianfranco, and Glaser, Shannon

Subjects
*RNA analysis, *BIOLOGICAL models, *CELL cycle, *CELL lines, *CELLULAR signal transduction, *GENE expression, *HEPATOCELLULAR carcinoma, *LIVER tumors, *DISEASE progression
Abstract

Liver cancer is a devastating cancer that ranges from relatively rare (around 2% of all cancers in the United States) to commonplace (up to 50% of cancers in underdeveloped countries). Depending upon the stage of pathogenesis, prognosis, or functional liver tissue present, transplantation or partial hepatectomy may be the only available treatment option. However, due to the rise in metabolic syndrome and the increasing demand for livers, patients often wait months or years for available organs. Due to this shortage, doctors must have other treatment options available. One promising area of cancer research lies in understanding the role of regulatory non-coding RNAs (ncRNAs) as oncogenic drivers and potential targets for prospective therapies. While the role of these ncRNAs was not initially clear, many of them have since been recognized to function as important players in the regulation of gene expression, epigenetic modification, and signal transduction in both normal and cancer cell cycles. Dysregulation of these different ncRNA subtypes has been implicated in the pathogenesis and progression of many major cancers including hepatocellular carcinoma. This review summarizes current findings on the roles noncoding RNAs play in the progression of liver cancer and the various animal models used in current research to elucidate those data. [ABSTRACT FROM AUTHOR]

Published
2019
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47. FGF1 Signaling Modulates Biliary Injury and Liver Fibrosis in the Mdr2 -/- Mouse Model of Primary Sclerosing Cholangitis.

Author

O'Brien A, Zhou T, White T, Medford A, Chen L, Kyritsi K, Wu N, Childs J, Stiles D, Ceci L, Chakraborty S, Ekser B, Baiocchi L, Carpino G, Gaudio E, Wu C, Kennedy L, Francis H, Alpini G, and Glaser S

Subjects
ATP Binding Cassette Transporter, Subfamily B metabolism, Animals, Disease Models, Animal, Fibroblast Growth Factor 1 genetics, Fibrosis, Humans, Inflammation, Liver Cirrhosis drug therapy, Male, Mice, Mice, Knockout, ATP-Binding Cassette Sub-Family B Member 4, Cholangitis, Sclerosing drug therapy, MicroRNAs genetics
Abstract

Fibroblast growth factor 1 (FGF1) belongs to a family of growth factors involved in cellular growth and division. MicroRNA 16 (miR-16) is a regulator of gene expression, which is dysregulated during liver injury and insult. However, the role of FGF1 in the progression of biliary proliferation, senescence, fibrosis, inflammation, angiogenesis, and its potential interaction with miR-16, are unknown. In vivo studies were performed in male bile duct-ligated (BDL, 12-week-old) mice, multidrug resistance 2 knockout (Mdr2 -/-) mice (10-week-old), and their corresponding controls, treated with recombinant human FGF1 (rhFGF1), fibroblast growth factor receptor (FGFR) antagonist (AZD4547), or anti-FGF1 monoclonal antibody (mAb). In vitro, the human cholangiocyte cell line (H69) and human hepatic stellate cells (HSCs) were used to determine the expression of proliferation, fibrosis, angiogenesis, and inflammatory genes following rhFGF1 treatment. PSC patient and control livers were used to evaluate FGF1 and miR-16 expression. Intrahepatic bile duct mass (IBDM), along with hepatic fibrosis and inflammation, increased in BDL mice treated with rhFGF1, with a corresponding decrease in miR-16, while treatment with AZD4547 or anti-FGF1 mAb decreased hepatic fibrosis, IBDM, and inflammation in BDL and Mdr2 -/- mice. In vitro, H69 and HSCs treated with rhFGF1 had increased expression of proliferation, fibrosis, and inflammatory markers. PSC samples also showed increased FGF1 and FGFRs with corresponding decreases in miR-16 compared with healthy controls. Conclusion: Our study demonstrates that suppression of FGF1 and miR-16 signaling decreases the presence of hepatic fibrosis, biliary proliferation, inflammation, senescence, and angiogenesis. Targeting the FGF1 and miR-16 axis may provide therapeutic options in treating cholangiopathies such as PSC., (© 2022 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of American Association for the Study of Liver Diseases.)

Published
2022
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