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Your search keyword '"De Paepe, Monique E."' showing total 330 results
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330 results on '"De Paepe, Monique E."'

1. Preexisting maternal immunity to AAV but not Cas9 impairs in utero gene editing in mice

Author

Riley, John S., Luks, Valerie L., Berkowitz, Cara L., Dumitru, Ana Maria, Kus, Nicole J., Dave, Apeksha, Menon, Pallavi, De Paepe, Monique E., Jain, Rajan, Li, Li, Dugoff, Lorraine, Teefey, Christina Paidas, Alameh, Mohamad-Gabriel, Zoltick, Philip W., and Peranteau, William H.

Subjects
Immunological research, Dependoviruses -- Research, Immunity -- Genetic aspects, Genetic vectors -- Research, Liver diseases -- Risk factors -- Models, Prenatal influences -- Genetic aspects -- Health aspects, Health care industry
Abstract

In utero gene editing (IUGE) is a potential treatment for inherited diseases that cause pathology before or soon after birth. Preexisting immunity to adeno-associated virus (AAV) vectors and Cas9 endonuclease may limit postnatal gene editing. The tolerogenic fetal immune system minimizes a fetal immune barrier to IUGE. However, the ability of maternal immunity to limit fetal gene editing remains a question. We investigated whether preexisting maternal immunity to AAV or Cas9 impairs IUGE. Using a combination of fluorescent reporter mice and a murine model of a metabolic liver disease, we demonstrated that maternal anti-AAV IgG antibodies were efficiently transferred from dam to fetus and impaired IUGE in a maternal titer-dependent fashion. By contrast, maternal cellular immunity was inefficiently transferred to the fetus, and neither maternal cellular nor humoral immunity to Cas9 impaired IUGE. Using human umbilical cord and maternal blood samples collected from mid- to late-gestation pregnancies, we demonstrated that maternal-fetal transmission of anti-AAV IgG was inefficient in midgestation compared with term, suggesting that the maternal immune barrier to clinical IUGE would be less relevant at midgestation. These findings support immunologic advantages for IUGE and inform maternal preprocedural testing protocols and exclusion criteria for future clinical trials., Introduction In utero gene editing (IUGE) is a potential treatment for inherited diseases that takes advantage of normal fetal developmental properties to institute the therapy before the onset of pathology. [...]

Published
2024
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29. Hyperoxia-induced apoptosis and Fas/FasL expression in lung epithelial cells

Author

De Paepe, Monique E., Mao, Quanfu, Chao, Yvonne, Powell, Jessica L., Rubin, Lewis P., and Sharma, Surendra

Subjects
Apoptosis -- Research, Epithelial cells -- Research, Lungs -- Research, Biological sciences
Abstract

Alveolar epithelial apoptosis is an important feature of hyperoxia-induced lung injury in vivo and has been described in the early stages of bronchopulmonary dysplasia (chronic lung disease of preterm newborn). Molecular regulation of hyperoxia-induced alveolar epithelial cell death remains incompletely understood. In view of functional involvement of Fas/FasL system in physiological postcanalicular type II cell apoptosis, we speculated this system may also be a critical regulator of hyperoxia-induced apoptosis. The aim of this study was to investigate the effects of hyperoxia on apoptosis and apoptotic gene expression in alveolar epithelial cells. Apoptosis was studied by TUNEL, electron microscopy, DNA size analysis, and caspase assays. Fas/FasL expression was determined by Western blot analysis and RPA. We determined that in MLE-12 cells exposed to hyperoxia, caspase-mediated apoptosis was the first morphologically and biochemically recognizable mode of cell death, followed by necrosis of residual adherent cells. The apoptotic stage was associated with a threefold upregulation of Fas mRNA and protein expression and increased susceptibility to direct Fas receptor activation, concomitant with a threefold increase of FasL protein levels. Fas gene silencing by siRNAs significantly reduced hyperoxia-induced apoptosis. In murine fetal type II cells, hyperoxia similarly induced markedly increased Fas/FasL protein expression, confirming validity of results obtained in transformed MLE-12 cells. Our findings implicate the Fas/FasL system as an important regulator of hyperoxia-induced type II cell apoptosis. Elucidation of regulation of hyperoxia-induced lung apoptosis may lead to alternative therapeutic strategies for perinatal or adult pulmonary diseases characterized by dysregulated type II cell apoptosis. programmed cell death; bronchopulmonary dysplasia; chronic lung disease; oxygen; alveolar epithelial type II cell

Published
2005

32. Fas/FasL-mediated apoptosis in perinatal murine lungs

Author

De Paepe, Monique E., Mao, Quanfu, Embree-Ku, Michelle, Rubin, Lewis P., and Luks, Francois I.

Subjects
Lungs -- Research, Apoptosis -- Research, Biological sciences
Abstract

Fas/FasL-mediated apoptosis in perinatal murine lungs. Am J Physiol Lung Cell Mol Physiol 287: L730-L742, 2004; 10.1152/ajplung.00120.2004.--Postcanalicular lung development is characterized by a time-specific increase in alveolar epithelial type II cell apoptosis. We have previously demonstrated that, in fetal rabbits, developmental type II cell apoptosis coincides with transient upregulation of the cell death regulator Fas ligand (FasL). The aims of this study were 1) to determine the spatiotemporal patterns of pulmonary apoptosis and Fas/FasL gene expression in the murine model [embryonic day 17 (E17) through postnatal day 5 (P5)], and 2) to investigate the functional involvement of the Fas/FasL system by determining the effect of Fas activation and inhibition on perinatal pulmonary apoptosis. The apoptotic activity of alveolar epithelial type II cells, determined by combined TUNEL labeling and anti-surfactant protein B immunohistochemistry, showed a dramatic increase during the perinatal transition (type II cell apoptotic index programmed cell death: lpr; CD95; lung development

Published
2004

36. Contributors

Author

Abdel-Razeq, Sonya S., Abrahams, Vikki M., Abu-Rustum, Reem S., Alshawabkeh, Laith, Aminoff, Michael J., Bahtiyar, Mert Ozan, Bairey Merz, C. Noel, Barbour, Linda A., Beall, Marie H., Beigi, Richard, Berghella, Vincenzo, Bixel, Kristin, Blanchard, Daniel G., Bodnar, Lisa M., Boelig, Rupsa C., Brady, Jennifer M., Branch, D. Ware, Bromley, Bryann, Buhimschi, Catalin S., Cambou, Mary Catherine, Campbell, Katherine Harper, Catalano, Patrick, Catov, Janet M., Chambers, Christina, Christian, Beth, Chung, Rebecca K., Cohn, David E., Copel, Joshua A., D’Alton, Mary E., Daniels, Lori B., De Paepe, Monique E., Douglas, Vanja C., Duff, Patrick, Dugoff, Lorraine, Fineman, Jeffrey R., Forray, Ariadna, Friedman, Jan M., Froehlich, Rosemary J., Ghidini, Alessandro, Gibson, Kelly S., Gilner, Jennifer, Grantz, Katherine Laughon, Greenberg, James M., Gregg, Anthony R., Grobman, William, Haberman, Beth B., Halscott, Torre L., Han, Christina S., Harper, Lorie M., Hawkins, Joy L., Heine, Robert Phillips, Himes, Katherine P., Hull, Andrew D., Humphreys, Meredith A., Kaimal, Anjali J., Karumanchi, S. Ananth, Keely, Erin, Kelly, Thomas F., Kennedy, Anne, Khan, Aliya, Kilpatrick, Sarah J., Kitahara, Sumire, Kominiarek, Michelle A., Kuller, Jeffrey A., LaCoursiere, D. Yvette, Lapinsky, Stephen R., Lawrence, Robert M., Lawrence, Ruth A., Leung, Ann, Lim, Ming Y., Liu, James H., Louis-Jacques, Adetola, Lye, Stephen J., Macones, George A., Mahendroo, Mala, Malone, Fergal D., Maltepe, Emin, Mari, Giancarlo, Mastrobattista, Joan M., McAdow, Molly, Megli, Christina J., Mercer, Brian M., Meschia, Giacomo, Mesiano, Sam, Metz, Torri D., Moise, Kenneth J., Jr., Monga, Manju, Montaney, Laura A., Monteagudo, Ana, Moore, Thomas R., Mor, Gil, Muglia, Louis J., Nageotte, Michael P., Narendran, Vivek, Nathan, Amy T., Nielsen-Saines, Karin, Nitsche, Joshua F., Običan, Sarah Gloria, Odibo, Anthony O., Paidas, Michael, Parast, Mana M., Pettker, Christian, Pippen, Jessica L., Plante, Lauren A., Powe, Camille E., Pretorius, Dolores H., Queenan, John, Rajkovic, Aleksandar, Ramaswamy, Bhuvaneswari, Rapini, Ronald P., Reddy, Uma M., Resnik, Robert, Roberts, Drucilla J., Ross, Michael G., Salmon, Jane E., Sammaritano, Lisa Rose, Savides, Thomas J., Sfakianaki, Anna Katerina, Shipp, Thomas D., Shrivastava, Vineet K., Silver, Robert M., Simhan, Hyagriv N., Sklansky, Mark Steven, Smid, Marcela C., Sottile, Peter, Terplan, Mishka, Thadhani, Ravi I., Thorp, John M., Jr., Timor-Tritsch, Ilan E., Tita, Alan, Tuuli, Methodius G., Valent, Amy M., Vaught, Arthur Jason, Wapner, Ronald J., Wilkening, Randall B., Wilkins, Isabelle, Wolf, Richard B., Woodward, Paula J., Wylie, Blair J., Yonkers, Kimberly A., and Young, Brett C.

Published
2023
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