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Dr. Pauline J.に依頼

France

Scientific & Medical Writing Expert | PhD in Life Sciences

プロフィール概要

I am a PhD-qualified scientist in Pharmaceutical Sciences with a strong background in biochemistry, molecular and cellular biology. My research focused on pre-clinical and translational models of cancer, inflammation, and neuro-immune interactions, where I gained extensive experience in project design, data analysis, and scientific communication. I have authored multiple peer-reviewed publications and secured competitive research grants. As a freelancer, I help biotech, pharma, and research organizations translate complex biology into clear, accurate outputs ranging from scientific and medical writing (manuscripts, grant applications, reports) to research consulting and project support. I combine academic rigor with industry insight to deliver reliable, detail-oriented work tailored to your needs. If you need expert scientific writing, literature reviews, experimental design input, or data interpretation/representation, I can provide timely, high-quality support for your projects.

専門分野

• ★ Preclinical Research
• ★ Cancer Research
• ★ Manuscript & Journal Article Writing
• ☆ Biostatistics
• ☆ Cell Biology
• ☆ Neuroscience
• ☆ Data Analysis
• ☆ Data Visualization
• ☆ Cell Culture
• ☆ Cytometry
• ☆ Drug Development
• ☆ Preclinical Pharmacology
• ☆ Cancer Biology
• ☆ Hypothesis
• ☆ Peer Review
• ☆ Research Methodology
• ☆ Fact Checking
• ☆ Literature Search
• ☆ Medical Writing
• ☆ Technical & Scientific Writing
• ☆ Journal Selection
• ☆ Experimental Protocols
• ☆ SOP & Protocol Writing
• ☆ Textbook Content Writing
• ☆ Science Communication
• ☆ Scientific Proofreading & Editing
• ☆ Course Content Writing
• ☆ Grant Writing

サービス

• Writing
• Research
• Consulting

Writing Technical Writing, Copywriting, Audio Transcription, General Proofreading & Editing, Translation

Research Fact Checking, Gray Literature Search, Scientific and Technical Research

Consulting Scientific and Technical Consulting

職務経験

Vrije Universiteit Brussel

- 現在

Pharmaceutical Sciences PhD candidate

Vrije Universiteit Brussel

3月 2019 - 1月 2025

Junior Scientist

UCB Pharmaceutical

9月 2017 - 2月 2019

学歴

Vrije Universiteit Brussel

- 現在

PhD in Pharmaceutical Sciences

Vrije Universiteit Brussel

3月 2019 - 1月 2025

Masters Biochemistry, Molecular and Cellular Biology

University of Namur

9月 2015 - 6月 2017

Bachelor’s in Biological sciences

University of Namur

9月 2012 - 6月 2015

認定資格

• 認定資格の詳細は未入力です。

出版物

JOURNAL ARTICLE

Compartmentalized role of xCT in supporting pancreatic tumor growth, inflammation and mood disturbance in mice @article{3381d303f3dc4096bf907c93349f56b2, title = "Compartmentalized role of xCT in supporting pancreatic tumor growth, inflammation and mood disturbance in mice", abstract = "xCT (Slc7a11), the specific subunit of the cystine/glutamate antiporter system xc-, is present in the brain and on immune cells, where it is known to modulate behavior and inflammatory responses. In a variety of cancers -including pancreatic ductal adenocarcinoma (PDAC)-, xCT is upregulated by tumor cells to support their growth and spread. Therefore, we studied the impact of xCT deletion in pancreatic tumor cells (Panc02) and/or the host (xCT-/- mice) on tumor burden, inflammation, cachexia and mood disturbances. Deletion of xCT in the tumor strongly reduced tumor growth. Targeting xCT in the host and not the tumor resulted only in a partial reduction of tumor burden, while it did attenuate tumor-related systemic inflammation and prevented an increase in immunosuppressive regulatory T cells. The latter effect could be replicated by specific xCT deletion in immune cells. xCT deletion in the host or the tumor differentially modulated neuroinflammation. When mice were grafted with xCT-deleted tumor cells, hypothalamic inflammation was reduced and, accordingly, food intake improved. Tumor bearing xCT-/- mice showed a trend of reduced hippocampal neuroinflammation with less anxiety- and depressive-like behavior. Taken together, targeting xCT may have beneficial effects on pancreatic cancer-related comorbidities, beyond reducing tumor burden. The search for novel and specific xCT inhibitors is warranted as they may represent a holistic therapy in pancreatic cancer.", author = "Olaya Lara and Pauline Janssen and Marco Mambretti and {De Pauw}, Laura and Gamze Ates and Liselotte Mackens and {De Munck}, Jolien and Jarne Walckiers and Zhaolong Pan and Pauline Beckers and Elisa Espinet and Hideyo Sato and {De Ridder}, Mark and Marks, {Daniel L} and Kurt Barb{\'e} and Joeri Aerts and Emmanuel Hermans and Ilse Rooman and Ann Massie", note = "Funding Information: This work was supported by Kom Op Tegen Kanker (ANI219 to AM and IR), a Strategic research Program of the Vrije Universiteit Brussel (SRP49 to AM), the Scientific Fund Willy Gepts (WFWG – UZ Brussel to PJ), G001619N project from Fund for Scientific Research Flanders (FWO to IR) and the Oncology Research Center (Vrije Universiteit Brussel to PJ). OL, LDP and GA are supported by the FWO (Aspirant fellowship 11C2719N to OL and 11658ON to LPD; postdoctoral fellowship 12B3223N to GA). IR was supported by an FWO Odysseus Fellowship G0F8916N. Publisher Copyright: {\textcopyright} 2024 The Authors", year = "2024", month = may, doi = "10.1016/j.bbi.2024.03.001", language = "English", volume = "118", pages = "275--286", journal = "Brain, Behavior, and Immunity", issn = "0889-1591", publisher = "Academic Press Inc.", } . Brain, Behavior, and Immunity.

P. Janssen, L. De Pauw, M. Mambretti, O. Lara, J. Walckiers, L. Mackens, I. Rooman, B. Guillaume, M. De Ridder, G. Ates, et al. (2024). Characterization of the long-term effects of lethal total body irradiation followed by bone marrow transplantation on the brain of C57BL/6 mice . International Journal of Radiation Biology.

Characterization of the long-term effects of lethal total body irradiation followed by bone marrow transplantation on the brain of C57BL/6 mice @article{01bef3a16bcd44eca27171bb98276d42, title = "Characterization of the long-term effects of lethal total body irradiation followed by bone marrow transplantation on the brain of C57BL/6 mice", abstract = "PURPOSE: Total body irradiation (TBI) followed by bone marrow transplantation (BMT) is used in pre-clinical research to generate mouse chimeras that allow to study the function of a protein specifically on immune cells. Adverse consequences of irradiation on the juvenile body and brain are well described and include general fatigue, neuroinflammation, neurodegeneration and cognitive impairment. Yet, the long-term consequences of TBI/BMT performed on healthy adult mice have been poorly investigated.MATERIAL AND METHODS: We developed a robust protocol to achieve near complete bone marrow replacement in mice using 2x550cGy TBI and evaluated the impact of the procedure on their general health, mood disturbances, memory, brain atrophy, neurogenesis, neuroinflammation and blood-brain barrier (BBB) permeability 2 and/or 16 months post-BMT.RESULTS: We found a persistent decrease in weight along with long-term impact on locomotion after TBI and BMT. Although the TBI/BMT procedure did not lead to anxiety- or depressive-like behavior 2- or 16-months post-BMT, long-term spatial memory of the irradiated mice was impaired. We also observed radiation-induced impaired neurogenesis and cortical microglia activation 2 months post-BMT. Moreover, higher levels of hippocampal IgG in aged BMT mice suggest an enhanced age-related increase in BBB permeability that could potentially contribute to the observed memory deficit.CONCLUSIONS: Overall health of the mice did not seem to be majorly impacted by TBI followed by BMT during adulthood. Yet, TBI-induced alterations in the brain and behavior could lead to erroneous conclusions on the function of a protein on immune cells when comparing mouse chimeras with different genetic backgrounds that might display altered susceptibility to radiation-induced damage. Ultimately, the BMT model we here present could also be used to study the related long-term consequences of TBI and BMT seen in patients.", keywords = "Total body irradiation, bone marrow transplantation, mood disturbances, memory, neuroinflammation, neurodegeneration, Neurogenesis", author = "P Janssen and {De Pauw}, L and M Mambretti and O Lara and J Walckiers and L Mackens and I Rooman and B Guillaume and {De Ridder}, M and G Ates and A Massie", note = "Publisher Copyright: {\textcopyright} 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.", year = "2024", month = mar, day = "3", doi = "10.1080/09553002.2023.2283092", language = "English", volume = "100", pages = "385--398", journal = "International Journal of Radiation Biology", issn = "0955-3002", publisher = "Taylor & Francis", number = "3", } . International Journal of Radiation Biology.

Pancreatic acinar cell fate relies on system xC- to prevent ferroptosis during stress @article{79f7dc9173584ddab5a0b6807e9e5806, title = "Pancreatic acinar cell fate relies on system xC- to prevent ferroptosis during stress", abstract = "Acinar cell dedifferentiation is one of the most notable features of acute and chronic pancreatitis. It can also be the initial step that facilitates pancreatic cancer development. In the present study, we further decipher the precise mechanisms and regulation using primary human cells and murine experimental models. Our RNAseq analysis indicates that, in both species, early acinar cell dedifferentiation is accompanied by multiple pathways related to cell survival that are highly enriched, and where SLC7A11 (xCT) is transiently upregulated. xCT is the specific subunit of the cystine/glutamate antiporter system xC-. To decipher its role, gene silencing, pharmacological inhibition and a knock-out mouse model were used. Acinar cells with depleted or reduced xCT function show an increase in ferroptosis relating to lipid peroxidation. Lower glutathione levels and more lipid ROS accumulation could be rescued by the antioxidant N-acetylcysteine or the ferroptosis inhibitor ferrostatin-1. In caerulein-induced acute pancreatitis in mice, xCT also prevents lipid peroxidation in acinar cells. In conclusion, during stress, acinar cell fate seems to be poised for avoiding several forms of cell death. xCT specifically prevents acinar cell ferroptosis by fueling the glutathione pool and maintaining ROS balance. The data suggest that xCT offers a druggable tipping point to steer the acinar cell fate in stress conditions.", keywords = "Animals, Mice, Acinar Cells, Acute Disease, Ferroptosis/genetics, Pancreatitis/genetics, Reactive Oxygen Species, Glutamic Acid", author = "Zhaolong Pan and {Van den Bossche}, Jan-Lars and Eva Rodriguez-Aznar and Pauline Janssen and Olaya Lara and Gamze Ates and Ann Massie and {De Paep}, {Diedert Luc} and Isabelle Houbracken and Marco Mambretti and Ilse Rooman", note = "Funding Information: This work was supported by the Research Foundation Flanders (FWO) (FWO research project G001619N to IR; Odysseus fellowship G0F8916N to IR; PhD fellowships 11L7722N to J-LVDB and 11C2719N to OL; Post-Doctoral fellowship 12B3223N to GA; I012118N to IR and I001420N to AM for infrastructure). PJ was financially supported by the Award Cancer Research - Oncology Center VUB (bequests of Ms. Esther Desmedt and Ms. Irma No{\"e}), and the Scientific Fund Willy Gepts – UZ Brussel. ERA was supported by EUTOPIA-SIF - Post-Doctoral Fellowship. AM was supported by OZR-VUB for infrastructure. Publisher Copyright: {\textcopyright} 2023, The Author(s).", year = "2023", month = aug, day = "21", doi = "10.1038/s41419-023-06063-w", language = "English", volume = "14", journal = "Cell & Death Disease", issn = "2041-4889", publisher = "Nature Publishing Group", number = "8", } . Cell & Death Disease.

Targeting SLC7A11 improves efferocytosis by dendritic cells and wound healing in diabetes @article{7b3b359f4c4341a4b91c193913af4abe, title = "Targeting SLC7A11 improves efferocytosis by dendritic cells and wound healing in diabetes", abstract = "Chronic non-healing wounds are a major complication of diabetes, which affects 1 in 10 people worldwide. Dying cells in the wound perpetuate the inflammation and contribute to dysregulated tissue repair1-3. Here we reveal that the membrane transporter SLC7A11 acts as a molecular brake on efferocytosis, the process by which dying cells are removed, and that inhibiting SLC7A11 function can accelerate wound healing. Transcriptomics of efferocytic dendritic cells in mouse identified upregulation of several SLC7 gene family members. In further analyses, pharmacological inhibition of SLC7A11, or deletion or knockdown of Slc7a11 using small interfering RNA enhanced efferocytosis in dendritic cells. Slc7a11 was highly expressed in dendritic cells in skin, and single-cell RNA sequencing of inflamed skin showed that Slc7a11 was upregulated in innate immune cells. In a mouse model of excisional skin wounding, inhibition or loss of SLC7A11 expression accelerated healing dynamics and reduced the apoptotic cell load in the wound. Mechanistic studies revealed a link between SLC7A11, glucose homeostasis and diabetes. SLC7A11-deficient dendritic cells were dependent on aerobic glycolysis using glucose derived from glycogen stores for increased efferocytosis; also, transcriptomics of efferocytic SLC7A11-deficient dendritic cells identified increased expression of genes linked to gluconeogenesis and diabetes. Further, Slc7a11 expression was higher in the wounds of diabetes-prone db/db mice, and targeting SLC7A11 accelerated their wound healing. The faster healing was also linked to the release of the TGFβ family member GDF15 from efferocytic dendritic cells. In sum, SLC7A11 is a negative regulator of efferocytosis, and removing this brake improves wound healing, with important implications for wound management in diabetes.", keywords = "SLC7A11, efferocytosis, dendritic cells, wound healing, diabetes", author = "Sophia Maschalidi and Parul Mehrotra and Ke{\c c}eli, {Burcu N} and {De Cleene}, {Hannah K L} and Kim Lecomte and {Van der Cruyssen}, Ren{\'e}e and Pauline Janssen and Jonathan Pinney and {van Loo}, Geert and Dirk Elewaut and Ann Massie and Esther Hoste and Ravichandran, {Kodi S}", note = "{\textcopyright} 2022. The Author(s), under exclusive licence to Springer Nature Limited.", year = "2022", month = jun, day = "23", doi = "10.1038/s41586-022-04754-6", language = "English", volume = "606", pages = "776--784", journal = "Nature", issn = "1476-4687", publisher = "Nature Publishing Group", number = "7915", } . Nature.

Lifespan extension with preservation of hippocampal function in aged system xc--deficient male mice @article{c4700a56c4ba4047b901b3b47ca00494, title = "Lifespan extension with preservation of hippocampal function in aged system xc--deficient male mice", abstract = "The cystine/glutamate antiporter system xc- has been identified as the major source of extracellular glutamate in several brain regions as well as a modulator of neuroinflammation, and genetic deletion of its specific subunit xCT (xCT-/-) is protective in mouse models for age-related neurological disorders. However, the previously observed oxidative shift in the plasma cystine/cysteine ratio of adult xCT-/- mice led to the hypothesis that system xc- deletion would negatively affect life- and healthspan. Still, till now the role of system xc- in physiological aging remains unexplored. We therefore studied the effect of xCT deletion on the aging process of mice, with a particular focus on the immune system, hippocampal function, and cognitive aging. We observed that male xCT-/- mice have an extended lifespan, despite an even more increased plasma cystine/cysteine ratio in aged compared to adult mice. This oxidative shift does not negatively impact the general health status of the mice. On the contrary, the age-related priming of the innate immune system, that manifested as increased LPS-induced cytokine levels and hypothermia in xCT+/+ mice, was attenuated in xCT-/- mice. While this was associated with only a very moderate shift towards a more anti-inflammatory state of the aged hippocampus, we observed changes in the hippocampal metabolome that were associated with a preserved hippocampal function and the retention of hippocampus-dependent memory in male aged xCT-/- mice. Targeting system xc- is thus not only a promising strategy to prevent cognitive decline, but also to promote healthy aging.", keywords = "Lifespan extension, aged system x c--deficient, male mice, preservation of hippocampal function", author = "Lise Verbruggen and Gamze Ates and Olaya Lara and {De Munck}, Jolien and Agn{\`e}s Villers and {De Pauw}, Laura and Sigrid Ottestad-Hansen and Sho Kobayashi and Pauline Beckers and Pauline Janssen and Hideyo Sato and Yun Zhou and Emmanuel Hermans and Rose Njemini and Lutgarde Arckens and Danbolt, {Niels C} and {De Bundel}, Dimitri and Aerts, {Joeri L} and Kurt Barb{\'e} and Benoit Guillaume and Laurence Ris and Eduard Bentea and Ann Massie", note = "{\textcopyright} 2022. The Author(s).", year = "2022", month = apr, doi = "10.1038/s41380-022-01470-5", language = "English", volume = "27", pages = "2355--2368", journal = "Molecular Psychiatry", issn = "1359-4184", publisher = "Nature Publishing Group", number = "4", } . Molecular Psychiatry.

Lifespan extension with preservation of hippocampal function in aged system xc−-deficient male mice <head> <META HTTP-EQUIV="Refresh" CONTENT="0;URL=/servlet/useragent"> </head> . Molecular Psychiatry.

Corticostriatal dysfunction and social interaction deficits in mice lacking the cystine/glutamate antiporter @article{c0078c901cd046da91ce47b7a9ea018d, title = "Corticostriatal dysfunction and social interaction deficits in mice lacking the cystine/glutamate antiporter", abstract = "The astrocytic cystine/glutamate antiporter system xc− represents an important source of extracellular glutamate in the central nervous system, with potential impact on excitatory neurotransmission. Yet, its function and importance in brain physiology remain incompletely understood. Employing slice electrophysiology and mice with a genetic deletion of the specific subunit of system xc−, xCT (xCT−/− mice), we uncovered decreased neurotransmission at corticostriatal synapses. This effect was partly mitigated by replenishing extracellular glutamate levels, indicating a defect linked with decreased extracellular glutamate availability. We observed no changes in the morphology of striatal medium spiny neurons, the density of dendritic spines, or the density or ultrastructure of corticostriatal synapses, indicating that the observed functional defects are not due to morphological or structural abnormalities. By combining electron microscopy with glutamate immunogold labeling, we identified decreased intracellular glutamate density in presynaptic terminals, presynaptic mitochondria, and in dendritic spines of xCT−/− mice. A proteomic and kinomic screen of the striatum of xCT−/− mice revealed decreased expression of presynaptic proteins and abnormal kinase network signaling, that may contribute to the observed changes in postsynaptic responses. Finally, these corticostriatal deregulations resulted in a behavioral phenotype suggestive of autism spectrum disorder in the xCT−/− mice; in tests sensitive to corticostriatal functioning we recorded increased repetitive digging behavior and decreased sociability. To conclude, our findings show that system xc− plays a previously unrecognized role in regulating corticostriatal neurotransmission and influences social preference and repetitive behavior.", author = "Bentea, {Eduard Mihai} and Agn{\`e}s Villiers and Cynthia Moore and Adam Funk and Sinead O'Donovan and Lise Verbruggen and Olaya Lara and Pauline Janssen and {De Pauw}, Laura and Noemi Declerck and Depasquale, {Erica A K} and Churchill, {Madeline J} and Hideyo Sato and Emmanuel Hermans and Lutgarde Arckens and Charles Meshul and Laurence RIS and Robert McCullumsmith and Ann Massie", note = "Funding Information: Acknowledgements We kindly thank Frank Van Der Kelen (Vrije Universiteit Brussel), Ria Vanlaer (Katholieke Universiteit Leuven), and Dr Joshua Anderson (University of Alabama Birmingham Kinome core) for their technical assistance. This work was supported by grants of the Vrije Universiteit Brussel (SRP49) and the “Wetenschappelijk Fonds Willy Gepts” of the UZ Brussel to AM, Research Foundation-Flanders (FWO) #1510218N to EB, Merit Review Grant #1BX 001643 and #1BX 000552 to CKM, from the United States (U.S.) Department of Veterans Affairs Biomedical Laboratory Research and Development, and NIMH R21 MH107916 to REM. This work was also supported with resources and the use of facilities at the VA Portland Health Care System. The MS data were acquired in the University of Cincinnati Proteomics Laboratory under the direction of Ken Greis, PhD on a mass spectrometer funded in part through the NIH S10 shared instrumentation grant (RR027015 Greis-PI). The contents do not represent the views of the U.S. Department of Veterans Affairs or the United States Government. Publisher Copyright: {\textcopyright} 2020, The Author(s). Copyright: Copyright 2023 Elsevier B.V., All rights reserved.", year = "2021", month = sep, doi = "10.1038/s41380-020-0751-3", language = "English", volume = "26", pages = "4754--4769", journal = "Molecular Psychiatry", issn = "1359-4184", publisher = "Nature Publishing Group", number = "9", } . Molecular Psychiatry.

Cystine-glutamate antiporter deletion accelerates motor recovery and improves histological outcomes following spinal cord injury in mice @article{5a02cc0ba1164571b3e20115fd0be629, title = "Cystine-glutamate antiporter deletion accelerates motor recovery and improves histological outcomes following spinal cord injury in mice", abstract = "xCT is the specific subunit of System xc-, an antiporter importing cystine while releasing glutamate. Although xCT expression has been found in the spinal cord, its expression and role after spinal cord injury (SCI) remain unknown. The aim of this study was to characterize the role of xCT on functional and histological outcomes following SCI induced in wild-type (xCT+/+) and in xCT-deficient mice (xCT-/-). In the normal mouse spinal cord, slc7a11/xCT mRNA was detected in meningeal fibroblasts, vascular mural cells, astrocytes, motor neurons and to a lesser extent in microglia. slc7a11/xCT gene and protein were upregulated within two weeks post-SCI. xCT-/- mice recovered muscular grip strength as well as pre-SCI weight faster than xCT+/+ mice. Histology of xCT-/- spinal cords revealed significantly more spared motor neurons and a higher number of quiescent microglia. In xCT-/- mice, inflammatory polarization shifted towards higher mRNA expression of ym1 and igf1 (anti-inflammatory) while lower levels of nox2 and tnf-a (pro-inflammatory). Although astrocyte polarization did not differ, we quantified an increased expression of lcn2 mRNA. Our results show that slc7a11/xCT is overexpressed early following SCI and is detrimental to motor neuron survival. xCT deletion modulates intraspinal glial activation by shifting towards an anti-inflammatory profile.", author = "Lindsay Sprimont and Pauline Janssen and {De Swert}, Kathleen and {Van Bulck}, Mathias and Ilse Rooman and Jacques Gilloteaux and Ann Massie and Charles Nicaise", year = "2021", month = jun, day = "9", doi = "10.1038/s41598-021-91698-y", language = "English", volume = "11", journal = "Scientific Reports", issn = "2045-2322", publisher = "Nature Publishing Group", number = "1", } . Scientific Reports.

Chronic Sulfasalazine Treatment in Mice Induces System xc- - Independent Adverse Effects @article{c72b08fdb9c5437ea10f41621a2dcf6d, title = "Chronic Sulfasalazine Treatment in Mice Induces System xc- - Independent Adverse Effects", abstract = "Despite ample evidence for the therapeutic potential of inhibition of the cystine/glutamate antiporter system xc- in neurological disorders and in cancer, none of the proposed inhibitors is selective. In this context, a lot of research has been performed using the EMA- and FDA-approved drug sulfasalazine (SAS). Even though this molecule is already on the market for decades as an anti-inflammatory drug, serious side effects due to its use have been reported. Whereas for the treatment of the main indications, SAS needs to be cleaved in the intestine into the anti-inflammatory compound mesalazine, it needs to reach the systemic circulation in its intact form to allow inhibition of system xc-. The higher plasma levels of intact SAS (or its metabolites) might induce adverse effects, independent of its action on system xc-. Some of these effects have however been attributed to system xc- inhibition, calling into question the safety of targeting system xc-. In this study we chronically treated system xc- - deficient mice and their wildtype littermates with two different doses of SAS (160 mg/kg twice daily or 320 mg/kg once daily, i.p.) and studied some of the adverse effects that were previously reported. SAS had a negative impact on the survival rate, the body weight, the thermoregulation and/or stress reaction of mice of both genotypes, and thus independent of its inhibitory action on system xc-. While SAS decreased the total distance travelled in the open-field test the first time the mice encountered the test, it did not influence this parameter on the long-term and it did not induce other behavioral changes such as anxiety- or depressive-like behavior. Finally, no major histological abnormalities were observed in the spinal cord. To conclude, we were unable to identify any undesirable system xc--dependent effect of chronic administration of SAS.", author = "Lise Verbruggen and Lindsay Sprimont and Eduard Bentea and Pauline Janssen and Azzedine Gharib and Lauren Deneyer and {De Pauw}, Laura and Olaya Lara and Hideyo Sato and Charles Nicaise and Ann Massie", note = "Copyright {\textcopyright} 2021 Verbruggen, Sprimont, Bentea, Janssen, Gharib, Deneyer, De Pauw, Lara, Sato, Nicaise and Massie.", year = "2021", month = may, day = "18", doi = "10.3389/fphar.2021.625699", language = "English", volume = "12", journal = "Frontiers in Pharmacology", issn = "1663-9812", publisher = "Frontiers Media S.A.", } . Frontiers in Pharmacology.

OTHER

Abstract 3378: Acinar cell susceptibility for tumor development in the pancreas: Targeting the critical regulators for therapy @article{0d04468a2c40489799b220b43e188a8b, title = "Abstract 3378: Acinar cell susceptibility for tumor development in the pancreas: Targeting the critical regulators for therapy", abstract = "Acinar to ductal metaplasia (ADM) or acinar cell dedifferentiation is one of the most notable features of chronic pancreatitis. It is also considered the initial step of pancreatic cancer development when oncogenic mutations accumulate. However, its precise mechanism and regulatory pathways remain unclear. This study profiled the transcriptome of dedifferentiated acinar cells from both humans and mice. Differential expression analysis integrated with a systematic literature search revealed several potential regulators (e.g., GDF15, GFRA1, MXRA5, CXCL17), of which the expression pattern over time was validated by qRT-PCR. We also focused on multiple conserved pathways of cell survival, among which SLC7A11 (xCT) is transiently upregulated in both species. The xCT subunit, integral to the cystine/glutamate antiporter system xc-, plays a critical role in cell survival across various cell types. To elucidate its role in acinar dedifferentiation, we employed gene silencing, pharmacological inhibition, and a knock-out mouse model. Acinar cells with diminished xCT function exhibit increased ferroptosis linked to lipid peroxidation. Antioxidants such as N-acetylcysteine and ferroptosis inhibitors like Ferrostatin-1 can mitigate lower glutathione levels and lipid ROS accumulation. Similarly, in mouse acute pancreatitis, xCT prevents lipid peroxidation. Our findings indicate that xCT fuels the glutathione pool and maintains ROS balance during ADM, thereby preventing pancreatic acinar cells from ferroptosis, a form of cell death rarely reported in relation to ADM. Next to xCT, a future and similar comprehensive study of the aforementioned genes could provide valuable insights into the dynamic changes that occur during acinar cell dedifferentiation and pave the way to the discovery of new intervention targets to suppress tumorigenesis in chronic pancreatitis.", author = "Zhaolong Pan and {Van den Bossche}, Jan-Lars and {Rodriguez Aznar}, Eva and Pauline Janssen and Olaya Lara and Gamze Ates and Ann Massie and {De Paep}, {Diedert Luc} and Isabelle Houbracken and Marco Mambretti and Ilse Rooman", year = "2024", month = mar, day = "15", doi = "10.1158/1538-7445.AM2024-3378", language = "English", volume = "84", journal = "Cancer Research", issn = "0008-5472", publisher = "American Association for Cancer Research Inc.", number = "6_supplement", note = "AACR Annual Meeting 2024 ; Conference date: 05-04-2024 Through 10-04-2024", } . Cancer Research.

Author Correction @article{af67fa405c7a41aaaf0360ca679bba35, title = "Author Correction: Targeting SLC7A11 improves efferocytosis by dendritic cells and wound healing in diabetes (Nature, (2022), 606, 7915, (776-784), 10.1038/s41586-022-04754-6)", abstract = "In the version of this article initially published, the flow cytometry plot shown in on the left (labelled 34%) in Fig. 3a was an inadvertent duplicate of the plot to the right (labelled 58%). The plot has been replaced in the HTML and PDF versions of the article.", keywords = "SLC7A11, efferocytosis, dendritic cells, wound healing, Diabetes", author = "Sophia Maschalidi and Parul Mehrotra and Ke{\c c}eli, {Burcu N} and {De Cleene}, {Hannah K L} and Kim Lecomte and {Van der Cruyssen}, Ren{\'e}e and Pauline Janssen and Jonathan Pinney and {van Loo}, Geert and Dirk Elewaut and Ann Massie and Esther Hoste and Ravichandran, {Kodi S}", year = "2022", month = jul, day = "27", doi = "10.1038/s41586-022-05101-5", language = "English", volume = "608", pages = "E29--E29", journal = "Nature", issn = "1476-4687", publisher = "Nature Publishing Group", number = "7923", } . Nature.

DISSERTATION THESIS

Pauline Janssen(2024). Specific involvement of system xc- on immune cells in two pathological conditions characterized by a systemic inflammatory phenotype .

CONFERENCE POSTER

Pauline Janssen(2023). Characterization of the long-term effects of lethal total body irradiation followed by bone marrow transplantation on the brain of C57BL/6 mice . Belgian Society for Neuroscience (BSN) Meeting 2023, 6/06/23.

Pauline Janssen(2023). Optimization and characterization of a bone marrow transplantation mouse model and its use to study the role of system xc- in LPS-induced neuroinflammation . Society for Neuroscience 2023, Washington, United States, 11/11/23.

Targeting system xc- in a mouse pancreatic cancer model reduces tumor growth, neuroinflammation and mood disturbances @conference{71fc0e660b8945ba8c5a83ac59fef886, title = "Targeting system xc- in a mouse pancreatic cancer model reduces tumor growth, neuroinflammation and mood disturbances", author = "Pauline Janssen", year = "2022", month = may, day = "22", language = "English", note = "Belgian Society for Neuroscience (BSN) Meeting 2022, BSN Meeting 2022 ; Conference date: 09-05-2022", } . Belgian Society for Neuroscience (BSN) Meeting 2022, Brussel, Belgium, 9/05/22.

xCT/Slc7a11 deletion accelerates motor recovery and improves histological outcomes follwong spinal cord injury. @conference{a201b548d7794cc783f0057e92c4a931, title = "xCT/Slc7a11 deletion accelerates motor recovery and improves histological outcomes follwong spinal cord injury.", author = "Lindsay Sprimont and Pauline Janssen and {Van Bulck}, Michiel and Ilse Rooman and H Sato and Joanna Bouchat and Jacques Gilloteaux and Ann Massie and Charles Nicaise", year = "2019", month = may, language = "English", note = "13th Bi-annual Scientific Meeting of the Belgian Society of Neuroscience ; Conference date: 23-05-2019", } . 13th Bi-annual Scientific Meeting of the Belgian Society of Neuroscience, Brussels, Belgium, 23/05/19.