scholarly journals Cell scientist to watch – Romain Levayer

2021 ◽  
Vol 134 (2) ◽  
pp. jcs256487
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Cell Biology ◽  
Young Scientist ◽  
Epithelial Morphogenesis ◽  
Cell Competition ◽  
Master's Degrees ◽  
Johns Hopkins University ◽  
University Of Bern ◽  
The University

ABSTRACTRomain Levayer did his bachelor's and master's degrees at École Normale Supérieure in Paris, France. In between these degrees, he did an internship in the lab of Geraldine Seydoux, at Johns Hopkins University in Baltimore, MD, USA. He then moved to Marseille, France, to join the laboratory of Thomas Lecuit at the Institut de Biologie du Développement de Marseille (IBDM) for his PhD. There, he studied epithelial morphogenesis during the early development of the Drosophila embryo. Postdoctoral work followed in the lab of Eduardo Moreno at the Institute of Cell Biology (IZB) at the University of Bern, Switzerland, where Romain investigated the mechanisms of epithelial cell competition. At the end of 2016, Romain returned to Paris to establish his research group at Institut Pasteur. His lab is trying to understand how the plasticity of behaviour of epithelial cells and the regulation of cell death modulate tissue morphogenesis and homeostasis. Romain was awarded an ERC Starting Grant in 2017 and the SBCF Young Scientist Award in 2018, and he was one of the laureates of La Fondation Schlumberger pour l'Education et la Recherche (FSER) in 2019.

scholarly journals Cell Scientist to Watch – Eurico Morais-de-Sá

2020 ◽  
Vol 133 (23) ◽  
pp. jcs256040
Keyword(s):  
Cell Division ◽  
Epithelial Cell ◽  
Cell Polarity ◽  
Research Group ◽  
Cell Biology ◽  
Epithelial Tissue ◽  
Marie Curie ◽  
Regulatory Processes ◽  
Spatial Asymmetry ◽  
The University

ABSTRACTEurico Morais-de-Sá graduated in biochemistry from the University of Porto, Portugal. After a research internship in protein crystallography at the Institute for Molecular and Cell Biology (IBMC) in Porto, Eurico moved to Cambridge, UK, to do his PhD with Daniel St Johnston at the Gurdon Institute. During this time, he studied cell polarity in the context of epithelial tissue and body-axis specification. In 2011, he was awarded EMBO and Marie Curie fellowships to return to Porto for his postdoctoral work with Claudio Sunkel at IBMC, where he used his cell polarity expertise to understand the regulatory processes of epithelial cell division. In 2018, Eurico established his own research group at Instituto de Inovação e Investigação em Saúde (i3S) focusing on the mechanisms by which epithelial cells modulate spatial asymmetry during cell division to maintain the function and integrity of proliferative tissues.

scholarly journals Polyhexamethylene Guanidine Phosphate Induces Apoptosis through Endoplasmic Reticulum Stress in Lung Epithelial Cells

2021 ◽  
Vol 22 (3) ◽  
pp. 1215
Author(s):  
Mi Ho Jeong ◽  
Mi Seon Jeon ◽  
Ga Eun Kim ◽  
Ha Ryong Kim
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Epithelial Cell ◽  
Er Stress ◽  
Lung Fibrosis ◽  
A549 Cells ◽  
Polyhexamethylene Guanidine ◽  
Lung Epithelial ◽  
Epithelial Cell Death ◽  
Guanidine Phosphate

Airway epithelial cell death contributes to the pathogenesis of lung fibrosis. Polyhexamethylene guanidine phosphate (PHMG-p), commonly used as a disinfectant, has been shown to be strongly associated with lung fibrosis in epidemiological and toxicological studies. However, the molecular mechanism underlying PHMG-p-induced epithelial cell death is currently unclear. We synthesized a PHMG-p–fluorescein isothiocyanate (FITC) conjugate and assessed its uptake into lung epithelial A549 cells. To examine intracellular localization, the cells were treated with PHMG-p–FITC; then, the cytoplasmic organelles were counterstained and observed with confocal microscopy. Additionally, the organelle-specific cell death pathway was investigated in cells treated with PHMG-p. PHMG-p–FITC co-localized with the endoplasmic reticulum (ER), and PHMG-p induced ER stress in A549 cells and mice. The ER stress inhibitor tauroursodeoxycholic acid (TUDCA) was used as a pre-treatment to verify the role of ER stress in PHMG-p-induced cytotoxicity. The cells treated with PHMG-p showed apoptosis, which was inhibited by TUDCA. Our results indicate that PHMG-p is rapidly located in the ER and causes ER-stress-mediated apoptosis, which is an initial step in PHMG-p-induced lung fibrosis.

scholarly journals Fibrillar α-synuclein induces neurotoxic astrocyte activation via RIP kinase signaling and NF-κB

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Tsui-Wen Chou ◽  
Nydia P. Chang ◽  
Medha Krishnagiri ◽  
Aisha P. Patel ◽  
Marissa Lindman ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Neurodegenerative Disorder ◽  
Neuronal Cell ◽  
Dopamine Neurons ◽  
Functional Markers ◽  
Kinase Signaling ◽  
Astrocyte Activation ◽  
Transcriptional Responses

AbstractParkinson’s disease (PD) is a neurodegenerative disorder characterized by the death of midbrain dopamine neurons. The pathogenesis of PD is poorly understood, though misfolded and/or aggregated forms of the protein α-synuclein have been implicated in several neurodegenerative disease processes, including neuroinflammation and astrocyte activation. Astrocytes in the midbrain play complex roles during PD, initiating both harmful and protective processes that vary over the course of the disease. However, despite their significant regulatory roles during neurodegeneration, the cellular and molecular mechanisms that promote pathogenic astrocyte activity remain mysterious. Here, we show that α-synuclein preformed fibrils (PFFs) induce pathogenic activation of human midbrain astrocytes, marked by inflammatory transcriptional responses, downregulation of phagocytic function, and conferral of neurotoxic activity. These effects required the necroptotic kinases RIPK1 and RIPK3, but were independent of MLKL and necroptosis. Instead, both transcriptional and functional markers of astrocyte activation occurred via RIPK-dependent activation of NF-κB signaling. Our study identifies a previously unknown function for α-synuclein in promoting neurotoxic astrocyte activation, as well as new cell death-independent roles for RIP kinase signaling in the regulation of glial cell biology and neuroinflammation. Together, these findings highlight previously unappreciated molecular mechanisms of pathologic astrocyte activation and neuronal cell death with implications for Parkinsonian neurodegeneration.

II. One size fits all: nonclassical MHC molecules fulfill multiple roles in epithelial cell function

1998 ◽  
Vol 274 (2) ◽  
pp. G227-G231 ◽  
Author(s):  
Richard S. Blumberg
Keyword(s):  
Epithelial Cell ◽  
Mhc Class I ◽  
Cell Biology ◽  
Cell Function ◽  
Surface Glycoprotein ◽  
Class I ◽  
Human Major Histocompatibility Complex ◽  
Cell Surface Glycoprotein ◽  
Mhc Molecules ◽  
Nonclassical Mhc

The human major histocompatibility complex (MHC) on chromosome 6 encodes three classical class I genes: human leukocyte antigen-A (HLA-A), HLA-B, and HLA-C. These polymorphic genes encode a 43- to 45-kDa cell surface glycoprotein that, in association with the 12-kDa β2-microglobulin molecule, functions in the presentation of nine amino acid peptides to the T cell receptor of CD8-bearing T lymphocytes and killer inhibitory receptors on natural killer cells. In addition to these ubiquitously expressed polymorphic proteins, the human genome also encodes a number of nonclassical MHC class I-like, or class Ib, genes that in general encode nonpolymorphic molecules involved in a variety of specific immunologic functions. Many of these genes, including CD1, the neonatal Fc receptor for immunoglobulin G, HLA-G, the MHC class I chain-related gene A, and Hfe, are prominently displayed on epithelial cells, suggesting an important role in epithelial cell biology.

Surinam Plantations in Dutch Archives

Itinerario ◽  
1982 ◽  
Vol 6 (1) ◽  
pp. 121-126
Author(s):  
Peter Boomgaard
Keyword(s):  
West Indies ◽  
Good News ◽  
University Of Minnesota ◽  
Indian History ◽  
East Indies ◽  
Plantation Economy ◽  
Indonesian Archipelago ◽  
Johns Hopkins University ◽  
The Caribbean ◽  
The University

The 1979 issue of Itinerario, (no. 2) opened with “A note on Suriname Plantation Archives at the University of Minnesota”, in which Richard Price of the Johns Hopkins University reported his discovery of some 2,000 manuscript pages on a number of Surinam plantations in the James Ford Bell Library at the University of Minnesota, Minneapolis. This, of course, is very good news. It is perhaps still better news that the Dutch archives contain vast and almost untapped (resources on a 200-odd plantations! I am, however, certainly not the first tone to make this ‘discovery’: Mrs. M.A.P. Meilink-Roelofsz not only mentioned it in her Ph.D. dissertation “Asian trade and European influence in the Indonesian Archipelago between 1500 and about 1630”, but she even ordered part of the archives herself. It must be the unbridgeable gap between scholars interested in the East Indies /and those who study West Indian history, that her enthusiastic remarks on the availability of plantation material went unheeded. When nine years later Th. Mathews published his article “Los estuadios sobre historia economica del Caribe (1585 - 1910)”2, he mentioned the Dutch West Indies as a blank on the Caribbean map as far as economic (plantation) history is concerned. Since Mathews wrote his article the historiographic situation has improved only slightly, and it is an ironic comment on Surinam historical scholarship that tiny Curaçao's XlXth century plantation economy by now has found its historian, while the Surinam plantations are still in search of an author.

scholarly journals Sirtuin 1 Promotes Hyperoxia-Induced Lung Epithelial Cell Death Independent of NF-E2–Related Factor 2 Activation

2016 ◽  
Vol 54 (5) ◽  
pp. 697-706 ◽  
Author(s):  
Haranatha R. Potteti ◽  
Subbiah Rajasekaran ◽  
Senthilkumar B. Rajamohan ◽  
Chandramohan R. Tamatam ◽  
Narsa M. Reddy ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Lung Epithelial Cell ◽  
Sirtuin 1 ◽  
Related Factor ◽  
Lung Epithelial ◽  
Epithelial Cell Death

Library Impact Practice Brief: Freshman Fellows: Implementing and Assessing a First-Year Primary-Source Research Program

2021 ◽  
Author(s):  
Margaret Burri ◽  
Joshua Everett ◽  
Heidi Herr ◽  
Jessica Keyes
Keyword(s):  
Primary Source ◽  
Structured Interview ◽  
First Year ◽  
Special Collections ◽  
Johns Hopkins University ◽  
College Career ◽  
Library Impact ◽  
Teaching Learning ◽  
The University ◽  
Impact Framework

This practice brief describes the assessment project undertaken by the Sheridan Libraries at Johns Hopkins University as part of the library’s participation in ARL’s Research Library Impact Framework initiative to address the question “(How) do the library’s special collections specifically support and promote teaching, learning, and research?” The research team investigated how the Freshman Fellows experience impacted the fellows’ studies and co-curricular activities at the university. Freshmen Fellows, established in 2016, is a signature opportunity to expose students to primary-source collections early in their college career by pairing four fellows with four curators on individual research projects. The program graduated its first cohort of fellows in spring 2020. The brief includes a semi-structured interview guide, program guidelines, and a primary research rubric.

scholarly journals Active elimination of intestinal cells drives oncogenic growth in organoids

2020 ◽  
Author(s):  
Ana Krotenberg Garcia ◽  
Arianna Fumagalli ◽  
Huy Quang Le ◽  
Owen J. Sansom ◽  
Jacco van Rheenen ◽  
...  
Keyword(s):  
Quality Control ◽  
Cell Death ◽  
Cancer Cells ◽  
Cell Fate ◽  
Crucial Role ◽  
Intestinal Cells ◽  
Dependent Manner ◽  
Wild Type ◽  
Cell Competition ◽  
Type Population

AbstractCompetitive cell-interactions play a crucial role in quality control during development and homeostasis. Here we show that cancer cells use such interactions to actively eliminate wild-type intestine cells in enteroid monolayers and organoids. This apoptosis-dependent process boosts proliferation of intestinal cancer cells. The remaining wild-type population activates markers of primitive epithelia and transits to a fetal-like state. Prevention of this cell fate transition avoids elimination of wild-type cells and, importantly, limits the proliferation of cancer cells. JNK signalling is activated in competing cells and is required for cell fate change and elimination of wild-type cells. Thus, cell competition drives growth of cancer cells by active out-competition of wild-type cells through forced cell death and cell fate change in a JNK dependent manner.

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