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Article ; Online: MCL-1 and BCL-XL: blood brothers.

Erlacher, Miriam / Labi, Verena

2021 Volume 137, Issue 14, Page(s) 1850–1851

MeSH term(s)	Humans ; bcl-X Protein/genetics ; Myeloid Cell Leukemia Sequence 1 Protein/genetics ; Proto-Oncogene Proteins c-bcl-2/genetics
Chemical Substances	bcl-X Protein ; Myeloid Cell Leukemia Sequence 1 Protein ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2021-01-22
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2020010569
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Zs.MO 364: Show issues

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Article ; Online: Cell signaling and the aging of B cells.

Labi, Verena / Derudder, Emmanuel

Experimental gerontology

2020 Volume 138, Page(s) 110985

Abstract: The uniqueness of each B cell lies in the structural diversity of the B-cell antigen receptor allowing the virtually limitless recognition of antigens, a necessity to protect individuals against a range of challenges. B-cell development and response to ... ...

Abstract	The uniqueness of each B cell lies in the structural diversity of the B-cell antigen receptor allowing the virtually limitless recognition of antigens, a necessity to protect individuals against a range of challenges. B-cell development and response to stimulation are exquisitely regulated by a group of cell surface receptors modulating various signaling cascades and their associated genetic programs. The effects of these signaling pathways in optimal antibody-mediated immunity or the aberrant promotion of immune pathologies have been intensely researched in the past in young individuals. In contrast, we are only beginning to understand the contribution of these pathways to the changes in B cells of old organisms. Thus, critical transcription factors such as E2A and STAT5 show differential expression or activity between young and old B cells. As a result, B-cell physiology appears altered, and antibody production is impaired. Here, we discuss selected phenotypic changes during B-cell aging and attempt to relate them to alterations of molecular mechanisms.
MeSH term(s)	Aging ; B-Lymphocytes ; Humans ; Lymphocyte Activation ; Receptors, Antigen, B-Cell ; Signal Transduction
Chemical Substances	Receptors, Antigen, B-Cell
Language	English
Publishing date	2020-06-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	390992-x
ISSN	1873-6815 ; 0531-5565
ISSN (online)	1873-6815
ISSN	0531-5565
DOI	10.1016/j.exger.2020.110985
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Zs.A 579: Show issues

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Article: Age-related neuroimmune signatures in dorsal root ganglia of a Fabry disease mouse model.

Choconta, Jeiny Luna / Labi, Verena / Dumbraveanu, Cristiana / Kalpachidou, Theodora / Kummer, Kai K / Kress, Michaela

Immunity & ageing : I & A

2023 Volume 20, Issue 1, Page(s) 22

Abstract: Pain in Fabry disease (FD) is generally accepted to result from neuronal damage in the peripheral nervous system as a consequence of excess lipid storage caused by alpha-galactosidase A (α-Gal A) deficiency. Signatures of pain arising from nerve injuries ...

Abstract	Pain in Fabry disease (FD) is generally accepted to result from neuronal damage in the peripheral nervous system as a consequence of excess lipid storage caused by alpha-galactosidase A (α-Gal A) deficiency. Signatures of pain arising from nerve injuries are generally associated with changes of number, location and phenotypes of immune cells within dorsal root ganglia (DRG). However, the neuroimmune processes in the DRG linked to accumulating glycosphingolipids in Fabry disease are insufficiently understood.Therefore, using indirect immune fluorescence microscopy, transmigration assays and FACS together with transcriptomic signatures associated with immune processes, we assessed age-dependent neuroimmune alterations in DRG obtained from mice with a global depletion of α-Gal A as a valid mouse model for FD. Macrophage numbers in the DRG of FD mice were unaltered, and BV-2 cells as a model for monocytic cells did not show augmented migratory reactions to glycosphingolipids exposure suggesting that these do not act as chemoattractants in FD. However, we found pronounced alterations of lysosomal signatures in sensory neurons and of macrophage morphology and phenotypes in FD DRG. Macrophages exhibited reduced morphological complexity indicated by a smaller number of ramifications and more rounded shape, which were age dependent and indicative of premature monocytic aging together with upregulated expression of markers CD68 and CD163.In our FD mouse model, the observed phenotypic changes in myeloid cell populations of the DRG suggest enhanced phagocytic and unaltered proliferative capacity of macrophages as compared to wildtype control mice. We suggest that macrophages may participate in FD pathogenesis and targeting macrophages at an early stage of FD may offer new treatment options other than enzyme replacement therapy.
Language	English
Publishing date	2023-05-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2168941-6
ISSN	1742-4933
ISSN	1742-4933
DOI	10.1186/s12979-023-00346-8
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Article ; Online: Efficacy of a Virtual Education Program for Family Caregivers of Persons Living with Dementia.

Noel, Margaret A / Lackey, Elizabeth / Labi, Vanna / Bouldin, Erin D

Journal of Alzheimer's disease : JAD

2022 Volume 86, Issue 4, Page(s) 1667–1678

Abstract: Background: Family caregivers of people with dementia often experience negative impacts including stress and burden. Psychoeducational programs can reduce these negative outcomes.: Objective: To evaluate whether this virtual caregiver education ... ...

Abstract	Background: Family caregivers of people with dementia often experience negative impacts including stress and burden. Psychoeducational programs can reduce these negative outcomes. Objective: To evaluate whether this virtual caregiver education program changes caregiver confidence, self-efficacy, and burden relative to controls. Methods: This was a pre-post comparison of a five-week, synchronous, virtual caregiver education program delivered by a clinician and caregiver support specialist covering aspects of dementia, including changes in cognition, behavior, functional abilities, caregiver-care recipient roles, communication, and caregiver self-care. Caregivers (n = 90) were surveyed at baseline, at completion of intervention, and three months thereafter; controls (n = 44) were surveyed at two points six weeks apart. We compared validated measures of caregiver confidence, self-efficacy, and burden using generalized estimating equations. Results: Participants' confidence and self-efficacy increased over follow-up compared with controls (p < 0.01 for interventiontime in regression models). There was no difference in burden. All participants (100%) reported perceived increased knowledge, 97% perceived increased confidence, and 95% perceived increased ability to manage dementia-related behaviors after the course. Conclusion:* This virtual caregiver education program was effective in improving caregiver confidence and self-efficacy and participants' self-reported impact was equivalent to those who had taken previous courses in person. Caregivers with greater confidence and self-efficacy have been shown to have better health outcomes and decreased stress and depressive symptoms. Health professionals, health care organizations, and public health agencies should consider using efficacious virtual caregiver education programs in rural and other community settings, during public health crises, or in standard practice as an alternative to in-person programs.
MeSH term(s)	Activities of Daily Living ; Caregivers/education ; Dementia ; Humans ; Self Efficacy ; Surveys and Questionnaires
Language	English
Publishing date	2022-02-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-215359
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Zs.A 6084: Show issues

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Article ; Online: miR-17∼92 in lymphocyte development and lymphomagenesis.

Labi, Verena / Schoeler, Katia / Melamed, Doron

Cancer letters

2019 Volume 446, Page(s) 73–80

Abstract: microRNAs (miRNAs) down-modulate the levels of proteins by sequence-specific binding to their respective target mRNAs, causing translational repression or mRNA degradation. The miR-17∼92 cluster encodes for six miRNAs whose target recognition ... ...

Abstract	microRNAs (miRNAs) down-modulate the levels of proteins by sequence-specific binding to their respective target mRNAs, causing translational repression or mRNA degradation. The miR-17∼92 cluster encodes for six miRNAs whose target recognition specificities are determined by their distinct sequence. In mice, the four miRNA families generated from the miR-17∼92 cluster coordinate to allow for proper lymphocyte development and effective adaptive immune responses following infection or immunization. Lymphocyte development and homeostasis rely on tight regulation of PI3K signaling to avoid autoimmunity or immunodeficiency, and the miR-17∼92 miRNAs appear as key mediators to appropriately tune PI3K activity. On the other hand, in lymphoid tumors overexpression of the miR-17∼92 miRNAs is a common oncogenic event. In this review, we touch on what we have learned so far about the miR-17∼92 miRNAs, particularly with respect to their role in lymphocyte development, homeostasis and pathology.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Lymphoma/genetics ; Lymphoma/immunology ; Lymphoma/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Phenotype ; Signal Transduction
Chemical Substances	MIRN17 microRNA, human ; MIRN18 microRNA, human ; MIRN19 microRNA, human ; MIRN92 microRNA, human ; MicroRNAs
Language	English
Publishing date	2019-01-17
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2018.12.020
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Zs.A 1177: Show issues

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Article ; Online: A protocol for harvesting biodiversity data from Facebook.

Chowdhury, Shawan / Ahmed, Sultan / Alam, Shofiul / Callaghan, Corey T / Das, Priyanka / Di Marco, Moreno / Di Minin, Enrico / Jarić, Ivan / Labi, Mahzabin Muzahid / Rokonuzzaman, Md / Roll, Uri / Sbragaglia, Valerio / Siddika, Asma / Bonn, Aletta

Conservation biology : the journal of the Society for Conservation Biology

2024 , Page(s) e14257

Abstract: The expanding use of community science platforms has led to an exponential increase in biodiversity data in global repositories. Yet, understanding of species distributions remains patchy. Biodiversity data from social media can potentially reduce the ... ...

Abstract	The expanding use of community science platforms has led to an exponential increase in biodiversity data in global repositories. Yet, understanding of species distributions remains patchy. Biodiversity data from social media can potentially reduce the global biodiversity knowledge gap. However, practical guidelines and standardized methods for harvesting such data are nonexistent. Following data privacy and protection safeguards, we devised a standardized method for extracting species distribution records from Facebook groups that allow access to their data. It involves 3 steps: group selection, data extraction, and georeferencing the record location. We present how to structure keywords, search for species photographs, and georeference localities for such records. We further highlight some challenges users might face when extracting species distribution data from Facebook and suggest solutions. Following our proposed framework, we present a case study on Bangladesh's biodiversity-a tropical megadiverse South Asian country. We scraped nearly 45,000 unique georeferenced records across 967 species and found a median of 27 records per species. About 12% of the distribution data were for threatened species, representing 27% of all species. We also obtained data for 56 DataDeficient species for Bangladesh. If carefully harvested, social media data can significantly reduce global biodiversity knowledge gaps. Consequently, developing an automated tool to extract and interpret social media biodiversity data is a research priority.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	58735-7
ISSN	1523-1739 ; 0888-8892
ISSN (online)	1523-1739
ISSN	0888-8892
DOI	10.1111/cobi.14257
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Article ; Online: Extra centrosomes delay DNA damage-driven tumorigenesis.

Braun, Vincent Z / Karbon, Gerlinde / Schuler, Fabian / Schapfl, Marina A / Weiss, Johannes G / Petermann, Paul Y / Spierings, Diana C J / Tijhuis, Andrea E / Foijer, Floris / Labi, Verena / Villunger, Andreas

Science advances

2024 Volume 10, Issue 13, Page(s) eadk0564

Abstract: Deregulated centrosome numbers are frequently found in human cancer and can promote malignancies in model organisms. Current research aims to clarify if extra centrosomes are cause or consequence of malignant transformation, and if their biogenesis can ... ...

Abstract	Deregulated centrosome numbers are frequently found in human cancer and can promote malignancies in model organisms. Current research aims to clarify if extra centrosomes are cause or consequence of malignant transformation, and if their biogenesis can be targeted for therapy. Here, we show that oncogene-driven blood cancer is inert to genetic manipulation of centrosome numbers, whereas the formation of DNA damage-induced malignancies is delayed. We provide first evidence that this unexpected phenomenon is connected to extra centrosomes eliciting a pro-death signal engaging the apoptotic machinery. Apoptosis induction requires the PIDDosome multi-protein complex, as it can be abrogated by loss of any of its three components,
MeSH term(s)	Humans ; Centrosome ; Apoptosis/genetics ; Neoplasms/metabolism ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; DNA Damage
Language	English
Publishing date	2024-03-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adk0564
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Article ; Online: How cell death shapes cancer.

Labi, V / Erlacher, M

Cell death & disease

2015 Volume 6, Page(s) e1675

Abstract: Apoptosis has been established as a mechanism of anti-cancer defense. Members of the BCL-2 family are critical mediators of apoptotic cell death in health and disease, often found to be deregulated in cancer and believed to lead to the survival of ... ...

Abstract	Apoptosis has been established as a mechanism of anti-cancer defense. Members of the BCL-2 family are critical mediators of apoptotic cell death in health and disease, often found to be deregulated in cancer and believed to lead to the survival of malignant clones. However, over the years, a number of studies pointed out that a model in which cell death resistance unambiguously acts as a barrier against malignant disease might be too simple. This is based on paradoxical observations made in tumor patients as well as mouse models indicating that apoptosis can indeed drive tumor formation, at least under certain circumstances. One possible explanation for this phenomenon is that apoptosis can promote proliferation critically needed to compensate for cell loss, for example, upon therapy, and to restore tissue homeostasis. However, this, at the same time, can promote tumor development by allowing expansion of selected clones. Usually, tissue resident stem/progenitor cells are a major source for repopulation, some of them potentially carrying (age-, injury- or therapy-induced) genetic aberrations deleterious for the host. Thereby, apoptosis might drive genomic instability by facilitating the emergence of pathologic clones during phases of proliferation and subsequent replication stress-associated DNA damage. Tumorigenesis initiated by repeated cell attrition and repopulation, as confirmed in different genetic models, has parallels in human cancers, exemplified in therapy-induced secondary malignancies and myelodysplastic syndromes in patients with congenital bone marrow failure syndromes. Here, we aim to review evidence in support of the oncogenic role of stress-induced apoptosis.
MeSH term(s)	Animals ; Apoptosis/physiology ; Cell Death/physiology ; Cell Transformation, Neoplastic ; DNA Damage/genetics ; DNA Damage/physiology ; Humans ; Mice ; Neoplasms/metabolism ; Neoplasms/pathology
Language	English
Publishing date	2015-03-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2015.20
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Article ; Online: Bacterial Infection with

Jakic, Bojana / Kimpel, Janine / Olson, William J / Labi, Verena / Hermann-Kleiter, Natascha

Bio-protocol

2021 Volume 11, Issue 23, Page(s) e4247

Abstract: Pathogens such as bacteria, viruses, fungi, or protozoa can cause acute and chronic infections in their hosts. The intracellular ... ...

Abstract	Pathogens such as bacteria, viruses, fungi, or protozoa can cause acute and chronic infections in their hosts. The intracellular bacterium
Language	English
Publishing date	2021-12-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4247
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Article ; Online: A role for the nuclear receptor NR2F6 in peritoneal B cell homeostasis.

Olson, William J / Jakic, Bojana / Labi, Verena / Woelk, Johannes / Derudder, Emmanuel / Baier, Gottfried / Hermann-Kleiter, Natascha

Frontiers in immunology

2022 Volume 13, Page(s) 845235

Abstract: B cells are key mediators of humoral immunity. Mature B cells fall into various sub-classes that can be separated by their ontogeny, expression of cell surface markers, anatomical location, and function. B1 subsets play important roles in natural ... ...

Abstract	B cells are key mediators of humoral immunity. Mature B cells fall into various sub-classes that can be separated by their ontogeny, expression of cell surface markers, anatomical location, and function. B1 subsets play important roles in natural immunity and constitute the majority of B cells in newborns. In the adult, B1 cells predominate in the pleural and peritoneal cavities, while the mature B2 follicular subset makes up the major fraction of B cells in lymphoid tissue, although important subsets of antibody-secreting B1 cells are also present at these sites. B1 cells are the main producers of natural IgM but can also contribute to elimination of some pathogens, while B2 cells primarily mediate response to foreign antigens. The differential molecular underpinning of the B1 and B2 subsets remains incompletely understood. Here we demonstrate that germline-deficiency of the orphan nuclear receptor NR2F6 causes a partial loss of B1b and B2 B cells in the peritoneum while leaving peritoneal B1a cells unaltered. A competitive bone marrow chimera in
MeSH term(s)	Animals ; B-Lymphocytes ; Homeostasis ; Mice ; Peritoneal Cavity ; Peritoneum ; Receptors, Cytoplasmic and Nuclear ; Repressor Proteins/metabolism
Chemical Substances	Nr2f6 protein, mouse ; Receptors, Cytoplasmic and Nuclear ; Repressor Proteins
Language	English
Publishing date	2022-08-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.845235
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