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  1. Article ; Online: Polyploidy in Lung Regeneration: Double Trouble or Dynamic Duo?

    Zemans, Rachel L

    American journal of respiratory cell and molecular biology

    2022  Volume 66, Issue 5, Page(s) 481–483

    MeSH term(s) Alveolar Epithelial Cells ; Humans ; Hypertrophy ; Lung Injury ; Polyploidy ; Thorax
    Language English
    Publishing date 2022-03-10
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0062ED
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    Zs.A 2851: Show issues Location:
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  2. Article ; Online: Interferon with Dogma in Cytokine Release Syndrome and Acute Lung Injury.

    Denstaedt, Scott J / Zemans, Rachel L

    American journal of respiratory cell and molecular biology

    2022  Volume 68, Issue 1, Page(s) 7–8

    MeSH term(s) Humans ; Interferons ; Cytokine Release Syndrome ; Cytokines ; Lung ; Acute Lung Injury
    Chemical Substances Interferons (9008-11-1) ; Cytokines
    Language English
    Publishing date 2022-10-20
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0396ED
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  3. Article ; Online: Neutrophil-mediated T-Cell Suppression in Influenza: Novel Finding Raising Additional Questions.

    Zemans, Rachel L

    American journal of respiratory cell and molecular biology

    2018  Volume 58, Issue 4, Page(s) 423–425

    MeSH term(s) Humans ; Influenza, Human ; Macrophage-1 Antigen ; Neutrophils ; Orthomyxoviridae Infections ; T-Lymphocytes
    Chemical Substances Macrophage-1 Antigen
    Language English
    Publishing date 2018-04-30
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2017-0425ED
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  4. Article ; Online: Diversity at the border.

    Zemans, Rachel L / Hagood, James S

    Nature immunology

    2020  Volume 21, Issue 2, Page(s) 112–114

    MeSH term(s) Epigenesis, Genetic ; Genetic Variation ; Linkage Disequilibrium ; Transcriptome
    Language English
    Publishing date 2020-01-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-019-0585-9
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  5. Article ; Online: Mechanisms of ATII-to-ATI Cell Differentiation during Lung Regeneration.

    Aspal, Mohit / Zemans, Rachel L

    International journal of molecular sciences

    2020  Volume 21, Issue 9

    Abstract: The alveolar epithelium consists of (ATI) and type II (ATII) cells. ATI cells cover the majority of the alveolar surface due to their thin, elongated shape and are largely responsible for barrier function and gas exchange. During lung injury, ATI cells ... ...

    Abstract The alveolar epithelium consists of (ATI) and type II (ATII) cells. ATI cells cover the majority of the alveolar surface due to their thin, elongated shape and are largely responsible for barrier function and gas exchange. During lung injury, ATI cells are susceptible to injury, including cell death. Under some circumstances, ATII cells also die. To regenerate lost epithelial cells, ATII cells serve as progenitor cells. They proliferate to create new ATII cells and then differentiate into ATI cells [
    MeSH term(s) Alveolar Epithelial Cells/cytology ; Alveolar Epithelial Cells/physiology ; Animals ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Humans ; Lung/cytology ; Lung/physiology ; Lung Injury/metabolism ; Signal Transduction/physiology
    Language English
    Publishing date 2020-04-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21093188
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  6. Article ; Online: Mechanisms of ATII-to-ATI Cell Differentiation during Lung Regeneration

    Mohit Aspal / Rachel L. Zemans

    International Journal of Molecular Sciences, Vol 21, Iss 3188, p

    2020  Volume 3188

    Abstract: The alveolar epithelium consists of (ATI) and type II (ATII) cells. ATI cells cover the majority of the alveolar surface due to their thin, elongated shape and are largely responsible for barrier function and gas exchange. During lung injury, ATI cells ... ...

    Abstract The alveolar epithelium consists of (ATI) and type II (ATII) cells. ATI cells cover the majority of the alveolar surface due to their thin, elongated shape and are largely responsible for barrier function and gas exchange. During lung injury, ATI cells are susceptible to injury, including cell death. Under some circumstances, ATII cells also die. To regenerate lost epithelial cells, ATII cells serve as progenitor cells. They proliferate to create new ATII cells and then differentiate into ATI cells [ 1 , 2 , 3 ]. Regeneration of ATI cells is critical to restore normal barrier and gas exchange function. Although the signaling pathways by which ATII cells proliferate have been explored [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 ], the mechanisms of ATII-to-ATI cell differentiation have not been well studied until recently. New studies have uncovered signaling pathways that mediate ATII-to-ATI differentiation. Bone morphogenetic protein (BMP) signaling inhibits ATII proliferation and promotes differentiation. Wnt/β-catenin and ETS variant transcription factor 5 (Etv5) signaling promote proliferation and inhibit differentiation. Delta-like 1 homolog (Dlk1) leads to a precisely timed inhibition of Notch signaling in later stages of alveolar repair, activating differentiation. Yes-associated protein/Transcriptional coactivator with PDZ-binding motif (YAP/TAZ) signaling appears to promote both proliferation and differentiation. We recently identified a novel transitional cell state through which ATII cells pass as they differentiate into ATI cells, and this has been validated by others in various models of lung injury. This intermediate cell state is characterized by the activation of Transforming growth factor beta (TGFβ) and other pathways, and some evidence suggests that TGFβ signaling induces and maintains this state. While the abovementioned signaling pathways have all been shown to be involved in ATII-to-ATI cell differentiation during lung regeneration, there is much that remains to be understood. The up- and ...
    Keywords alveolar epithelium ; lung injury ; lung regeneration ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 333
    Language English
    Publishing date 2020-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: What drives neutrophils to the alveoli in ARDS?

    Zemans, Rachel L / Matthay, Michael A

    Thorax

    2017  Volume 72, Issue 1, Page(s) 1–3

    Language English
    Publishing date 2017-01
    Publishing country England
    Document type Editorial
    ZDB-ID 204353-1
    ISSN 1468-3296 ; 0040-6376
    ISSN (online) 1468-3296
    ISSN 0040-6376
    DOI 10.1136/thoraxjnl-2016-209170
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  8. Article ; Online: Cellular senescence: friend or foe to respiratory viral infections?

    Kelley, William J / Zemans, Rachel L / Goldstein, Daniel R

    The European respiratory journal

    2020  Volume 56, Issue 6

    Abstract: Cellular senescence permanently arrests the replication of various cell types and contributes to age-associated diseases. In particular, cellular senescence may enhance chronic lung diseases including COPD and idiopathic pulmonary fibrosis. However, the ... ...

    Abstract Cellular senescence permanently arrests the replication of various cell types and contributes to age-associated diseases. In particular, cellular senescence may enhance chronic lung diseases including COPD and idiopathic pulmonary fibrosis. However, the role cellular senescence plays in the pathophysiology of acute inflammatory diseases, especially viral infections, is less well understood. There is evidence that cellular senescence prevents viral replication by increasing antiviral cytokines, but other evidence shows that senescence may enhance viral replication by downregulating antiviral signalling. Furthermore, cellular senescence leads to the secretion of inflammatory mediators, which may either promote host defence or exacerbate immune pathology during viral infections. In this Perspective article, we summarise how senescence contributes to physiology and disease, the role of senescence in chronic lung diseases, and how senescence impacts acute respiratory viral infections. Finally, we develop a potential framework for how senescence may contribute, both positively and negatively, to the pathophysiology of viral respiratory infections, including severe acute respiratory syndrome due to the coronavirus SARS-CoV-2.
    MeSH term(s) Cellular Senescence ; Humans ; Lung/pathology ; Respiratory Tract Infections/pathology ; Respiratory Tract Infections/virology ; Virus Diseases/pathology ; Virus Diseases/virology
    Keywords covid19
    Language English
    Publishing date 2020-12-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.02708-2020
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    Zs.A 2322: Show issues Location:
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    Zs.MO 292: Show issues

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  9. Article ; Online: Early-life pulmonary viral infection leads to long-term functional and lower airway structural changes in the lungs.

    Malinczak, Carrie-Anne / Fonseca, Wendy / Hrycaj, Steven M / Morris, Susan B / Rasky, Andrew J / Yagi, Kazuma / Wellik, Deneen M / Ziegler, Steven F / Zemans, Rachel L / Lukacs, Nicholas W

    American journal of physiology. Lung cellular and molecular physiology

    2024  Volume 326, Issue 3, Page(s) L280–L291

    Abstract: Early-life respiratory virus infections have been correlated with enhanced development of childhood asthma. In particular, significant numbers of respiratory syncytial virus (RSV)-hospitalized infants go on to develop lung disease. It has been suggested ... ...

    Abstract Early-life respiratory virus infections have been correlated with enhanced development of childhood asthma. In particular, significant numbers of respiratory syncytial virus (RSV)-hospitalized infants go on to develop lung disease. It has been suggested that early-life viral infections may lead to altered lung development or repair that negatively impacts lung function later in life. Our data demonstrate that early-life RSV infection modifies lung structure, leading to decreased lung function. At 5 wk postneonatal RSV infection, significant defects are observed in baseline pulmonary function test (PFT) parameters consistent with decreased lung function as well as enlarged alveolar spaces. Lung function changes in the early-life RSV-infected group continue at 3 mo of age. The altered PFT and structural changes induced by early-life RSV were mitigated in
    MeSH term(s) Humans ; Infant ; Animals ; Mice ; Respiratory Syncytial Virus Infections ; Lung/pathology ; Pneumonia/complications ; Lung Diseases/complications ; Respiratory Syncytial Virus, Human ; Mice, Inbred BALB C
    Language English
    Publishing date 2024-01-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00300.2023
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  10. Article ; Online: MAP kinase phosphatase-1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution.

    Fortier, Sean M / Walker, Natalie M / Penke, Loka R / Baas, Jared D / Shen, Qinxue / Speth, Jennifer M / Huang, Steven K / Zemans, Rachel L / Bennett, Anton M / Peters-Golden, Marc

    The Journal of clinical investigation

    2024  

    Abstract: Fibrosis following tissue injury is distinguished from normal repair by the accumulation of pathogenic and apoptosis-resistant myofibroblasts (MFs), which arise primarily by differentiation from resident fibroblasts. Endogenous molecular brakes that ... ...

    Abstract Fibrosis following tissue injury is distinguished from normal repair by the accumulation of pathogenic and apoptosis-resistant myofibroblasts (MFs), which arise primarily by differentiation from resident fibroblasts. Endogenous molecular brakes that promote MF dedifferentiation and clearance during spontaneous resolution of experimental lung fibrosis may provide insights that could inform and improve treatment of progressive pulmonary fibrosis in patients. Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP1) influences cellular phenotype and fate through precise and timely regulation of MAPK activity within various cell types and tissues, yet its role in lung fibroblasts and pulmonary fibrosis has not been explored. Utilizing gain- and loss-of-function studies, we found that MKP1 promoted lung MF dedifferentiation and restored their sensitivity to apoptosis - effects determined to be mainly dependent upon its dephosphorylation of p38α MAPK (p38α). Fibroblast-specific deletion of MKP1 following peak bleomycin-induced lung fibrosis largely abrogated its subsequent spontaneous resolution. Such resolution was restored by treating these transgenic mice with the p38α inhibitor VX-702. We conclude that MKP1 is a critical antifibrotic brake whose inhibition of pathogenic p38α in lung fibroblasts is necessary for fibrosis resolution following lung injury.
    Language English
    Publishing date 2024-03-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI172826
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