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  1. Article: Cell competition drives bronchiolization and pulmonary fibrosis.

    Warren, Rachel / Klinkhammer, Kylie / Lyu, Handeng / Yao, Changfu / Stripp, Barry / De Langhe, Stijn P

    Research square

    2024  

    Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive scarring disease arising from the maladaptive differentiation of lung stem cells into bronchial epithelial cells rather than into alveolar type 1 (AT1) cells, which are responsible for gas exchange. ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is a progressive scarring disease arising from the maladaptive differentiation of lung stem cells into bronchial epithelial cells rather than into alveolar type 1 (AT1) cells, which are responsible for gas exchange. Here, we report that healthy lungs maintain their stem cells through tonic Hippo and β-catenin signaling, which promote Yap/Taz degradation and allow for low level expression of the Wnt target gene
    Language English
    Publishing date 2024-04-22
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-4177351/v1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Hippo signaling impairs alveolar epithelial regeneration in pulmonary fibrosis.

    Warren, Rachel / Lyu, Handeng / Klinkhammer, Kylie / De Langhe, Stijn P

    eLife

    2023  Volume 12

    Abstract: Idiopathic pulmonary fibrosis (IPF) consists of fibrotic alveolar remodeling and progressive loss of pulmonary function. Genetic and experimental evidence indicates that chronic alveolar injury and failure to properly repair the respiratory epithelium ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) consists of fibrotic alveolar remodeling and progressive loss of pulmonary function. Genetic and experimental evidence indicates that chronic alveolar injury and failure to properly repair the respiratory epithelium are intrinsic to IPF pathogenesis. Loss of alveolar type 2 (AT2) stem cells or mutations that either impair their self-renewal and/or impair their differentiation into AT1 cells can serve as a trigger of pulmonary fibrosis. Recent reports indicate increased YAP activity in respiratory epithelial cells in IPF lungs. Individual IPF epithelial cells with aberrant YAP activation in bronchiolized regions frequently co-express AT1, AT2, conducting airway selective markers and even mesenchymal or EMT markers, demonstrating 'indeterminate' states of differentiation and suggesting that aberrant YAP signaling might promote pulmonary fibrosis. Yet, Yap and Taz have recently also been shown to be important for AT1 cell maintenance and alveolar epithelial regeneration after
    MeSH term(s) Humans ; Hippo Signaling Pathway ; Lung/pathology ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Transcription Factors/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Bleomycin/toxicity ; Bleomycin/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; Transcription Factors ; Intracellular Signaling Peptides and Proteins ; Bleomycin (11056-06-7)
    Language English
    Publishing date 2023-05-11
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.85092
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Protocol for the use of signal amplification by exchange reaction-fluorescence in situ hybridization on adult formalin-fixed paraffin-embedded mouse lung tissue.

    Warren, Rachel / Shaik, Aftab / Teubner, Lauren / Lyu, Handeng / De Langhe, Stijn

    STAR protocols

    2023  Volume 4, Issue 2, Page(s) 102353

    Abstract: Fluorescence in situ hybridization (FISH) is a useful tool for analyzing RNA expression, but difficulties arise with low-abundance RNA and in tissues that are formalin-fixed paraffin-embedded (FFPE) because reagents can be expensive. In this protocol, we ...

    Abstract Fluorescence in situ hybridization (FISH) is a useful tool for analyzing RNA expression, but difficulties arise with low-abundance RNA and in tissues that are formalin-fixed paraffin-embedded (FFPE) because reagents can be expensive. In this protocol, we adapt a previously designed FISH amplification protocol (SABER [signal amplification by exchange reaction]) for adult mouse FFPE lung sections by using probes that are extended and branched to amplify the signal. We combine FISH and immunostaining to identify cell-specific RNA. For complete details on the use and execution of this protocol, please refer to Kishi et al.
    Language English
    Publishing date 2023-06-09
    Publishing country United States
    Document type Journal Article
    ISSN 2666-1667
    ISSN (online) 2666-1667
    DOI 10.1016/j.xpro.2023.102353
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  4. Article ; Online: Niche-mediated repair of airways is directed in an occupant-dependent manner.

    Lyu, Handeng / Warren, Rachel / Gao, Shan / Klinkhammer, Kylie / Yuan, Tingting / Zhang, Jin-San / Brownfield, Douglas / Li, Xiaokun / De Langhe, Stijn P

    Cell reports

    2022  Volume 41, Issue 12, Page(s) 111863

    Abstract: In injured airways of the adult lung, epithelial progenitors are called upon to repair by nearby mesenchymal cells via signals transmitted through the niche. Currently, it is unclear whether repair is coordinated by the mesenchymal cells that maintain ... ...

    Abstract In injured airways of the adult lung, epithelial progenitors are called upon to repair by nearby mesenchymal cells via signals transmitted through the niche. Currently, it is unclear whether repair is coordinated by the mesenchymal cells that maintain the niche or by the airway epithelial cells that occupy it. Here, we show that the spatiotemporal expression of Fgf10 by the niche is primarily orchestrated by the niche's epithelial occupants-both those that reside prior to, and following, injury. During homeostasis, differentiated airway epithelial cells secrete Sonic hedgehog (Shh) to inhibit Fgf10 expression by Gli1
    MeSH term(s) Hedgehog Proteins/metabolism ; Lung/metabolism ; Cell Differentiation ; Epithelial Cells/metabolism ; Mesenchymal Stem Cells/metabolism ; Zinc Finger Protein GLI1/metabolism
    Chemical Substances Hedgehog Proteins ; Zinc Finger Protein GLI1
    Language English
    Publishing date 2022-11-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.111863
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: FGF10 Therapeutic Administration Promotes Mobilization of Injury-Activated Alveolar Progenitors in a Mouse Fibrosis Model.

    Lv, Yu-Qing / Cai, Ge-Fu / Zeng, Ping-Ping / Dhlamini, Qhaweni / Chen, Le-Fu / Chen, Jun-Jie / Lyu, Han-Deng / Mossahebi-Mohammadi, Majid / Ahmadvand, Negah / Bellusci, Saverio / Li, Xiaokun / Chen, Chengshui / Zhang, Jin-San

    Cells

    2022  Volume 11, Issue 15

    Abstract: Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease with dire consequences and in urgent need of improved therapies. Compelling evidence indicates that damage or dysfunction of AT2s is of central importance in the development ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease with dire consequences and in urgent need of improved therapies. Compelling evidence indicates that damage or dysfunction of AT2s is of central importance in the development of IPF. We recently identified a novel AT2 subpopulation characterized by low SFTPC expression but that is enriched for PD-L1 in mice. These cells represent quiescent, immature AT2 cells during normal homeostasis and expand upon pneumonectomy (PNX) and were consequently named injury-activated alveolar progenitors (IAAPs). FGF10 is shown to play critical roles in lung development, homeostasis, and injury repair demonstrated in genetically engineered mice. In an effort to bridge the gap between the promising properties of endogenous Fgf10 manipulation and therapeutic reality, we here investigated whether the administration of exogenous recombinant FGF10 protein (rFGF10) can provide preventive and/or therapeutic benefit in a mouse model of bleomycin-induced pulmonary fibrosis with a focus on its impact on IAAP dynamics. C57BL/6 mice and
    MeSH term(s) Animals ; Bleomycin/therapeutic use ; Body Weight ; Disease Models, Animal ; Fibroblast Growth Factor 10/pharmacology ; Lung/pathology ; Mice ; Mice, Inbred C57BL ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/metabolism
    Chemical Substances Fgf10 protein, mouse ; Fibroblast Growth Factor 10 ; Bleomycin (11056-06-7)
    Language English
    Publishing date 2022-08-03
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11152396
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Temporospatial Expression of Fgfr1 and 2 During Lung Development, Homeostasis, and Regeneration.

    Yuan, Tingting / Klinkhammer, Kylie / Lyu, Handeng / Gao, Shan / Yuan, Jie / Hopkins, Seantel / Zhang, Jin-San / De Langhe, Stijn P

    Frontiers in pharmacology

    2020  Volume 11, Page(s) 120

    Abstract: Fgfr1 (Fibroblast growth factor receptor 1) and Fgfr2 are dynamically expressed during lung development, homeostasis, and regeneration. Our current analysis indicates that Fgfr2 is expressed in distal epithelial progenitors AT2, AT1, club, and basal ... ...

    Abstract Fgfr1 (Fibroblast growth factor receptor 1) and Fgfr2 are dynamically expressed during lung development, homeostasis, and regeneration. Our current analysis indicates that Fgfr2 is expressed in distal epithelial progenitors AT2, AT1, club, and basal cells but not in ciliated or neuroendocrine cells during lung development and homeostasis. However, after injury, Fgfr2 becomes upregulated in neuroendocrine cells and distal club cells. Epithelial Fgfr1 expression is minimal throughout lung development, homeostasis, and regeneration. We further find both Fgfr1 and Fgfr2 strongly expressed in cartilage progenitors and airway smooth muscle cells during lung development, whereas Fgfr1 but not Fgfr2 was expressed in lipofibroblasts and vascular smooth muscle cells. In the adult lung, Fgfr1 and Fgfr2 were mostly downregulated in smooth muscle cells but became upregulated after injury. Fgfr1 remained expressed in mesenchymal alveolar niche cells or lipofibroblasts with lower levels of expression in their descendant (alveolar) myofibroblasts during alveologenesis.
    Language English
    Publishing date 2020-03-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2020.00120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Erratum: The WW domains dictate isoform-specific regulation of YAP1 stability and pancreatic cancer cell malignancy: Erratum.

    Guo, Qiang / Quan, Meiyu / Dong, Jinglai / Bai, Jing / Wang, Jie / Han, Rui / Wang, Wei / Cai, Yaxin / Lv, Yu-Qing / Chen, Qianjie / Xu, Huijing / Lyu, Han-Deng / Deng, Liancheng / Zhou, Depu / Xiao, Xueyuan / De Langhe, Stijn / Billadeau, Daniel D / Lou, Zhenkun / Zhang, Jin-San

    Theranostics

    2020  Volume 10, Issue 22, Page(s) 10341–10344

    Abstract: This corrects the article DOI: 10.7150/thno.42795.]. ...

    Abstract [This corrects the article DOI: 10.7150/thno.42795.].
    Language English
    Publishing date 2020-08-18
    Publishing country Australia
    Document type Journal Article ; Published Erratum
    ZDB-ID 2592097-2
    ISSN 1838-7640 ; 1838-7640
    ISSN (online) 1838-7640
    ISSN 1838-7640
    DOI 10.7150/thno.51728
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The WW domains dictate isoform-specific regulation of YAP1 stability and pancreatic cancer cell malignancy.

    Guo, Qiang / Quan, Meiyu / Dong, Jinglai / Bai, Jing / Wang, Jie / Han, Rui / Wang, Wei / Cai, Yaxin / Lv, Yu-Qing / Chen, Qianjie / Xu, Huijing / Lyu, Han-Deng / Deng, Liancheng / Zhou, Depu / Xiao, Xueyuan / De Langhe, Stijn / Billadeau, Daniel D / Lou, Zhenkun / Zhang, Jin-San

    Theranostics

    2020  Volume 10, Issue 10, Page(s) 4422–4436

    Abstract: YAP1 is a key mediator of the Hippo pathway capable of exerting a profound effect on organ size as well as tumorigenesis. Alternative mRNA splicing of human YAP1 results in at least 8 protein isoforms that differ within the ... ...

    Abstract YAP1 is a key mediator of the Hippo pathway capable of exerting a profound effect on organ size as well as tumorigenesis. Alternative mRNA splicing of human YAP1 results in at least 8 protein isoforms that differ within the 2
    MeSH term(s) Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/metabolism ; Adenocarcinoma/metabolism ; Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Invasiveness ; Pancreatic Neoplasms/metabolism ; Protein Isoforms/chemistry ; Protein Isoforms/metabolism ; RNA, Messenger/metabolism ; Transcription Factors/chemistry ; Transcription Factors/metabolism ; WW Domains ; YAP-Signaling Proteins ; Pancreatic Neoplasms
    Chemical Substances Adaptor Proteins, Signal Transducing ; Protein Isoforms ; RNA, Messenger ; Transcription Factors ; YAP-Signaling Proteins ; YAP1 protein, human
    Language English
    Publishing date 2020-03-15
    Publishing country Australia
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2592097-2
    ISSN 1838-7640 ; 1838-7640
    ISSN (online) 1838-7640
    ISSN 1838-7640
    DOI 10.7150/thno.42795
    Database MEDical Literature Analysis and Retrieval System OnLINE

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