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  1. Article: Drug like HSP27 cross linkers with chromenone structure ameliorates pulmonary fibrosis.

    Yoo, Young Jo / Jeon, Seulgi / Jin, Hee / Won, Hee Yeon / Jeong, Mi Gyeong / Cho, Yeseul / Hwang, Eun Sook / Na, Younghwa / Cho, Jaeho / Lee, Yun-Sil

    Frontiers in pharmacology

    2023  Volume 14, Page(s) 1203033

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2023-07-04
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1203033
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Therapeutic potential of targeting cathepsin S in pulmonary fibrosis.

    Yoo, YoungJo / Choi, Eun / Kim, Yejin / Cha, Yunyoung / Um, Eunhye / Kim, Younghwa / Kim, Yunji / Lee, Yun-Sil

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2021  Volume 145, Page(s) 112245

    Abstract: Cathepsin S (CTSS), a lysosomal protease, belongs to a family of cysteine cathepsin proteases that promote degradation of damaged proteins in the endolysosomal pathway. Aberrant CTSS expression and regulation are associated with the pathogenesis of ... ...

    Abstract Cathepsin S (CTSS), a lysosomal protease, belongs to a family of cysteine cathepsin proteases that promote degradation of damaged proteins in the endolysosomal pathway. Aberrant CTSS expression and regulation are associated with the pathogenesis of several diseases, including lung diseases. CTSS overexpression causes a variety of pathological processes, including pulmonary fibrosis, with increased CTSS secretion and accelerated extracellular matrix remodeling. Compared to many other cysteine cathepsin family members, CTSS has unique features that it presents limited tissue expression and retains its enzymatic activity at a neutral pH, suggesting its decisive involvement in disease microenvironments. In this review, we investigated the role of CTSS in lung disease, exploring recent studies that have indicated that CTSS mediates fibrosis in unique ways, along with its structure, substrates, and distinct regulation. We also outlined examples of CTSS inhibitors in clinical and preclinical development and proposed CTSS as a potential therapeutic target for pulmonary fibrosis.
    MeSH term(s) Animals ; Cathepsins/antagonists & inhibitors ; Cathepsins/metabolism ; Drug Development ; Extracellular Matrix/metabolism ; Humans ; Hydrogen-Ion Concentration ; Molecular Targeted Therapy ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/physiopathology
    Chemical Substances Cathepsins (EC 3.4.-) ; cathepsin S (EC 3.4.22.27)
    Language English
    Publishing date 2021-11-10
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2021.112245
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.198: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Di-2-ethylhexylphthalate promotes thyroid cell proliferation and DNA damage through activating thyrotropin-receptor-mediated pathways in vitro and in vivo.

    Kim, Seoyoung / Park, Ga-Young / Yoo, Young Jo / Jeong, Ji Seong / Nam, Ki Taek / Jee, Sun-Ha / Lim, Kyung-Min / Lee, Yun-Sil

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2018  Volume 124, Page(s) 265–272

    Abstract: Phthalates are being suggested to be associated with altered thyroid function and proliferative changes, but detailed mechanisms remain unclear. Here, we examined the effects of di-(2-ethylhexyl) phthalate (DEHP) on DNA damage and proliferation in ... ...

    Abstract Phthalates are being suggested to be associated with altered thyroid function and proliferative changes, but detailed mechanisms remain unclear. Here, we examined the effects of di-(2-ethylhexyl) phthalate (DEHP) on DNA damage and proliferation in thyroid using thyroid carcinoma cell line, 8505C, in vitro and the rats orally treated with DEHP at 0, 0.3, 3, 30 and 150 mg/kg for 90 days from post-natal day 9 in vivo. Exposure to DHEP (1-50 μM) induced cellular proliferation, as evidenced by increased cell viability and DNA synthesis. Activation of γH2AX, a sensitive biomarker for DNA damage was observed following the exposure to DHEP (from 5 to 50 μM) with increased comet tail moment (5-100 μM) in comet assay, reflecting that DNA damage also occurred. When upstream signaling was examined, both thyrotropin receptor (TSHR)-ERK1/2 axis and TSHR-AKT axis were activated with upregulation of Pax8, a master transcriptional factor for thyroid differentiation and proliferation. Thyroid tissue from juvenile rats orally exposed to DEHP also confirmed DNA damage responses and the activation of TSHR signaling, which was evident from 0.3 to 3 mg/kg respectively. Notably, deletion of TSHR through siRNA attenuated these DEHP-induced events in vitro. Collectively these results suggest that DEHP induces DNA damage and cellular proliferation in thyroid, which appears to be from TSHR activation, providing an important insight into endocrine disrupting activities of phthalates on thyroid.
    MeSH term(s) Animals ; Cell Line, Tumor ; Cell Proliferation/drug effects ; DNA Damage/drug effects ; Diethylhexyl Phthalate/adverse effects ; Female ; Histones/metabolism ; Humans ; Male ; Phosphoproteins/metabolism ; Rats, Sprague-Dawley ; Receptors, Thyrotropin/metabolism ; Signal Transduction/drug effects ; Thyroid Gland/drug effects ; Thyroid Gland/pathology
    Chemical Substances Histones ; Phosphoproteins ; Receptors, Thyrotropin ; gamma-H2AX protein, rat ; Diethylhexyl Phthalate (C42K0PH13C)
    Language English
    Publishing date 2018-12-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2018.12.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 529: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: The Hsp27-Mediated IkBα-NFκB Signaling Axis Promotes Radiation-Induced Lung Fibrosis.

    Kim, Jee-Youn / Jeon, Seulgi / Yoo, Young Jo / Jin, Hee / Won, Hee Yeon / Yoon, Kyeonghee / Hwang, Eun Sook / Lee, Yoon-Jin / Na, Younghwa / Cho, Jaeho / Lee, Yun-Sil

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2019  Volume 25, Issue 17, Page(s) 5364–5375

    Abstract: Purpose: Lung fibrosis is a major side effect experienced by patients after lung cancer radiotherapy. However, effective protection strategies and underlying treatment targets remain unclear. In an effort to improve clinical outcomes, pharmacologic ... ...

    Abstract Purpose: Lung fibrosis is a major side effect experienced by patients after lung cancer radiotherapy. However, effective protection strategies and underlying treatment targets remain unclear. In an effort to improve clinical outcomes, pharmacologic treatment of fibrosis is becoming increasingly popular; however, no ideal therapeutic strategy is yet available.
    Experimental design: We used a mouse model to irradiate high focal (90 or 75 Gy) to 3-mm volume of the left lung. Lung tissues of mice were subjected to microarray, mRNA expression, and immunohistochemical analysis. Correlations of radiation (IR)-induced epithelial-mesenchymal transition (EMT) were validated in lung cell lines using appropriate treatments to activate or inhibit selected pathways.
    Results: The expression of Hsp27 was increased during IR-induced lung fibrosis in a mouse model. Inhibition of functional Hsp27 using shRNA and a synthetic small molecule inhibitor (J2) in lung cells alleviated IR-mediated EMT. The activation of NFkB pathways via direct interaction between Hsp27 and IkBα resulted in increased expressions of Twist, IL-1β, and IL-6 and facilitated IR-mediated EMT, which was identified as an underlying mechanism of Hsp27-mediated fibrosis after IR. J2 also inhibited IR-induced lung fibrosis in an orthotopic lung cancer model, and IR-induced lung fibrotic tissues from patients showed higher expression of Hsp27 than unirradiated lungs.
    Conclusions: Collectively, IkBα-NFkB signaling activation by Hsp27, which resulted in the facilitation of Twist, IL1β, and IL6 expression, is involved in the EMT process that is tightly connected to the development of IR-induced lung fibrosis. Our findings also suggest that inhibition of Hsp27 has the potential to become a valuable therapeutic strategy for IR-induced lung fibrosis.
    MeSH term(s) Animals ; Disease Models, Animal ; Epithelial-Mesenchymal Transition ; Gamma Rays ; Gene Expression Profiling ; HSP27 Heat-Shock Proteins/metabolism ; Heat-Shock Proteins/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Chaperones/metabolism ; NF-KappaB Inhibitor alpha/metabolism ; NF-kappa B/metabolism ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Radiation Injuries/etiology ; Radiation Injuries/metabolism ; Radiation Injuries/pathology ; Signal Transduction ; Tumor Cells, Cultured
    Chemical Substances HSP27 Heat-Shock Proteins ; HSPB1 protein, human ; Heat-Shock Proteins ; Hspb2 protein, mouse ; Molecular Chaperones ; NF-kappa B ; NF-KappaB Inhibitor alpha (139874-52-5)
    Language English
    Publishing date 2019-05-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-18-3900
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4223: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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