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  1. Article ; Online: The Authors' Reply.

    Lee, Tzu-Han / Yeh, Huan-Jui

    American journal of physical medicine & rehabilitation

    2022  Volume 101, Issue 10, Page(s) e156–e157

    Language English
    Publishing date 2022-05-14
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 219390-5
    ISSN 1537-7385 ; 0002-9491 ; 0894-9115
    ISSN (online) 1537-7385
    ISSN 0002-9491 ; 0894-9115
    DOI 10.1097/PHM.0000000000002049
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: SARS-CoV-2 infection reduces Krüppel-Like Factor 2 in human lung autopsy.

    Lee, Tzu-Han / Wu, David / Guzy, Robert / Schoettler, Nathan / Adegunsoye, Ayodeji / Mueller, Jeffrey / Hussein, Aliya / Sperling, Anne / Mutlu, Gokhan M / Fang, Yun

    bioRxiv : the preprint server for biology

    2021  

    Abstract: Acute respiratory distress syndrome (ARDS) occurred in ~12% of hospitalized COVID-19 patients in a recent New York City cohort. Pulmonary endothelial dysfunction, characterized by increased expression of inflammatory genes and increased monolayer ... ...

    Abstract Acute respiratory distress syndrome (ARDS) occurred in ~12% of hospitalized COVID-19 patients in a recent New York City cohort. Pulmonary endothelial dysfunction, characterized by increased expression of inflammatory genes and increased monolayer permeability, is a major component of ARDS. Vascular leak results in parenchymal accumulation of leukocytes, protein, and extravascular water, leading to pulmonary edema, ischemia, and activation of coagulation associated with COVID-19. Endothelial inflammation further contributes to uncontrolled cytokine storm in ARDS. We have recently demonstrated that Kruppel-like factor 2 (KLF2), a transcription factor which promotes endothelial quiescence and monolayer integrity, is significantly reduced in experimental models of ARDS. Lung inflammation and high-tidal volume ventilation result in reduced KLF2, leading to pulmonary endothelial dysfunction and acute lung injury. Mechanistically, we found that KLF2 is a potent transcriptional activator of Rap guanine nucleotide exchange factor 3 (RAPGEF3) which orchestrates and maintains vascular integrity. Moreover, KLF2 regulates multiple genome-wide association study (GWAS)-implicated ARDS genes. Whether lung KLF2 is regulated by SARS-CoV-2 infection is unknown. Here we report that endothelial KLF2 is significantly reduced in human lung autopsies from COVID-19 patients, which supports that ARDS due to SARS-CoV-2 is a vascular phenotype possibly attributed to KLF2 down-regulation. We provide additional data demonstrating that KLF2 is down-regulated in SARS-CoV infection in mice.
    Language English
    Publishing date 2021-01-18
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2021.01.15.426691
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: SARS-CoV-2 Infection Is Associated with Reduced Krüppel-like Factor 2 in Human Lung Autopsy.

    Wu, David / Lee, Tzu-Han / Huang, Ru-Ting / D Guzy, Robert / Schoettler, Nathan / Adegunsoye, Ayodeji / Mueller, Jeffrey / Husain, Aliya / I Sperling, Anne / Mutlu, Gökhan M / Fang, Yun

    American journal of respiratory cell and molecular biology

    2021  Volume 65, Issue 2, Page(s) 222–226

    MeSH term(s) Autopsy ; COVID-19/metabolism ; COVID-19/pathology ; Female ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Lung/metabolism ; Lung/pathology ; Lung/virology ; Male ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Respiratory Mucosa/virology ; SARS-CoV-2/metabolism
    Chemical Substances KLF2 protein, human ; Kruppel-Like Transcription Factors
    Language English
    Publishing date 2021-07-23
    Publishing country United States
    Document type Letter
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2020-0564LE
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Cervical cord injury after massage.

    Lee, Tzu-Han / Chiu, Jan-Wei / Chan, Rai-Chi

    American journal of physical medicine & rehabilitation

    2011  Volume 90, Issue 10, Page(s) 856–859

    Abstract: We present the case of a 47-yr-old gentleman with cervical cord injury after he received massage in the neck area. Magnetic resonance imaging of the cervical spine showed a herniation of the nucleus pulposus and compressive myelopathy. The patient ... ...

    Abstract We present the case of a 47-yr-old gentleman with cervical cord injury after he received massage in the neck area. Magnetic resonance imaging of the cervical spine showed a herniation of the nucleus pulposus and compressive myelopathy. The patient required surgical intervention and rehabilitation. Despite 6 mos of rehabilitation, residual hand dysfunction and minor ambulation problems persisted. Although massage has many benefits, this case reminds us that there is potential danger in performing neck massage.
    MeSH term(s) Cervical Vertebrae ; Humans ; Intervertebral Disc Displacement/diagnosis ; Intervertebral Disc Displacement/etiology ; Intervertebral Disc Displacement/therapy ; Male ; Massage/adverse effects ; Middle Aged ; Spinal Cord Compression/diagnosis ; Spinal Cord Compression/etiology ; Spinal Cord Compression/therapy
    Language English
    Publishing date 2011-10
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 219390-5
    ISSN 1537-7385 ; 0002-9491 ; 0894-9115
    ISSN (online) 1537-7385
    ISSN 0002-9491 ; 0894-9115
    DOI 10.1097/PHM.0b013e318228c27c
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: SARS-CoV-2 infection reduces Krüppel-Like Factor 2 in human lung autopsy

    Lee, Tzu-Han / Wu, David / Guzy, Robert / Schoettler, Nathan / Adegunsoye, Ayodeji / Mueller, Jeffrey / Hussein, Aliya / Sperling, Anne / Mutlu, Gokhan M / Fang, Yun

    bioRxiv

    Abstract: Acute respiratory distress syndrome (ARDS) occurred in ~12% of hospitalized COVID-19 patients in a recent New York City cohort. Pulmonary endothelial dysfunction, characterized by increased expression of inflammatory genes and increased monolayer ... ...

    Abstract Acute respiratory distress syndrome (ARDS) occurred in ~12% of hospitalized COVID-19 patients in a recent New York City cohort. Pulmonary endothelial dysfunction, characterized by increased expression of inflammatory genes and increased monolayer permeability, is a major component of ARDS. Vascular leak results in parenchymal accumulation of leukocytes, protein, and extravascular water, leading to pulmonary edema, ischemia, and activation of coagulation associated with COVID-19. Endothelial inflammation further contributes to uncontrolled cytokine storm in ARDS. We have recently demonstrated that Kruppel-like factor 2 (KLF2), a transcription factor which promotes endothelial quiescence and monolayer integrity, is significantly reduced in experimental models of ARDS. Lung inflammation and high-tidal volume ventilation result in reduced KLF2, leading to pulmonary endothelial dysfunction and acute lung injury. Mechanistically, we found that KLF2 is a potent transcriptional activator of Rap guanine nucleotide exchange factor 3 (RAPGEF3) which orchestrates and maintains vascular integrity. Moreover, KLF2 regulates multiple genome-wide association study (GWAS)-implicated ARDS genes. Whether lung KLF2 is regulated by SARS-CoV-2 infection is unknown. Here we report that endothelial KLF2 is significantly reduced in human lung autopsies from COVID-19 patients, which supports that ARDS due to SARS-CoV-2 is a vascular phenotype possibly attributed to KLF2 down-regulation. We provide additional data demonstrating that KLF2 is down-regulated in SARS-CoV infection in mice.
    Keywords covid19
    Language English
    Publishing date 2021-01-18
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2021.01.15.426691
    Database COVID19

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  6. Article ; Online: Fibroblast-enriched endoplasmic reticulum protein TXNDC5 promotes pulmonary fibrosis by augmenting TGFβ signaling through TGFBR1 stabilization.

    Lee, Tzu-Han / Yeh, Chih-Fan / Lee, Ying-Tung / Shih, Ying-Chun / Chen, Yen-Ting / Hung, Chen-Ting / You, Ming-Yi / Wu, Pei-Chen / Shentu, Tzu-Pin / Huang, Ru-Ting / Lin, Yu-Shan / Wu, Yueh-Feng / Lin, Sung-Jan / Lu, Frank-Leigh / Tsao, Po-Nien / Lin, Tzu-Hung / Lo, Shen-Chuan / Tseng, Yi-Shuan / Wu, Wan-Lin /
    Chen, Chiung-Nien / Wu, Chau-Chung / Lin, Shuei-Liong / Sperling, Anne I / Guzy, Robert D / Fang, Yun / Yang, Kai-Chien

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 4254

    Abstract: Pulmonary fibrosis (PF) is a major public health problem with limited therapeutic options. There is a clear need to identify novel mediators of PF to develop effective therapeutics. Here we show that an ER protein disulfide isomerase, thioredoxin domain ... ...

    Abstract Pulmonary fibrosis (PF) is a major public health problem with limited therapeutic options. There is a clear need to identify novel mediators of PF to develop effective therapeutics. Here we show that an ER protein disulfide isomerase, thioredoxin domain containing 5 (TXNDC5), is highly upregulated in the lung tissues from both patients with idiopathic pulmonary fibrosis and a mouse model of bleomycin (BLM)-induced PF. Global deletion of Txndc5 markedly reduces the extent of PF and preserves lung function in mice following BLM treatment. Mechanistic investigations demonstrate that TXNDC5 promotes fibrogenesis by enhancing TGFβ1 signaling through direct binding with and stabilization of TGFBR1 in lung fibroblasts. Moreover, TGFβ1 stimulation is shown to upregulate TXNDC5 via ER stress/ATF6-dependent transcriptional control in lung fibroblasts. Inducing fibroblast-specific deletion of Txndc5 mitigates the progression of BLM-induced PF and lung function deterioration. Targeting TXNDC5, therefore, could be a novel therapeutic approach against PF.
    MeSH term(s) Animals ; Bleomycin/toxicity ; Disease Models, Animal ; Endoplasmic Reticulum Stress ; Gene Deletion ; Humans ; Idiopathic Pulmonary Fibrosis/etiology ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Protein Disulfide-Isomerases/genetics ; Protein Disulfide-Isomerases/metabolism ; Protein Folding ; Protein Stability ; Pulmonary Fibrosis/etiology ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Receptor, Transforming Growth Factor-beta Type I/chemistry ; Receptor, Transforming Growth Factor-beta Type I/metabolism ; Signal Transduction ; Thioredoxins/antagonists & inhibitors ; Thioredoxins/genetics ; Thioredoxins/metabolism ; Transforming Growth Factor beta1/metabolism ; Up-Regulation
    Chemical Substances PC-TRP protein, mouse ; Transforming Growth Factor beta1 ; Bleomycin (11056-06-7) ; Thioredoxins (52500-60-4) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Protein Disulfide-Isomerases (EC 5.3.4.1) ; TXNDC5 protein, human (EC 5.3.4.1)
    Language English
    Publishing date 2020-08-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-18047-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Endoplasmic Reticulum Protein TXNDC5 Augments Myocardial Fibrosis by Facilitating Extracellular Matrix Protein Folding and Redox-Sensitive Cardiac Fibroblast Activation.

    Shih, Ying-Chun / Chen, Chao-Ling / Zhang, Yan / Mellor, Rebecca L / Kanter, Evelyn M / Fang, Yun / Wang, Hua-Chi / Hung, Chen-Ting / Nong, Jing-Yi / Chen, Hui-Ju / Lee, Tzu-Han / Tseng, Yi-Shuan / Chen, Chiung-Nien / Wu, Chau-Chung / Lin, Shuei-Liong / Yamada, Kathryn A / Nerbonne, Jeanne M / Yang, Kai-Chien

    Circulation research

    2018  Volume 122, Issue 8, Page(s) 1052–1068

    Abstract: Rationale: Cardiac fibrosis plays a critical role in the pathogenesis of heart failure. Excessive accumulation of extracellular matrix (ECM) resulting from cardiac fibrosis impairs cardiac contractile function and increases arrhythmogenicity. Current ... ...

    Abstract Rationale: Cardiac fibrosis plays a critical role in the pathogenesis of heart failure. Excessive accumulation of extracellular matrix (ECM) resulting from cardiac fibrosis impairs cardiac contractile function and increases arrhythmogenicity. Current treatment options for cardiac fibrosis, however, are limited, and there is a clear need to identify novel mediators of cardiac fibrosis to facilitate the development of better therapeutics. Exploiting coexpression gene network analysis on RNA sequencing data from failing human heart, we identified TXNDC5 (thioredoxin domain containing 5), a cardiac fibroblast (CF)-enriched endoplasmic reticulum protein, as a potential novel mediator of cardiac fibrosis, and we completed experiments to test this hypothesis directly.
    Objective: The objective of this study was to determine the functional role of TXNDC5 in the pathogenesis of cardiac fibrosis.
    Methods and results: RNA sequencing and Western blot analyses revealed that TXNDC5 mRNA and protein were highly upregulated in failing human left ventricles and in hypertrophied/failing mouse left ventricle. In addition, cardiac TXNDC5 mRNA expression levels were positively correlated with those of transcripts encoding transforming growth factor β1 and ECM proteins in vivo. TXNDC5 mRNA and protein were increased in human CF (hCF) under transforming growth factor β1 stimulation in vitro. Knockdown of
    Conclusions: The endoplasmic reticulum protein TXNDC5 promotes cardiac fibrosis by facilitating ECM protein folding and CF activation via redox-sensitive c-Jun N-terminal kinase signaling. Loss of TXNDC5 protects against β agonist-induced cardiac fibrosis and contractile dysfunction. Targeting TXNDC5, therefore, could be a powerful new therapeutic approach to mitigate excessive cardiac fibrosis, thereby improving cardiac function and outcomes in patients with heart failure.
    MeSH term(s) Activating Transcription Factor 6/biosynthesis ; Activating Transcription Factor 6/genetics ; Animals ; Cardiomyopathy, Hypertrophic/metabolism ; Cardiomyopathy, Hypertrophic/pathology ; Cells, Cultured ; Extracellular Matrix Proteins/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibrosis/metabolism ; Gene Expression Regulation ; Heart Failure/chemically induced ; Heart Failure/metabolism ; Heart Failure/pathology ; Humans ; Isoproterenol/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; Myocardium/pathology ; NADPH Oxidase 4/biosynthesis ; NADPH Oxidase 4/genetics ; NIH 3T3 Cells ; Oxidation-Reduction ; Protein Disulfide-Isomerases/antagonists & inhibitors ; Protein Disulfide-Isomerases/genetics ; Protein Disulfide-Isomerases/physiology ; Protein Folding ; RNA Interference ; RNA, Small Interfering/pharmacology ; Thioredoxins/antagonists & inhibitors ; Thioredoxins/genetics ; Thioredoxins/physiology
    Chemical Substances Activating Transcription Factor 6 ; Atf6 protein, mouse ; Extracellular Matrix Proteins ; PC-TRP protein, mouse ; RNA, Small Interfering ; Thioredoxins (52500-60-4) ; NADPH Oxidase 4 (EC 1.6.3.-) ; NOX4 protein, human (EC 1.6.3.-) ; Protein Disulfide-Isomerases (EC 5.3.4.1) ; TXNDC5 protein, human (EC 5.3.4.1) ; Isoproterenol (L628TT009W)
    Language English
    Publishing date 2018-03-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.117.312130
    Database MEDical Literature Analysis and Retrieval System OnLINE

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