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  1. Article ; Online: Rodent Model for Orthotopic Implantation of Engineered Liver Devices.

    Sahakyants, Tatevik / Lieberthal, Tyler J / Comer, Carly D / Hancock, Matthew J / Spann, Andrew P / Neville, Craig M / Vacanti, Joseph P

    Tissue engineering. Part C, Methods

    2022  Volume 29, Issue 1, Page(s) 20–29

    Abstract: This study presents a novel surgical model developed to provide hematological support for implanted cellularized devices augmenting or replacing liver tissue function. Advances in bioengineering provide tools and materials to create living tissue ... ...

    Abstract This study presents a novel surgical model developed to provide hematological support for implanted cellularized devices augmenting or replacing liver tissue function. Advances in bioengineering provide tools and materials to create living tissue replacements designed to restore that lost to disease, trauma, or congenital deformity. Such substitutes are often assembled and matured
    MeSH term(s) Humans ; Rats ; Animals ; Rodentia ; Liver Transplantation/methods ; Liver/blood supply ; Hepatectomy/methods ; Tissue Engineering
    Language English
    Publishing date 2022-12-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2420585-0
    ISSN 1937-3392 ; 1937-3384
    ISSN (online) 1937-3392
    ISSN 1937-3384
    DOI 10.1089/ten.TEC.2022.0174
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Talin: a mechanosensitive molecule in health and disease.

    Haining, Alexander W M / Lieberthal, Tyler J / Del Río Hernández, Armando

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2016  Volume 30, Issue 6, Page(s) 2073–2085

    Abstract: Talin is a ubiquitous, large focal adhesion protein that links intracellular networks with the extracellular matrix (ECM) via its connection with the actin cytoskeleton and membrane integrins. It is one of a handful molecules that can expose new ... ...

    Abstract Talin is a ubiquitous, large focal adhesion protein that links intracellular networks with the extracellular matrix (ECM) via its connection with the actin cytoskeleton and membrane integrins. It is one of a handful molecules that can expose new recognition sites when undergoing force-induced mechanical unfolding, and it can bind and recruit cytoskeletal proteins that are involved in mechanotransduction. Talin has attracted great interest in the field of mechanobiology because of its plasticity in undergoing conformational changes under force stimulation as well as its cellular localization that bridges the cytoskeleton with the ECM. In addition to these roles in healthy cells, the dysregulation of talin activators can lead to disease states in which aberrant integrin activation and mechanotransduction precipitate changes in cell spreading, migration, and survival. New data have implicated a role for talin in diseases that are highly regulated by mechanical cues. In this review, we present the current understanding of talin structure, its relationship to binding partners, and its role in disease states.-Haining, A. W. M., Lieberthal, T. J., del Río Hernández, A. Talin: a mechanosensitive molecule in health and disease.
    MeSH term(s) Animals ; Cytoskeleton/physiology ; Gene Expression Regulation/physiology ; Hematologic Diseases/metabolism ; Mechanotransduction, Cellular/physiology ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/therapy ; Protein Binding ; Talin/chemistry ; Talin/genetics ; Talin/metabolism
    Chemical Substances Talin
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.201500080R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 296: Show issues

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  3. Article: Navigating the Collagen Jungle: The Biomedical Potential of Fiber Organization in Cancer.

    Ouellette, Jonathan N / Drifka, Cole R / Pointer, Kelli B / Liu, Yuming / Lieberthal, Tyler J / Kao, W John / Kuo, John S / Loeffler, Agnes G / Eliceiri, Kevin W

    Bioengineering (Basel, Switzerland)

    2021  Volume 8, Issue 2

    Abstract: Recent research has highlighted the importance of key tumor microenvironment features, notably the collagen-rich extracellular matrix (ECM) in characterizing tumor invasion and progression. This led to great interest from both basic researchers and ... ...

    Abstract Recent research has highlighted the importance of key tumor microenvironment features, notably the collagen-rich extracellular matrix (ECM) in characterizing tumor invasion and progression. This led to great interest from both basic researchers and clinicians, including pathologists, to include collagen fiber evaluation as part of the investigation of cancer development and progression. Fibrillar collagen is the most abundant in the normal extracellular matrix, and was revealed to be upregulated in many cancers. Recent studies suggested an emerging theme across multiple cancer types in which specific collagen fiber organization patterns differ between benign and malignant tissue and also appear to be associated with disease stage, prognosis, treatment response, and other clinical features. There is great potential for developing image-based collagen fiber biomarkers for clinical applications, but its adoption in standard clinical practice is dependent on further translational and clinical evaluations. Here, we offer a comprehensive review of the current literature of fibrillar collagen structure and organization as a candidate cancer biomarker, and new perspectives on the challenges and next steps for researchers and clinicians seeking to exploit this information in biomedical research and clinical workflows.
    Language English
    Publishing date 2021-01-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2746191-9
    ISSN 2306-5354
    ISSN 2306-5354
    DOI 10.3390/bioengineering8020017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Chemically Functionalised Graphene FET Biosensor for the Label-free Sensing of Exosomes.

    Kwong Hong Tsang, Deana / Lieberthal, Tyler J / Watts, Clare / Dunlop, Iain E / Ramadan, Sami / Del Rio Hernandez, Armando E / Klein, Norbert

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 13946

    Abstract: A graphene field-effect transistor (gFET) was non-covalently functionalised with 1-pyrenebutyric acid N-hydroxysuccinimide ester and conjugated with anti-CD63 antibodies for the label-free detection of exosomes. Using a microfluidic channel, part of a ... ...

    Abstract A graphene field-effect transistor (gFET) was non-covalently functionalised with 1-pyrenebutyric acid N-hydroxysuccinimide ester and conjugated with anti-CD63 antibodies for the label-free detection of exosomes. Using a microfluidic channel, part of a graphene film was exposed to solution. The change in electrical properties of the exposed graphene created an additional minimum alongside the original Dirac point in the drain-source current (I
    Language English
    Publishing date 2019-09-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-50412-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: ATRA modulates mechanical activation of TGF-β by pancreatic stellate cells.

    Sarper, Muge / Cortes, Ernesto / Lieberthal, Tyler J / Del Río Hernández, Armando

    Scientific reports

    2016  Volume 6, Page(s) 27639

    Abstract: The hallmark of pancreatic ductal adenocarcinoma (PDAC) is abundant desmoplasia, which is orchestrated by pancreatic stellate cells (PSCs) and accounts for the majority of the stroma surrounding the tumour. Healthy PSCs are quiescent, but upon activation ...

    Abstract The hallmark of pancreatic ductal adenocarcinoma (PDAC) is abundant desmoplasia, which is orchestrated by pancreatic stellate cells (PSCs) and accounts for the majority of the stroma surrounding the tumour. Healthy PSCs are quiescent, but upon activation during disease progression, they adopt a myofibroblast-contractile phenotype and secrete and concomitantly reorganise the stiff extracellular matrix (ECM). Transforming growth factor β (TGF-β) is a potent activator of PSCs, and its activation requires spatiotemporal organisation of cellular and extracellular cues to liberate it from an inactive complex with latent TGF-β binding protein (LTBP). Here we study the mechanical activation of TGF-β by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-β through a mechanism involving myosin II dependent contractility. Therefore, ATRA inhibits the ability of PSCs to mechanically release active TGF-β, which might otherwise act in an autocrine manner to sustain PSCs in an active state and a tumour-favouring stiff microenvironment.
    MeSH term(s) Actomyosin/chemistry ; Alternative Splicing ; Carcinoma, Pancreatic Ductal/metabolism ; Cytoskeleton/chemistry ; Disease Progression ; Fibronectins/metabolism ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Integrin beta1/metabolism ; Latent TGF-beta Binding Proteins/metabolism ; Myofibroblasts/metabolism ; Myosin Type II/metabolism ; Pancreatic Neoplasms ; Pancreatic Stellate Cells/metabolism ; Phenotype ; Stress, Mechanical ; Transforming Growth Factor beta1/metabolism ; Tretinoin/metabolism ; Tumor Microenvironment ; Pancreatic Neoplasms
    Chemical Substances Fibronectins ; Integrin beta1 ; LTBP1 protein, human ; Latent TGF-beta Binding Proteins ; TGFB1 protein, human ; Transforming Growth Factor beta1 ; Tretinoin (5688UTC01R) ; Actomyosin (9013-26-7) ; Myosin Type II (EC 3.6.1.-)
    Language English
    Publishing date 2016-07-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep27639
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Liver epithelial focal adhesion kinase modulates fibrogenesis and hedgehog signaling.

    Weng, Yun / Lieberthal, Tyler J / Zhou, Vivian X / Lopez-Ichikawa, Maya / Armas-Phan, Manuel / Bond, Tristan K / Yoshida, Miya C / Choi, Won-Tak / Chang, Tammy T

    JCI insight

    2020  Volume 5, Issue 20

    Abstract: Focal adhesion kinase (FAK) is an important mediator of extracellular matrix-integrin mechano-signal transduction that regulates cell motility, survival, and proliferation. As such, FAK is being investigated as a potential therapeutic target for ... ...

    Abstract Focal adhesion kinase (FAK) is an important mediator of extracellular matrix-integrin mechano-signal transduction that regulates cell motility, survival, and proliferation. As such, FAK is being investigated as a potential therapeutic target for malignant and fibrotic diseases, and numerous clinical trials of FAK inhibitors are underway. The function of FAK in nonmalignant, nonmotile epithelial cells is not well understood. We previously showed that hepatocytes demonstrated activated FAK near stiff collagen tracts in fibrotic livers. In this study, we examined the role of liver epithelial FAK by inducing fibrotic liver disease in mice with liver epithelial FAK deficiency. We found that mice that lacked FAK in liver epithelial cells developed more severe liver injury and worse fibrosis as compared with controls. Increased fibrosis in liver epithelial FAK-deficient mice was linked to the activation of several profibrotic pathways, including the hedgehog/smoothened pathway. FAK-deficient hepatocytes produced increased Indian hedgehog in a manner dependent on matrix stiffness. Furthermore, expression of the hedgehog receptor, smoothened, was increased in macrophages and biliary cells of hepatocyte-specific FAK-deficient fibrotic livers. These results indicate that liver epithelial FAK has important regulatory roles in the response to liver injury and progression of fibrosis.
    MeSH term(s) Animals ; Cell Movement/genetics ; Cell Proliferation/genetics ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Extracellular Matrix/genetics ; Extracellular Matrix/metabolism ; Focal Adhesion Kinase 1/genetics ; Hedgehog Proteins/genetics ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Liver/injuries ; Liver/pathology ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Mice ; Mice, Knockout ; Signal Transduction/genetics ; Smoothened Receptor/genetics
    Chemical Substances Hedgehog Proteins ; Smo protein, mouse ; Smoothened Receptor ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; Ptk2 protein, mouse (EC 2.7.10.2)
    Language English
    Publishing date 2020-10-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.141217
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Tamoxifen mechanically reprograms the tumor microenvironment via HIF-1A and reduces cancer cell survival.

    Cortes, Ernesto / Lachowski, Dariusz / Robinson, Benjamin / Sarper, Muge / Teppo, Jaakko S / Thorpe, Stephen D / Lieberthal, Tyler J / Iwamoto, Kazunari / Lee, David A / Okada-Hatakeyama, Mariko / Varjosalo, Markku T / Del Río Hernández, Armando E

    EMBO reports

    2018  Volume 20, Issue 1

    Abstract: The tumor microenvironment is fundamental to cancer progression, and the influence of its mechanical properties is increasingly being appreciated. Tamoxifen has been used for many years to treat estrogen-positive breast cancer. Here we report that ... ...

    Abstract The tumor microenvironment is fundamental to cancer progression, and the influence of its mechanical properties is increasingly being appreciated. Tamoxifen has been used for many years to treat estrogen-positive breast cancer. Here we report that tamoxifen regulates the level and activity of collagen cross-linking and degradative enzymes, and hence the organization of the extracellular matrix, via a mechanism involving both the G protein-coupled estrogen receptor (GPER) and hypoxia-inducible factor-1 alpha (HIF-1A). We show that tamoxifen reduces HIF-1A levels by suppressing myosin-dependent contractility and matrix stiffness mechanosensing. Tamoxifen also downregulates hypoxia-regulated genes and increases vascularization in PDAC tissues. Our findings implicate the GPER/HIF-1A axis as a master regulator of peri-tumoral stromal remodeling and the fibrovascular tumor microenvironment and offer a paradigm shift for tamoxifen from a well-established drug in breast cancer hormonal therapy to an alternative candidate for stromal targeting strategies in PDAC and possibly other cancers.
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Animals ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cellular Reprogramming/drug effects ; Fibroblasts/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Mice ; Myosins/genetics ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/pathology ; Receptors, Estrogen/genetics ; Receptors, G-Protein-Coupled/genetics ; Signal Transduction/drug effects ; Tamoxifen/administration & dosage ; Tumor Microenvironment/drug effects
    Chemical Substances GPER1 protein, human ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Receptors, Estrogen ; Receptors, G-Protein-Coupled ; Tamoxifen (094ZI81Y45) ; Myosins (EC 3.6.4.1)
    Language English
    Publishing date 2018-12-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.201846557
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 41: Show issues

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