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Article ; Online: Harnessing Mechanobiology for Tissue Engineering.

Kim, Sudong / Uroz, Marina / Bays, Jennifer L / Chen, Christopher S

2021 Volume 56, Issue 2, Page(s) 180–191

Abstract: A primary challenge in tissue engineering is to recapitulate both the structural and functional features of whole tissues and organs. In vivo, patterning of the body plan and constituent tissues emerges from the carefully orchestrated interactions ... ...

Abstract	A primary challenge in tissue engineering is to recapitulate both the structural and functional features of whole tissues and organs. In vivo, patterning of the body plan and constituent tissues emerges from the carefully orchestrated interactions between the transcriptional programs that give rise to cell types and the mechanical forces that drive the bending, twisting, and extensions critical to morphogenesis. Substantial recent progress in mechanobiology-understanding how mechanics regulate cell behaviors and what cellular machineries are responsible-raises the possibility that one can begin to use these insights to help guide the strategy and design of functional engineered tissues. In this perspective, we review and propose the development of different approaches, from providing appropriate extracellular mechanical cues to interfering with cellular mechanosensing machinery, to aid in controlling cell and tissue structure and function.
MeSH term(s)	Animals ; Biomechanical Phenomena ; Biophysics ; Cell Differentiation ; Humans ; Mechanotransduction, Cellular ; Morphogenesis ; Tissue Engineering/methods
Language	English
Publishing date	2021-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2020.12.017
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Zs.A 5742: 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)
Zs.MG 76: Show issues

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Article ; Online: Differential vascular endothelial cell toxicity of established and novel BCR-ABL tyrosine kinase inhibitors.

Wang, Yihua / Travers, Richard J / Farrell, Alanna / Lu, Qing / Bays, Jennifer L / Stepanian, Alec / Chen, Christopher / Jaffe, Iris Z

PloS one

2023 Volume 18, Issue 11, Page(s) e0294438

Abstract: BCR-ABL tyrosine kinase inhibitors (TKIs) have dramatically improved survival in Philadelphia chromosome-positive leukemias. Newer BCR-ABL TKIs provide superior cancer outcomes but with increased risk of acute arterial thrombosis, which further increases ...

Abstract	BCR-ABL tyrosine kinase inhibitors (TKIs) have dramatically improved survival in Philadelphia chromosome-positive leukemias. Newer BCR-ABL TKIs provide superior cancer outcomes but with increased risk of acute arterial thrombosis, which further increases in patients with cardiovascular comorbidities and mitigates survival benefits compared to imatinib. Recent studies implicate endothelial cell (EC) damage in this toxicity by unknown mechanisms with few side-by-side comparisons of multiple TKIs and with no available data on endothelial impact of recently approved TKIs or novels TKIs being tested in clinical trials. To characterize BCR-ABL TKI induced EC dysfunction we exposed primary human umbilical vein ECs in 2D and 3D culture to clinically relevant concentrations of seven BCR-ABL TKIs and quantified their impact on EC scratch-wound healing, viability, inflammation, and permeability mechanisms. Dasatinib, ponatinib, and nilotinib, the TKIs associated with thrombosis in patients, all significantly impaired EC wound healing, survival, and proliferation compared to imatinib, but only dasatinib and ponatinib impaired cell migration and only nilotinib enhanced EC necrosis. Dasatinib and ponatinib increased leukocyte adhesion to ECs with upregulation of adhesion molecule expression in ECs (ICAM1, VCAM1, and P-selectin) and leukocytes (PSGL1). Dasatinib increased permeability and impaired cell junctional integrity in human engineered microvessels, consistent with its unique association with pleural effusions. Of the new agents, bafetinib decreased EC viability and increased microvessel permeability while asciminib and radotinib did not impact any EC function tested. In summary, the vasculotoxic TKIs (dasatinib, ponatinib, nilotinib) cause EC toxicity but with mechanistic differences, supporting the potential need for drug-specific vasculoprotective strategies. Asciminib and radotinib do not induce EC toxicity at clinically relevant concentrations suggesting a better safety profile.
MeSH term(s)	Humans ; Imatinib Mesylate/adverse effects ; Dasatinib/adverse effects ; Tyrosine Kinase Inhibitors ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Protein Kinase Inhibitors/toxicity ; Endothelial Cells ; Thrombosis/drug therapy ; Fusion Proteins, bcr-abl ; Antineoplastic Agents/therapeutic use
Chemical Substances	Imatinib Mesylate (8A1O1M485B) ; Dasatinib (RBZ1571X5H) ; 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-pyrazin-2-ylpyrimidin-2-ylamino)benzamide ; Tyrosine Kinase Inhibitors ; Protein Kinase Inhibitors ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Antineoplastic Agents
Language	English
Publishing date	2023-11-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0294438
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Article ; Online: Ankyrin G organizes membrane components to promote coupling of cell mechanics and glucose uptake.

Salvi, Alicia M / Bays, Jennifer L / Mackin, Samantha R / Mege, René-Marc / DeMali, Kris A

Nature cell biology

2021 Volume 23, Issue 5, Page(s) 457–466

Abstract: The response of cells to forces is critical for their function and occurs via rearrangement of the actin ... ...

Abstract	The response of cells to forces is critical for their function and occurs via rearrangement of the actin cytoskeleton
MeSH term(s)	Ankyrins/metabolism ; Biological Transport/physiology ; Carrier Proteins/metabolism ; Cell Membrane/metabolism ; Cytoskeleton/metabolism ; Glucose/metabolism ; Glucose Transporter Type 1/metabolism ; Humans ; Signal Transduction/physiology
Chemical Substances	Ankyrins ; Carrier Proteins ; Glucose Transporter Type 1 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-05-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-021-00677-y
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Zs.A 5169: 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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Article ; Online: Notch1 and Notch3 coordinate for pericyte-induced stabilization of vasculature.

Tefft, Juliann B / Bays, Jennifer L / Lammers, Alex / Kim, Sudong / Eyckmans, Jeroen / Chen, Christopher S

American journal of physiology. Cell physiology

2021 Volume 322, Issue 2, Page(s) C185–C196

Abstract: The Notch pathway regulates complex patterning events in many species and is critical for the proper formation and function of the vasculature. Despite this importance, how the various components of the Notch pathway work in concert is still not well ... ...

Abstract	The Notch pathway regulates complex patterning events in many species and is critical for the proper formation and function of the vasculature. Despite this importance, how the various components of the Notch pathway work in concert is still not well understood. For example, NOTCH1 stabilizes homotypic endothelial junctions, but the role of NOTCH1 in heterotypic interactions is not entirely clear. NOTCH3, on the other hand, is essential for heterotypic interactions of pericytes with the endothelium, but how NOTCH3 signaling in pericytes impacts the endothelium remains elusive. Here, we use in vitro vascular models to investigate whether pericyte-induced stabilization of the vasculature requires the cooperation of NOTCH1 and NOTCH3. We observe that both pericyte NOTCH3 and endothelial NOTCH1 are required for the stabilization of the endothelium. Loss of either NOTCH3 or NOTCH1 decreases the accumulation of VE-cadherin at endothelial adherens junctions and increases the frequency of wider, more motile junctions. We found that DLL4 was the key ligand for simulating NOTCH1 activation in endothelial cells and observed that DLL4 expression in pericytes is dependent on NOTCH3. Altogether, these data suggest that an interplay between pericyte NOTCH3 and endothelial NOTCH1 is critical for pericyte-induced vascular stabilization.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Adaptor Proteins, Signal Transducing/pharmacology ; Calcium-Binding Proteins/metabolism ; Calcium-Binding Proteins/pharmacology ; Cells, Cultured ; Coculture Techniques ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; HEK293 Cells ; Humans ; Microvessels/cytology ; Microvessels/drug effects ; Microvessels/metabolism ; Pericytes/drug effects ; Pericytes/metabolism ; Receptor, Notch1/agonists ; Receptor, Notch1/metabolism ; Receptor, Notch3/agonists ; Receptor, Notch3/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Calcium-Binding Proteins ; DLL4 protein, human ; NOTCH1 protein, human ; NOTCH3 protein, human ; Receptor, Notch1 ; Receptor, Notch3
Language	English
Publishing date	2021-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00320.2021
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Uc I Zs.89: Show issues

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Article ; Online: Differential vascular endothelial cell toxicity of established and novel BCR-ABL tyrosine kinase inhibitors.

Yihua Wang / Richard J Travers / Alanna Farrell / Qing Lu / Jennifer L Bays / Alec Stepanian / Christopher Chen / Iris Z Jaffe

PLoS ONE, Vol 18, Iss 11, p e

2023 Volume 0294438

Abstract	BCR-ABL tyrosine kinase inhibitors (TKIs) have dramatically improved survival in Philadelphia chromosome-positive leukemias. Newer BCR-ABL TKIs provide superior cancer outcomes but with increased risk of acute arterial thrombosis, which further increases in patients with cardiovascular comorbidities and mitigates survival benefits compared to imatinib. Recent studies implicate endothelial cell (EC) damage in this toxicity by unknown mechanisms with few side-by-side comparisons of multiple TKIs and with no available data on endothelial impact of recently approved TKIs or novels TKIs being tested in clinical trials. To characterize BCR-ABL TKI induced EC dysfunction we exposed primary human umbilical vein ECs in 2D and 3D culture to clinically relevant concentrations of seven BCR-ABL TKIs and quantified their impact on EC scratch-wound healing, viability, inflammation, and permeability mechanisms. Dasatinib, ponatinib, and nilotinib, the TKIs associated with thrombosis in patients, all significantly impaired EC wound healing, survival, and proliferation compared to imatinib, but only dasatinib and ponatinib impaired cell migration and only nilotinib enhanced EC necrosis. Dasatinib and ponatinib increased leukocyte adhesion to ECs with upregulation of adhesion molecule expression in ECs (ICAM1, VCAM1, and P-selectin) and leukocytes (PSGL1). Dasatinib increased permeability and impaired cell junctional integrity in human engineered microvessels, consistent with its unique association with pleural effusions. Of the new agents, bafetinib decreased EC viability and increased microvessel permeability while asciminib and radotinib did not impact any EC function tested. In summary, the vasculotoxic TKIs (dasatinib, ponatinib, nilotinib) cause EC toxicity but with mechanistic differences, supporting the potential need for drug-specific vasculoprotective strategies. Asciminib and radotinib do not induce EC toxicity at clinically relevant concentrations suggesting a better safety profile.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: It takes energy to resist force.

Bays, Jennifer L / DeMali, Kris A

Cell cycle (Georgetown, Tex.)

2017 Volume 16, Issue 19, Page(s) 1733–1734

MeSH term(s)	AMP-Activated Protein Kinases ; Cadherins ; Mechanotransduction, Cellular ; Microscopy, Atomic Force
Chemical Substances	Cadherins ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2017-08-18
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2017.1360654
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Zs.A 5881: Show issues

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Article ; Online: Directing Cholangiocyte Morphogenesis in Natural Biomaterial Scaffolds.

Smith, Quinton / Bays, Jennifer / Li, Linqing / Shareef, Haniyah / Chen, Christopher S / Bhatia, Sangeeta N

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2022 Volume 9, Issue 14, Page(s) e2201951

Language	English
Publishing date	2022-05-12
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202201951
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Article ; Online: Vinculin in cell-cell and cell-matrix adhesions.

Bays, Jennifer L / DeMali, Kris A

Cellular and molecular life sciences : CMLS

2017 Volume 74, Issue 16, Page(s) 2999–3009

Abstract: Vinculin was identified as a component of focal adhesions and adherens junctions nearly 40 years ago. Since that time, remarkable progress has been made in understanding its activation, regulation and function. Here we discuss the current understanding ... ...

Abstract	Vinculin was identified as a component of focal adhesions and adherens junctions nearly 40 years ago. Since that time, remarkable progress has been made in understanding its activation, regulation and function. Here we discuss the current understanding of the roles of vinculin in cell-cell and cell-matrix adhesions. Emphasis is placed on the how vinculin is recruited, activated and regulated. We also highlight the recent understanding of how vinculin responds to and transmits force at integrin- and cadherin-containing adhesion complexes to the cytoskeleton. Furthermore, we discuss roles of vinculin in binding to and rearranging the actin cytoskeleton.
MeSH term(s)	Actin Cytoskeleton/metabolism ; Adherens Junctions/metabolism ; Animals ; Cadherins/metabolism ; Cell Adhesion ; Cell Movement ; Focal Adhesions/metabolism ; Humans ; Integrins/metabolism ; Mechanotransduction, Cellular ; Models, Molecular ; Protein Interaction Maps ; Vinculin/analysis ; Vinculin/metabolism
Chemical Substances	Cadherins ; Integrins ; Vinculin (125361-02-6)
Language	English
Publishing date	2017-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-017-2511-3
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Article: Vinculin in cellâcell and cellâmatrix adhesions

Bays, Jennifer L / Kris A. DeMali

Cellular and molecular life sciences. 2017 Aug., v. 74, no. 16

2017

Abstract	Vinculin was identified as a component of focal adhesions and adherens junctions nearly 40 years ago. Since that time, remarkable progress has been made in understanding its activation, regulation and function. Here we discuss the current understanding of the roles of vinculin in cellâcell and cellâmatrix adhesions. Emphasis is placed on the how vinculin is recruited, activated and regulated. We also highlight the recent understanding of how vinculin responds to and transmits force at integrin- and cadherin-containing adhesion complexes to the cytoskeleton. Furthermore, we discuss roles of vinculin in binding to and rearranging the actin cytoskeleton.
Keywords	adherens junctions ; adhesion ; focal adhesions ; microfilaments
Language	English
Dates of publication	2017-08
Size	p. 2999-3009.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-017-2511-3
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Directing Cholangiocyte Morphogenesis in Natural Biomaterial Scaffolds.

Smith, Quinton / Bays, Jennifer / Li, Linqing / Shareef, Haniyah / Chen, Christopher S / Bhatia, Sangeeta N

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2021 Volume 9, Issue 3, Page(s) e2102698

Abstract: Patients with Alagille syndrome carry monogenic mutations in the Notch signaling pathway and face complications such as jaundice and cholestasis. Given the presence of intrahepatic ductopenia in these patients, Notch2 receptor signaling is implicated in ... ...

Abstract	Patients with Alagille syndrome carry monogenic mutations in the Notch signaling pathway and face complications such as jaundice and cholestasis. Given the presence of intrahepatic ductopenia in these patients, Notch2 receptor signaling is implicated in driving normal biliary development and downstream branching morphogenesis. As a result, in vitro model systems of liver epithelium are needed to further mechanistic insight of biliary tissue assembly. Here, primary human intrahepatic cholangiocytes as a candidate population for such a platform are systematically evaluated, and conditions that direct their branching morphogenesis are described. It is found that extracellular matrix presentation, coupled with mitogen stimulation, promotes biliary branching in a Notch-dependent manner. These results demonstrate the utility of using 3D scaffolds for mechanistic investigation of cholangiocyte branching and provide a gateway to integrate biliary architecture in additional in vitro models of liver tissue.
MeSH term(s)	Adult ; Alagille Syndrome/metabolism ; Biliary Tract/metabolism ; Biocompatible Materials/metabolism ; Cells, Cultured ; Epithelial Cells/metabolism ; Humans ; Liver/metabolism ; Morphogenesis ; Organoids/metabolism ; Signal Transduction ; Tissue Scaffolds
Chemical Substances	Biocompatible Materials
Language	English
Publishing date	2021-11-16
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202102698
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