1
40
8
-
Text
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URL Address
<a href="http://doi.org/10.1080/03008207.2020.1828380" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/03008207.2020.1828380</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-14
ISSN
1607-8438 0300-8207
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Update Year & Number
October 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED College of Pharmacy
NEOMED Department
Department of Anatomy & Neurobiology
Department of Pharmacy Practice
NEOMED Student Publications
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A retrotransposon gag-like-3 gene RTL3 and SOX-9 co-regulate the expression of COL2A1 in chondrocytes.
Publisher
An entity responsible for making the resource available
Connective Tissue Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-10-12
Subject
The topic of the resource
gene regulation; chondrogenesis; extracellular matrix; chondrocyte; ZCCHC5/RTL3; RTL3; ZCCHC5
Creator
An entity primarily responsible for making the resource
Ball HC;Ansari M Y;Ahmad N;Novak K;Haqqi TM
Description
An account of the resource
PURPOSE: Transposable elements are known to remodel gene structure and provide a known source of genetic variation. Retrotransposon gag-like-3 (RTL3) is a mammalian retrotransposon-derived transcript (MART) whose function in the skeletal tissue is unknown. This study aimed to elucidate the biological significance of RTL3 in chondrogenesis and type-II collagen (COL2A1) gene expression in chondrocytes. MATERIALS AND METHODS: Expression of RTL3, SOX-9 and COL2A1 mRNAs was determined by TaqMan assays and the protein expression by immunoblotting. RTL3 and Sox-9 depletion in human chondrocytes was achieved using validated siRNAs. An RTL3 mutant (∆RTL3) lacking the zinc finger domain was created using in vitro mutagenesis. Forced expression of RTL3, ∆RTL3, and SOX-9 was achieved using CMV promoter containing expression plasmids. CRISPR-Cas9 was utilized to delete Rtl3 and create a stable ATDC5(Rlt3-/-) cell line. Matrix deposition and Col2a1 quantification during chondrogenesis were determined by Alcian blue staining and Sircol™ Soluble Collagen Assay, respectively. RESULTS: RTL3 is not ubiquitously expressed but showed strong expression in cartilage, chondrocytes and synoviocytes but not in muscle, brain, or other tissues analyzed. Loss-of-function and gain-of-function studies demonstrated a critical role of RTL3 in the regulation of SOX-9 and COL2A1 expression and matrix synthesis during chondrogenesis. Both RTL3 and SOX-9 displayed co-regulated expression in chondrocytes. Gene regulatory activity of RTL3 requires the c-terminal CCHC zinc-finger binding domain. CONCLUSIONS: Our results identify a novel regulatory mechanism of COL2A1 expression in chondrocytes that may help to further understand the skeletal development and the pathogenesis of diseases with altered COL2A1 expression.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1080/03008207.2020.1828380" target="_blank" rel="noreferrer noopener">10.1080/03008207.2020.1828380</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
Ahmad N
Ansari M Y
Ball HC
chondrocyte
chondrogenesis
Connective tissue research
Department of Anatomy & Neurobiology
Department of Pharmacy Practice
Extracellular Matrix
Gene Regulation
Haqqi TM
journalArticle
NEOMED College of Medicine
NEOMED College of Pharmacy
NEOMED Student Publications
Novak K
October 2020 List
RTL3
ZCCHC5
ZCCHC5/RTL3
-
Text
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URL Address
<a href="http://doi.org/10.1007/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-020-0775-5</a>
Pages
14-14
Issue
2
Volume
115
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Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
TRPV4 deletion protects heart from myocardial infarction-induced adverse remodeling via modulation of cardiac fibroblast differentiation.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-01
Subject
The topic of the resource
Mechanotransduction; TRPV4; Myocardial infarction; Myocardial infarction; TGF-beta1; Rho/Rho kinase; Mechanotransduction; TGF-β1; Myocardial infarction; EXTRACELLULAR matrix; HEART failure; HEART fibrosis; HEART; Cardiac fibroblast; Cardiac fibrosis; Rho/Rho kinase; TRPV4; Cardiac fibroblast; Cardiac fibrosis; DELETION mutation
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Kanugula Anantha K; Paruchuri Sailaja; Chilian William M; Thodeti Charles K
Description
An account of the resource
Cardiac fibrosis caused by adverse cardiac remodeling following myocardial infarction can eventually lead to heart failure. Although the role of soluble factors such as TGF-beta is well studied in cardiac fibrosis following myocardial injury, the physiological role of mechanotransduction is not fully understood. Here, we investigated the molecular mechanism and functional role of TRPV4 mechanotransduction in cardiac fibrosis. TRPV4KO mice, 8 weeks following myocardial infarction (MI), exhibited preserved cardiac function compared to WT mice. Histological analysis demonstrated reduced cardiac fibrosis in TRPV4KO mice. We found that WT CF exhibited hypotonicity-induced calcium influx and extracellular matrix (ECM)-stiffness-dependent differentiation in response to
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-020-0775-5" target="_blank" rel="noreferrer noopener">10.1007/s00395-020-0775-5</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2020
Adapala Ravi K
Basic research in cardiology
cardiac fibroblast
Cardiac fibrosis
Chilian William M
DELETION mutation
Department of Integrative Medical Sciences
Extracellular Matrix
heart
Heart failure
HEART fibrosis
Kanugula Anantha K
Mechanotransduction
myocardial infarction
NEOMED College of Medicine
NEOMED Postdoc Publications
Paruchuri Sailaja
Rho/Rho kinase
TGF-beta1
TGF-β1
Thodeti Charles K
TRPV4
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-1
Volume
117
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Dublin Core
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Title
A name given to the resource
Knockout of Type VI Collagen Preserves Mitochondrial Structure and Function Following Myocardial Infarction
Publisher
An entity responsible for making the resource available
Circulation Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-07
Subject
The topic of the resource
ischemia; Extracellular matrix; Cardiovascular System & Cardiology; Hematology; cardiac remodeling
Creator
An entity primarily responsible for making the resource
Meszaros J G; Luther D J; Kang P T; Chen Y R; Miller R L; Bonaldo P; Chilian W M; Thodeti C K
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2015
Bonaldo P
cardiac remodeling
Cardiovascular System & Cardiology
Chen Y R
Chilian W M
Circulation research
Extracellular Matrix
Hematology
ischemia
Journal Article or Conference Abstract Publication
Kang P T
Luther D J
Meszaros J G
Miller R L
Thodeti C K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1039/c0ib00034e" target="_blank" rel="noreferrer noopener">http://doi.org/10.1039/c0ib00034e</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
435-442
Issue
9
Volume
2
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Title
A name given to the resource
Ultra-rapid activation of TRPV4 ion channels by mechanical forces applied to cell surface beta 1 integrins
Publisher
An entity responsible for making the resource available
Integrative Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010
Subject
The topic of the resource
cytoskeleton; mechanotransduction; integrin; Cell Biology; Extracellular matrix; pathways; kinase; shear-stress; focal adhesions; living cells; stretch
Creator
An entity primarily responsible for making the resource
Matthews B D; Thodeti C K; Tytell J D; Mammoto A; Overby D R; Ingber D E
Description
An account of the resource
Integrins are ubiquitous transmembrane mechanoreceptors that elicit changes in intracellular biochemistry in response to mechanical force application, but these alterations generally proceed over seconds to minutes. Stress-sensitive ion channels represent another class of mechanoreceptors that are activated much more rapidly (within msec), and recent findings suggest that calcium influx through Transient Receptor Potential Vanilloid-4 (TRPV4) channels expressed in the plasma membrane of bovine capillary endothelial cells is required for mechanical strain-induced changes in focal adhesion assembly, cell orientation and directional migration. However, whether mechanically stretching a cell's extracellular matrix (ECM) adhesions might directly activate cell surface ion channels remains unknown. Here we show that forces applied to beta 1 integrins result in ultra-rapid (within 4 msec) activation of calcium influx through TRPV4 channels. The TRPV4 channels were specifically activated by mechanical strain in the cytoskeletal backbone of the focal adhesion, and not by deformation of the lipid bilayer or submembranous cortical cytoskeleton alone. This early-immediate calcium signaling response required the distal region of the b1 integrin cytoplasmic tail that contains a binding site for the integrin-associated transmembrane CD98 protein, and external force application to CD98 within focal adhesions activated the same ultra-rapid calcium signaling response. Local direct strain-dependent activation of TRPV4 channels mediated by force transfer from integrins and CD98 may therefore enable compartmentalization of calcium signaling within focal adhesions that is critical for mechanical control of many cell behaviors that underlie cell and tissue development.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1039/c0ib00034e" target="_blank" rel="noreferrer noopener">10.1039/c0ib00034e</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2010
Cell Biology
cytoskeleton
Extracellular Matrix
Focal Adhesions
Ingber D E
Integrative Biology
integrin
Journal Article or Conference Abstract Publication
Kinase
living cells
Mammoto A
Matthews B D
Mechanotransduction
Overby D R
pathways
shear-stress
stretch
Thodeti C K
Tytell J D
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
E88-E88
Issue
12
Volume
115
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Dublin Core
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Title
A name given to the resource
TRPV4 Channel Deletion Improves Cardiac Function and Remodeling Following Myocardial Infarction and Transverse Aortic Constriction via Modulation of Rho/MRTF-A Pathway
Publisher
An entity responsible for making the resource available
Circulation Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-12
Subject
The topic of the resource
Cardiac hypertrophy; Cardiovascular System & Cardiology; Extracellular matrix; fibrosis; Hematology; Ion channels; Myocardial infarction
Creator
An entity primarily responsible for making the resource
Adapala R K; Thoppil R; Cappelli H; Ohanyan V A; Luli J; Luther D J; Paruchuri S; Chilian W M; Meszaros J G; Thodeti C K
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2014
Adapala R K
Cappelli H
Cardiac hypertrophy
Cardiovascular System & Cardiology
Chilian W M
Circulation research
Extracellular Matrix
Fibrosis
Hematology
Ion Channels
Journal Article or Conference Abstract Publication
Luli J
Luther D J
Meszaros J G
myocardial infarction
Ohanyan V A
Paruchuri S
Thodeti C K
Thoppil R
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-1
Issue
21
Volume
124
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Dublin Core
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Title
A name given to the resource
Mechanosensitive Trpv4 Channels Mediate Cardiac Myofibroblast Differentitation
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-11
Subject
The topic of the resource
Cardiovascular System & Cardiology; Extracellular matrix; fibrosis; Ion channels; Myocardial infarction; Signal transduction
Creator
An entity primarily responsible for making the resource
Adapala R; Luther D; Shah S; Meszaros J G; Chilian W M; Thodeti C K
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2011
Adapala R
Cardiovascular System & Cardiology
Chilian W M
Circulation
Extracellular Matrix
Fibrosis
Ion Channels
Journal Article or Conference Abstract Publication
Luther D
Meszaros J G
myocardial infarction
Shah S
Signal Transduction
Thodeti C K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3389/fnana.2013.00053" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fnana.2013.00053</a>
Pages
53–53
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Perineuronal nets and GABAergic cells in the inferior colliculus of guinea pigs.
Publisher
An entity responsible for making the resource available
Frontiers in neuroanatomy
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-07
Subject
The topic of the resource
GABA; auditory; plasticity; extracellular matrix; inhibition; midbrain
Creator
An entity primarily responsible for making the resource
Foster Nichole L; Mellott Jeffrey G; Schofield Brett R
Description
An account of the resource
Perineuronal nets (PNs) are aggregates of extracellular matrix that have been associated with neuronal plasticity, critical periods, fast-spiking cells and protection from oxidative stress. Although PNs have been reported in the auditory system in several species, there is disagreement about the distribution of PNs within the inferior colliculus (IC), an important auditory hub in the midbrain. Furthermore, PNs in many brain areas are preferentially associated with GABAergic cells, but whether such an association exists in the IC has not been addressed. We used Wisteria floribunda agglutinin staining and immunohistochemistry in guinea pigs to examine PNs within the IC. PNs are present in all IC subdivisions and are densest in the central portions of the IC. Throughout the IC, PNs are preferentially associated with GABAergic cells. Not all GABAergic cells are surrounded by PNs, so the presence of PNs can be used to subdivide IC GABAergic cells into "netted" and "non-netted" categories. Finally, PNs in the IC, like those in other brain areas, display molecular heterogeneity that suggests a multitude of functions.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3389/fnana.2013.00053" target="_blank" rel="noreferrer noopener">10.3389/fnana.2013.00053</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Auditory
Department of Anatomy & Neurobiology
Extracellular Matrix
Foster Nichole L
Frontiers in neuroanatomy
GABA
inhibition
Mellott Jeffrey G
midbrain
NEOMED College of Medicine
plasticity
Schofield Brett R
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/jcp.25900" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcp.25900</a>
Pages
409–421
Issue
1
Volume
233
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Osteoactivin regulates head and neck squamous cell carcinoma invasion by modulating matrix metalloproteases.
Publisher
An entity responsible for making the resource available
Journal of cellular physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
*Cell Movement; Carcinoma; Cell Line; cell lines; Enzymologic; extracellular matrix; Gene Expression Regulation; Head and Neck Neoplasms/*enzymology/genetics/pathology; human; Humans; matrix metalloproteinases; Matrix Metalloproteinases; Membrane Glycoproteins/genetics/*metabolism; Messenger/genetics/metabolism; neoplasm invasion; Neoplasm Invasiveness; Neoplastic; RNA; RNA Interference; Secreted/genetics/*metabolism; Signal Transduction; Squamous Cell Carcinoma of Head and Neck; Squamous Cell/*enzymology/genetics/pathology; Transfection; Tumor
Creator
An entity primarily responsible for making the resource
Arosarena Oneida A; Barr Eric W; Thorpe Ryan; Yankey Hilary; Tarr Joseph T; Safadi Fayez F
Description
An account of the resource
Nearly 60% of patients with head and neck squamous cell carcinoma (HNSCC) die of metastases or locoregional recurrence. Metastasis is mediated by cancer cell migration and invasion, which are in part dependent on extracellular matrix degradation by matrix metalloproteinases. Osteoactivin (OA) overexpression plays a role in metastases in several malignancies, and has been shown to upregulate matrix metalloproteinase (MMP) expression and activity. To determine how OA modulates MMP expression and activity in HNSCC, and to investigate OA effects on cell invasion, we assessed effects of OA treatment on MMP mRNA and protein expression, as well as gelatinase and caseinolytic activity in HNSCC cell lines. We assessed the effects of OA gene silencing on MMP expression, gelatinase and caseinolytic activity, and cell invasion. OA treatment had differential effects on MMP mRNA expression. OA treatment upregulated MMP-10 expression in UMSCC14a (p = 0.0431) and SCC15 (p \textless 0.0001) cells, but decreased MMP-9 expression in UMSCC14a cells (p = 0.0002). OA gene silencing decreased MMP-10 expression in UMSCC12 cells (p = 0.0001), and MMP-3 (p = 0.0005) and -9 (p = 0.0036) expression in SCC25 cells. In SCC15 and SCC25 cells, OA treatment increased MMP-2 (p = 0.0408) and MMP-9 gelatinase activity (p \textless 0.0001), respectively. OA depletion decreased MMP-2 (p = 0.0023) and -9 (p \textless 0.0001) activity in SCC25 cells. OA treatment increased 70 kDa caseinolytic activity in UMSCC12 cells consistent with tissue type plasminogen activator (p = 0.0078). OA depletion decreased invasive capacity of UMSCC12 cells (p \textless 0.0001). OA's effects on MMP expression in HNSCC are variable, and may promote cancer cell invasion.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jcp.25900" target="_blank" rel="noreferrer noopener">10.1002/jcp.25900</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cell Movement
2018
Arosarena Oneida A
Barr Eric W
Carcinoma
Cell Line
cell lines
Department of Anatomy & Neurobiology
Enzymologic
Extracellular Matrix
Gene Expression Regulation
Head and Neck Neoplasms/*enzymology/genetics/pathology
Human
Humans
Journal of cellular physiology
matrix metalloproteinases
Membrane Glycoproteins/genetics/*metabolism
Messenger/genetics/metabolism
NEOMED College of Medicine
neoplasm invasion
Neoplasm Invasiveness
Neoplastic
RNA
RNA Interference
Safadi Fayez F
Secreted/genetics/*metabolism
Signal Transduction
Squamous Cell Carcinoma of Head and Neck
Squamous Cell/*enzymology/genetics/pathology
Tarr Joseph T
Thorpe Ryan
Transfection
Tumor
Yankey Hilary