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Article ; Online: Inadequate Intimal Angiogenesis as a Source of Coronary Plaque Instability: Implications for Healing.

Brezinski, Mark / Willard, Frank / Rupnick, Maria

2019 Volume 140, Issue 23, Page(s) 1857–1859

MeSH term(s)	Acute Coronary Syndrome/etiology ; Acute Coronary Syndrome/physiopathology ; Coronary Vessels/pathology ; Coronary Vessels/physiology ; Humans ; Microvessels/ultrastructure ; Models, Cardiovascular ; Neovascularization, Pathologic/complications ; Neovascularization, Pathologic/physiopathology ; Neovascularization, Physiologic/physiology ; Plaque, Atherosclerotic/complications ; Plaque, Atherosclerotic/pathology ; Plaque, Atherosclerotic/physiopathology ; Regeneration ; Rupture, Spontaneous ; Silicones ; Tissue Embedding ; Tomography, Optical Coherence ; Tunica Intima/pathology ; Vasa Vasorum/pathology
Chemical Substances	Silicones
Language	English
Publishing date	2019-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.119.042192
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Article: Can We Advance Macroscopic Quantum Systems Outside the Framework of Complex Decoherence Theory?

Brezinski, Mark E / Rupnick, Maria

Journal of computer science and systems biology

2014 Volume 7, Issue 4, Page(s) 119–136

Abstract: Macroscopic quantum systems (MQS) are macroscopic systems driven by quantum rather than classical mechanics, a long studied area with minimal success till recently. Harnessing the benefits of quantum mechanics on a macroscopic level would revolutionize ... ...

Abstract	Macroscopic quantum systems (MQS) are macroscopic systems driven by quantum rather than classical mechanics, a long studied area with minimal success till recently. Harnessing the benefits of quantum mechanics on a macroscopic level would revolutionize fields ranging from telecommunication to biology, the latter focused on here for reasons discussed. Contrary to misconceptions, there are no known physical laws that prevent the development of MQS. Instead, they are generally believed universally lost in complex systems from environmental entanglements (decoherence). But we argue success is achievable MQS with decoherence compensation developed, naturally or artificially, from top-down rather current reductionist approaches. This paper advances the MQS field by a complex systems approach to decoherence. First, why complex system decoherence approaches (top-down) are needed is discussed. Specifically, complex adaptive systems (CAS) are not amenable to reductionist models (and their master equations) because of emergent behaviour, approximation failures, not accounting for quantum compensatory mechanisms, ignoring path integrals, and the subentity problem. In addition, since MQS must exist within the context of the classical world, where rapid decoherence and prolonged coherence are both needed. Nature has already demonstrated this for quantum subsystems such as photosynthesis and magnetoreception. Second, we perform a preliminary study that illustrates a top-down approach to potential MQS. In summary, reductionist arguments against MQS are not justifiable. It is more likely they are not easily detectable in large intact classical systems or have been destroyed by reductionist experimental set-ups. This complex systems decoherence approach, using top down investigations, is critical to paradigm shifts in MQS research both in biological and non-biological systems.
Language	English
Publishing date	2014-05-22
Publishing country	India
Document type	Journal Article
ZDB-ID	2495283-7
ISSN	0974-7230
ISSN	0974-7230
DOI	10.4172/jcsb.1000147
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Article ; Online: QHREDGS enhances tube formation, metabolism and survival of endothelial cells in collagen-chitosan hydrogels.

Miklas, Jason W / Dallabrida, Susan M / Reis, Lewis A / Ismail, Nesreen / Rupnick, Maria / Radisic, Milica

PloS one

2013 Volume 8, Issue 8, Page(s) e72956

Abstract: Cell survival in complex, vascularized tissues, has been implicated as a major bottleneck in advancement of therapies based on cardiac tissue engineering. This limitation motivates the search for small, inexpensive molecules that would simultaneously be ... ...

Abstract	Cell survival in complex, vascularized tissues, has been implicated as a major bottleneck in advancement of therapies based on cardiac tissue engineering. This limitation motivates the search for small, inexpensive molecules that would simultaneously be cardio-protective and vasculogenic. Here, we present peptide sequence QHREDGS, based upon the fibrinogen-like domain of angiopoietin-1, as a prime candidate molecule. We demonstrated previously that QHREDGS improved cardiomyocyte metabolism and mitigated serum starved apoptosis. In this paper we further demonstrate the potency of QHREDGS in its ability to enhance endothelial cell survival, metabolism and tube formation. When endothelial cells were exposed to the soluble form of QHREDGS, improvements in endothelial cell barrier functionality, nitric oxide production and cell metabolism (ATP levels) in serum starved conditions were found. The functionality of the peptide was then examined when conjugated to collagen-chitosan hydrogel, a potential carrier for in vivo application. The presence of the peptide in the hydrogel mitigated paclitaxel induced apoptosis of endothelial cells in a dose dependent manner. Furthermore, the peptide modified hydrogels stimulated tube-like structure formation of encapsulated endothelial cells. When integrin αvβ3 or α5β1 were antibody blocked during cell encapsulation in peptide modified hydrogels, tube formation was abolished. Therefore, the dual protective nature of the novel peptide QHREDGS may position this peptide as an appealing augmentation for collagen-chitosan hydrogels that could be used for biomaterial delivered cell therapies in the settings of myocardial infarction.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Angiopoietin-1/chemistry ; Cell Survival/drug effects ; Cells, Cultured ; Cells, Immobilized/cytology ; Cells, Immobilized/metabolism ; Chitosan/chemistry ; Chitosan/pharmacology ; Collagen/chemistry ; Collagen/pharmacology ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Humans ; Hydrogels/chemistry ; Hydrogels/pharmacology ; Integrin alpha5beta1/biosynthesis ; Integrin alphaVbeta3/biosynthesis ; Peptides/chemistry ; Peptides/pharmacology
Chemical Substances	ANGPT1 protein, human ; Angiopoietin-1 ; Hydrogels ; Integrin alpha5beta1 ; Integrin alphaVbeta3 ; Peptides ; Adenosine Triphosphate (8L70Q75FXE) ; Collagen (9007-34-5) ; Chitosan (9012-76-4)
Language	English
Publishing date	2013-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0072956
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Article ; Online: Contrary effects of the receptor tyrosine kinase inhibitor vandetanib on constitutive and flow-stimulated nitric oxide elaboration in humans.

Mayer, Erica L / Dallabrida, Susan M / Rupnick, Maria A / Redline, Whitney M / Hannagan, Keri / Ismail, Nesreen S / Burstein, Harold J / Beckman, Joshua A

Hypertension (Dallas, Tex. : 1979)

2011 Volume 58, Issue 1, Page(s) 85–92

Abstract: Vascular endothelial growth factor regulates neoplastic angiogenesis through production of endothelium-derived NO. We performed a prospective evaluation of vascular function during treatment with vandetanib, a vascular endothelial growth receptor 2 and 3 ...

Abstract	Vascular endothelial growth factor regulates neoplastic angiogenesis through production of endothelium-derived NO. We performed a prospective evaluation of vascular function during treatment with vandetanib, a vascular endothelial growth receptor 2 and 3 receptor tyrosine kinase inhibitor, to determine the effects of vascular endothelial growth receptor signal interruption on endothelial function in humans. Seventeen patients with stage IV breast cancer received dose-escalated vandetanib in combination with low-dose oral chemotherapy. We measured blood pressure, systemic nitrate/nitrite levels, and brachial artery vascular function. In vitro analyses of cultured endothelial cells were performed to determine the effect of vandetanib on NO production, akt(473) phosphorylation, and endothelial NO synthase protein content and membrane localization. Vandetanib treatment for 6 weeks significantly increased blood pressure, decreased resting brachial artery diameter, and decreased plasma systemic nitrate/nitrite levels compared with baseline. Flow-mediated vasodilation was preserved, and no change was noted in nitroglycerin-mediated vasodilation. In vitro, endothelial cell nitrite levels and akt(473) phosphorylation were reduced and vascular endothelial growth receptor 2 levels did not change, but endothelial NO synthase membrane concentration doubled. Vandetanib reduces constitutive NO production and increases blood pressure, yet flow-stimulated NO bioavailability was preserved. Changes in vascular function with tyrosine kinase inhibition are complex and require further study in humans.
MeSH term(s)	Administration, Oral ; Adult ; Aged ; Blood Pressure/drug effects ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/physiopathology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Enzyme-Linked Immunosorbent Assay ; Female ; Follow-Up Studies ; Humans ; Middle Aged ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Neovascularization, Pathologic/prevention & control ; Nitric Oxide/biosynthesis ; Piperidines/administration & dosage ; Prospective Studies ; Quinazolines/administration & dosage ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction/drug effects ; Tumor Cells, Cultured ; Vasodilation/drug effects
Chemical Substances	Piperidines ; Quinazolines ; Nitric Oxide (31C4KY9ESH) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; vandetanib (YO460OQ37K)
Language	English
Publishing date	2011-04-11
Publishing country	United States
Document type	Clinical Trial, Phase I ; Comparative Study ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.110.168120
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Article ; Online: Photocrosslinkable chitosan modified with angiopoietin-1 peptide, QHREDGS, promotes survival of neonatal rat heart cells.

Rask, Fiona / Dallabrida, Susan M / Ismail, Nesreen S / Amoozgar, Zohreh / Yeo, Yoon / Rupnick, Maria A / Radisic, Milica

Journal of biomedical materials research. Part A

2011 Volume 95, Issue 1, Page(s) 105–117

Abstract: Myocardial infarction (MI) results in the death of cardiomyocytes (CM), which causes scar formation and pathological remodeling of the heart. The delivery of healthy myocytes or bone marrow cells reduces pathological remodeling after MI, however, current ...

Abstract	Myocardial infarction (MI) results in the death of cardiomyocytes (CM), which causes scar formation and pathological remodeling of the heart. The delivery of healthy myocytes or bone marrow cells reduces pathological remodeling after MI, however, current cell injection methods have low cell survival rates and high cell loss. The main objective of this work was to develop a novel hydrogel that can promote survival of CMs. Photocrosslinkable azidobenzoic acid modified chitosan (Az-chitosan) was conjugated with the angiopoietin-1-derived peptide, QHREDGS. This novel peptide is thought to mediate attachment and survival responses of CM to angiopoietin-1 via integrin binding. Thin layers of Az-chitosan, Az-chitosan-QHREDGS, and Az-chitosan-DGQESHR (scrambled peptide control) were spin coated on glass slides and photocrosslinked with application of UV light (365 nm). Neonatal rat heart cells cultured up to 5 days, demonstrated significantly higher attachment and viability on Az-chitosan-QHREDGS compared to cells on other hydrogel controls. Surfaces were also stained for the CM-specific marker troponin I, demonstrating significantly higher percentage of CMs on Az-chitosan-QHREDGS compared to Az-chitosan. The cells cultivated on Az-chitosan-QHREDGS demonstrated significantly lower levels of caspase 3/7 activation after taxol treatment in comparison to cells cultivated on the control hydrogels, glass substrate, or Az-chitosan linked to RGD, an established integrin binding peptide that did not protect against apoptosis. Thus, Az-chitosan-QHREDGS supports attachment and survival of neonatal rat heart cells.
MeSH term(s)	Amino Acid Sequence ; Angiopoietin-1/chemistry ; Angiopoietin-1/pharmacology ; Animals ; Animals, Newborn ; Apoptosis/drug effects ; Azides/pharmacology ; Cell Adhesion/drug effects ; Cell Survival/drug effects ; Cells, Cultured ; Chitosan/pharmacology ; Cross-Linking Reagents/pharmacology ; Microscopy, Electron, Scanning ; Molecular Sequence Data ; Myocardium/cytology ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Peptides/chemistry ; Peptides/pharmacology ; Rats ; Rats, Sprague-Dawley ; Surface Properties/drug effects ; Troponin I/metabolism ; Ultraviolet Rays
Chemical Substances	Angiopoietin-1 ; Azides ; Cross-Linking Reagents ; Peptides ; Troponin I ; 4-azidobenzoic acid (6427-66-3) ; Chitosan (9012-76-4)
Language	English
Publishing date	2011-05-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2099989-6
ISSN	1552-4965 ; 1549-3296 ; 0021-9304
ISSN (online)	1552-4965
ISSN	1549-3296 ; 0021-9304
DOI	10.1002/jbm.a.32808
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Article ; Online: Angiopoietin-1 promotes cardiac and skeletal myocyte survival through integrins.

Dallabrida, Susan M / Ismail, Nesreen / Oberle, Julianne R / Himes, Blanca E / Rupnick, Maria A

Circulation research

2005 Volume 96, Issue 4, Page(s) e8–24

Abstract: Cardiac myocyte loss, regardless of insult, can trigger compensatory myocardial remodeling leading to heart failure. Identifying mediators of cardiac myocyte survival may advance clinical efforts toward myocardial preservation. Angiopoietin-1 limits ... ...

Abstract	Cardiac myocyte loss, regardless of insult, can trigger compensatory myocardial remodeling leading to heart failure. Identifying mediators of cardiac myocyte survival may advance clinical efforts toward myocardial preservation. Angiopoietin-1 limits ischemia-induced cardiac injury. This benefit is ascribed to angiogenesis because the receptor, tie2, is largely endothelial-specific. We propose that direct, non-tie2 interactions of angiopoietin-1 on cardiac myocytes contribute to this cardioprotection. We found that mouse C2C12 skeletal myocytes lack tie2, yet dose-dependently adhered to angiopoietin-1 and angiopoietin-2 similarly to laminin, fibronectin, vitronectin, and more than to collagen-I, -III, and -IV. Adhesion was divalent cation-mediated (Mn2+, Ca2+, not Mg2+), blocked with EDTA/EGTA, RGD-based peptides, and select integrin subunit antibodies. Similar findings were obtained with human skeletal myocytes (HSMs) and freshly isolated rat neonatal cardiac myocytes (NCMs). Furthermore, angiopoietin-1 conferred significant survival advantage exceeding that of most cell matrices, which was not fully explained by differences in cell adhesion. Angiopoietin-1 promoted survival of serum-starved C2C12, HSM, and NCM (MTT, trypan blue) and prevented taxol-induced apoptosis (caspase-3). Immobilized and soluble angiopoietin-1 phosphorylated Akt(S473) and MAPK(p42/44), (not FAK(Y397)) in C2C12 more than in endothelial cells and more than did angiopoietin-2 or cell matrices. EDTA, RGD-based peptides, and some integrin antibodies blocked these responses. Angiopoietin-1 activated HSM and NCM Akt(S473) and MAPK(p42/44) survival pathways. We propose that this novel function contributes to developmental and cardioprotective actions of angiopoietin-1 presently attributed to vascular effects alone. Angiopoietin-1 may prove therapeutically valuable in cardiac remodeling by supporting myocyte viability and preserving pump function. The full text of this article is available online at http://circres.ahajournals.org.
MeSH term(s)	Amino Acid Substitution ; Angiopoietin-1/genetics ; Angiopoietin-1/pharmacology ; Angiopoietin-1/physiology ; Angiopoietin-2/pharmacology ; Animals ; Animals, Newborn ; Apoptosis/drug effects ; Cell Adhesion/drug effects ; Cells, Cultured/cytology ; Cells, Cultured/drug effects ; Cells, Cultured/metabolism ; Edetic Acid/pharmacology ; Extracellular Matrix Proteins/physiology ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Humans ; Integrins/physiology ; MAP Kinase Signaling System/drug effects ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Muscle Fibers, Skeletal/cytology ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Oligopeptides/pharmacology ; Phosphorylation ; Protein Processing, Post-Translational ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley ; Receptor, TIE-2/physiology ; Recombinant Fusion Proteins/pharmacology
Chemical Substances	ANGPT1 protein, human ; Angiopoietin-1 ; Angiopoietin-2 ; Extracellular Matrix Proteins ; Integrins ; Oligopeptides ; Proto-Oncogene Proteins ; Recombinant Fusion Proteins ; arginyl-glycyl-aspartic acid (78VO7F77PN) ; Edetic Acid (9G34HU7RV0) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, TIE-2 (EC 2.7.10.1) ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; PTK2 protein, human (EC 2.7.10.2) ; Ptk2 protein, rat (EC 2.7.10.2) ; AKT1 protein, human (EC 2.7.11.1) ; Akt1 protein, rat (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24)
Language	English
Publishing date	2005-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/01.RES.0000158285.57191.60
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Article ; Online: Endostatin lowers blood pressure via nitric oxide and prevents hypertension associated with VEGF inhibition.

Sunshine, Sarah B / Dallabrida, Susan M / Durand, Ellen / Ismail, Nesreen S / Bazinet, Lauren / Birsner, Amy E / Sohn, Regina / Ikeda, Sadakatsu / Pu, William T / Kulke, Matthew H / Javaherian, Kashi / Zurakowski, David / Folkman, Judah M / Rupnick, Maria

Proceedings of the National Academy of Sciences of the United States of America

2012 Volume 109, Issue 28, Page(s) 11306–11311

Abstract: Antiangiogenesis therapy has become a vital part of the armamentarium against cancer. Hypertension is a dose-limiting toxicity for VEGF inhibitors. Thus, there is a pressing need to address the associated adverse events so these agents can be better used. ...

Abstract	Antiangiogenesis therapy has become a vital part of the armamentarium against cancer. Hypertension is a dose-limiting toxicity for VEGF inhibitors. Thus, there is a pressing need to address the associated adverse events so these agents can be better used. The hypertension may be mediated by reduced NO bioavailability resulting from VEGF inhibition. We proposed that the hypertension may be prevented by coadministration with endostatin (ES), an endogenous angiogenesis inhibitor with antitumor effects shown to increase endothelial NO production in vitro. We determined that Fc-conjugated ES promoted NO production in endothelial and smooth muscle cells. ES also lowered blood pressure in normotensive mice and prevented hypertension induced by anti-VEGF antibodies. This effect was associated with higher circulating nitrate levels and was absent in eNOS-knockout mice, implicating a NO-mediated mechanism. Retrospective study of patients treated with ES in a clinical trial revealed a small but significant reduction in blood pressure, suggesting that the findings may translate to the clinic. Coadministration of ES with VEGF inhibitors may offer a unique strategy to prevent drug-related hypertension and enhance antiangiogenic tumor suppression.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Animals ; Antibodies/chemistry ; Blood Pressure/physiology ; Clinical Trials, Phase II as Topic ; Endostatins/metabolism ; Female ; Heart/drug effects ; Humans ; Hypertension/metabolism ; Hypertension/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Neovascularization, Pathologic/prevention & control ; Nitric Oxide/metabolism ; Vascular Endothelial Growth Factor A/antagonists & inhibitors
Chemical Substances	Angiogenesis Inhibitors ; Antibodies ; Endostatins ; Vascular Endothelial Growth Factor A ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2012-06-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1203275109
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Zs.A 1148: Show issues

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Article ; Online: Vascular progenitor cells isolated from human embryonic stem cells give rise to endothelial and smooth muscle like cells and form vascular networks in vivo.

Ferreira, Lino S / Gerecht, Sharon / Shieh, Hester F / Watson, Nicki / Rupnick, Maria A / Dallabrida, Susan M / Vunjak-Novakovic, Gordana / Langer, Robert

Circulation research

2007 Volume 101, Issue 3, Page(s) 286–294

Abstract: We report that human embryonic stem cells contain a population of vascular progenitor cells that have the ability to differentiate into endothelial-like and smooth muscle (SM)-like cells. Vascular progenitor cells were isolated from EBs grown in ... ...

Abstract	We report that human embryonic stem cells contain a population of vascular progenitor cells that have the ability to differentiate into endothelial-like and smooth muscle (SM)-like cells. Vascular progenitor cells were isolated from EBs grown in suspension for 10 days and were characterized by expression of the endothelial/hematopoietic marker CD34 (CD34+ cells). When these cells are subsequently cultured in EGM-2 (endothelial growth medium) supplemented with vascular endothelial growth factor-165 (50 ng/mL), they give rise to endothelial-like cells characterized by a cobblestone cell morphology, expression of endothelial markers (platelet endothelial cell-adhesion molecule-1, CD34, KDR/Flk-1, vascular endothelial cadherin, von Willebrand factor), incorporation of acetylated low-density lipoprotein, and formation of capillary-like structures when placed in Matrigel. In contrast, when CD34+ cells are cultured in EGM-2 supplemented with platelet-derived growth factor-BB (50 ng/mL), they give rise to SM-like cells characterized by spindle-shape morphology, expression of SM cell markers (alpha-SM actin, SM myosin heavy chain, calponin, caldesmon, SM alpha-22), and the ability to contract and relax in response to common pharmacological agents such as carbachol and atropine but rarely form capillary-like structures when placed in Matrigel. Implantation studies in nude mice show that both cell types contribute to the formation of human microvasculature. Some microvessels contained mouse blood cells, which indicates functional integration with host vasculature. Therefore, the vascular progenitors isolated from human embryonic stem cells using methods established in the present study could provide a means to examine the mechanisms of endothelial and SM cell development, and they could also provide a potential source of cells for vascular tissue engineering.
MeSH term(s)	Animals ; Antigens, CD34/biosynthesis ; Biomarkers ; Blood Vessels/cytology ; Blood Vessels/ultrastructure ; Cattle ; Cell Differentiation/drug effects ; Cell Lineage ; Cells, Cultured/cytology ; Cells, Cultured/drug effects ; Cells, Cultured/metabolism ; Cells, Cultured/transplantation ; Collagen ; Culture Media/pharmacology ; Drug Combinations ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/drug effects ; Embryonic Stem Cells/metabolism ; Embryonic Stem Cells/transplantation ; Endothelial Cells/cytology ; Fetal Blood ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Humans ; Injections, Subcutaneous ; Laminin ; Mice ; Mice, Nude ; Morphogenesis ; Muscle Proteins/biosynthesis ; Myocytes, Smooth Muscle/cytology ; Neovascularization, Physiologic ; Organ Specificity ; Platelet-Derived Growth Factor/pharmacology ; Proteoglycans ; Proto-Oncogene Proteins c-sis ; Tissue Engineering ; Vascular Endothelial Growth Factor A/pharmacology
Chemical Substances	Antigens, CD34 ; Biomarkers ; Culture Media ; Drug Combinations ; Laminin ; Muscle Proteins ; Platelet-Derived Growth Factor ; Proteoglycans ; Proto-Oncogene Proteins c-sis ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; matrigel (119978-18-6) ; becaplermin (1B56C968OA) ; Collagen (9007-34-5)
Language	English
Publishing date	2007-08-03
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.107.150201
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Article: Nonsteroidal antiinflammatory drugs differentially suppress endometriosis in a murine model.

Efstathiou, Jason A / Sampson, David A / Levine, Zalman / Rohan, Richard M / Zurakowski, David / Folkman, Judah / D'Amato, Robert J / Rupnick, Maria A

Fertility and sterility

2005 Volume 83, Issue 1, Page(s) 171–181

Abstract: Objective: To determine whether nonsteroidal antiinflammatory drugs (NSAIDs) affect the establishment and progression of endometriotic lesions in a murine model.: Design: Pharmacologic intervention in a surgically induced murine model of abdominal/ ... ...

Abstract	Objective: To determine whether nonsteroidal antiinflammatory drugs (NSAIDs) affect the establishment and progression of endometriotic lesions in a murine model. Design: Pharmacologic intervention in a surgically induced murine model of abdominal/peritoneal endometriosis. Setting: Animal research facility. Patient(s): Eight-week-old, female C57BL/6 mice. Intervention(s): After implantation of autologous endometrium, mice were randomized into groups and treated with one of several NSAIDs or the vehicle-matched control for 4 weeks. Main outcome measure(s): Establishment, growth, and total burden of endometriotic lesions. Result(s): The NSAIDs differentially inhibited lesion establishment and growth, resulting in significantly reduced disease burden. Compared with controls (5.7 +/- 2.3 mm(2)), lesion burden was reduced by celecoxib (1.3 +/- 1.2 mm(2)), indomethacin (1.4 +/- 1.4 mm(2)), naproxen (2.7 +/- 1.2 mm(2)), sulindac (3.1 +/- 1.5 mm(2)), rofecoxib (3.4 +/- 3.0 mm(2)), and ibuprofen (4.1 +/- 1.4 mm(2)). In contrast, aspirin (5.9 +/- 1.2 mm(2)) had no statistically significant effect. Uninterrupted estrus cycling was confirmed by vaginal exams and smears in celecoxib-treated mice. Conclusion(s): Chronic administration of certain NSAIDs limits the progression of endometriosis in this murine model. The data suggest that NSAID selection in the treatment of endometriosis should be extended beyond pain management to maximize the inhibitory effect on disease burden.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Celecoxib ; Cyclooxygenase Inhibitors/therapeutic use ; Disease Models, Animal ; Endometriosis/drug therapy ; Endometriosis/pathology ; Female ; Humans ; Mice ; Mice, Inbred C57BL ; Pyrazoles/therapeutic use ; Sulfonamides/therapeutic use
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase Inhibitors ; Pyrazoles ; Sulfonamides ; Celecoxib (JCX84Q7J1L)
Language	English
Publishing date	2005-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80133-1
ISSN	1556-5653 ; 0015-0282
ISSN (online)	1556-5653
ISSN	0015-0282
DOI	10.1016/j.fertnstert.2004.06.058
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Integrin binding angiopoietin-1 monomers reduce cardiac hypertrophy

Dallabrida, Susan M / Ismail, Nesreen S / Pravda, Elke A / Parodi, Emily M / Dickie, Renee / Durand, Ellen M / Lai, Jean / Cassiola, Flavia / Rogers, Rick A / Rupnick, Maria A

FASEB journal. 2008 Aug., v. 22, no. 8

2008

Abstract: Angiopoietins were thought to be endothelial cell-specific via the tie2 receptor. We showed that angiopoietin-1 (ang1) also interacts with integrins on cardiac myocytes (CMs) to increase survival. Because ang1 monomers bind and activate integrins (not ... ...

Abstract	Angiopoietins were thought to be endothelial cell-specific via the tie2 receptor. We showed that angiopoietin-1 (ang1) also interacts with integrins on cardiac myocytes (CMs) to increase survival. Because ang1 monomers bind and activate integrins (not tie2), we determined their function in vivo. We examined monomer and multimer expressions during physiological and pathological cardiac remodeling and overexpressed ang1 monomers in phenylephrine-induced cardiac hypertrophy. Cardiac ang1 levels (mRNA, protein) increased during postnatal development and decreased with phenylephrine-induced cardiac hypertrophy, whereas tie2 phosphorylations were unchanged. We found that most or all of the changes during cardiac remodeling were in monomers, offering an explanation for unchanged tie2 activity. Heart tissue contains abundant ang1 monomers and few multimers (Western blotting). We generated plasmids that produce ang1 monomers (ang1-256), injected them into mice, and confirmed cardiac expression (immunohistochemistry, RT-PCR). Ang1 monomers localize to CMs, smooth muscle cells, and endothelial cells. In phenylephrine-induced cardiac hypertrophy, ang1-256 reduced left ventricle (LV)/tibia ratios, fetal gene expressions (atrial and brain natriuretic peptides, skeletal actin, β-myosin heavy chain), and fibrosis (collagen III), and increased LV prosurvival signaling (akt, MAPKp₄₂/₄₄), and AMPKT₁₇₂. However, tie2 phosphorylations were unchanged. Ang1-256 increased integrin-linked kinase, a key regulator of integrin signaling and cardiac health. Collectively, these results suggest a role for ang1 monomers in cardiac remodeling.--Dallabrida, S. M., Ismail, N. S., Pravda, E. A., Parodi, E. M., Dickie, R., Durand, E. M., Lai, J., Cassiola, F., Rogers, R. A., Rupnick, M. A. Integrin binding angiopoietin-1 monomers reduce cardiac hypertrophy.
Language	English
Dates of publication	2008-08
Size	p. 3010-3023.
Publishing place	The Federation of American Societies for Experimental Biology
Document type	Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
Database	NAL-Catalogue (AGRICOLA)

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