scholarly journals Activation of Notch Signaling DuringEx VivoExpansion Maintains Donor Muscle Cell Engraftment

Stem Cells ◽  
2012 ◽  
Vol 30 (10) ◽  
pp. 2212-2220 ◽  
Author(s):  
Maura H. Parker ◽  
Carol Loretz ◽  
Ashlee E. Tyler ◽  
William J. Duddy ◽  
John K. Hall ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Muscle Cell ◽  
Cell Engraftment ◽  
Donor Muscle

scholarly journals Inhibition of CD26/DPP-IV enhances donor muscle cell engraftment and stimulates sustained donor cell proliferation

2012 ◽  
Vol 2 (1) ◽  
pp. 4 ◽  
Author(s):  
Maura H Parker ◽  
Carol Loretz ◽  
Ashlee E Tyler ◽  
Lauren Snider ◽  
Rainer Storb ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Muscle Cell ◽  
Donor Cell ◽  
Dpp Iv ◽  
Cell Engraftment ◽  
Donor Muscle

scholarly journals Delta-like ligand 4–Notch signaling regulates bone marrow–derived pericyte/vascular smooth muscle cell formation

Blood ◽  
2011 ◽  
Vol 117 (2) ◽  
pp. 719-726 ◽  
Author(s):  
Keri Schadler Stewart ◽  
Zhichao Zhou ◽  
Patrick Zweidler-McKay ◽  
Eugenie S. Kleinerman
Keyword(s):  
Bone Marrow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Notch Signaling ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Ewing Sarcoma

Abstract Delta-like ligand 4 (DLL4) is essential for the formation of mature vasculature. However, the role of DLL4-Notch signaling in pericyte/vascular smooth muscle cell (vSMC) development is poorly understood. We sought to determine whether DLL4-Notch signaling is involved in pericyte/vSMC formation in vitro and during vasculogenesis in vivo using 2 Ewing sarcoma mouse models. Inhibition of DLL4 with the antibody YW152F inhibited pericyte/vSMC marker expression by bone marrow (BM) cells in vitro. Conversely, transfection of 10T1/2 cells with the active domains of Notch receptors led to increased expression of pericyte/vSMC markers. Furthermore, the blood vessels of Ewing sarcoma tumors from mice treated with YW152F had reduced numbers of BM-derived pericytes/vSMCs, fewer open lumens, and were less functional than the vessels in tumors of control-treated mice. Tumor growth was also inhibited. These data demonstrate a specific role for DLL4 in the formation of BM-derived pericytes/vSMCs and indicate that DLL4 may be a novel therapeutic target for the inhibition of vasculogenesis.

scholarly journals Notch signaling inhibits muscle cell differentiation through a CBF1-independent pathway

Development ◽  
1996 ◽  
Vol 122 (12) ◽  
pp. 3765-3773 ◽  
Author(s):  
C. Shawber ◽  
D. Nofziger ◽  
J.J. Hsieh ◽  
C. Lindsell ◽  
O. Bogler ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Notch Signaling ◽  
Cell Fate ◽  
Muscle Cell ◽  
Cellular Differentiation ◽  
C2c12 Myoblasts ◽  
Muscle Cell Differentiation ◽  
Binding Factor ◽  
Exogenous Expression ◽  
Enhancer Of Split

Notch controls cell fate by inhibiting cellular differentiation, presumably through activation of the transcriptional regulator human C promoter Binding Factor (CBF1), which transactivates the hairy and Enhancer of split (HES-1) gene. However, we describe constitutively active forms of Notch1, which inhibit muscle cell differentiation but do not interact with CBF1 or upregulate endogenous HES-1 expression. In addition, Jagged-Notch interactions that prevent the expression of muscle cell specific genes do not involve the upregulation of endogenous HES-1. In fact, exogenous expression of HES-1 in C2C12 myoblasts does not block myogenesis. Our data demonstrate the existence of a CBF1-independent pathway by which Notch inhibits differentiation. We therefore propose that Notch signaling activates at least two different pathways: one which involves CBF1 as an intermediate and one which does not.

scholarly journals Differential effects of alcohol and its metabolite acetaldehyde on vascular smooth muscle cell Notch signaling and growth

2018 ◽  
Vol 314 (1) ◽  
pp. H131-H137 ◽  
Author(s):  
Ekaterina Hatch ◽  
David Morrow ◽  
Weimin Liu ◽  
Paul A. Cahill ◽  
Eileen M. Redmond
Keyword(s):  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Cell Growth ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Notch Signaling ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Notch Receptor ◽  
Secretase Activity

Alcohol (EtOH) consumption can variously affect cardiovascular disease. Our aim was to compare the effects of EtOH and its primary metabolite acetaldehyde (ACT) on vascular smooth muscle Notch signaling and cell growth, which are important for atherogenesis. Human coronary artery smooth muscle cells (HCASMCs) were treated with EtOH (25 mM) or ACT (10 or 25 μM). As previously reported, EtOH inhibited Notch signaling and growth of HCASMCs. In contrast, ACT treatment stimulated HCASMC proliferation (cell counts) and increased proliferating cell nuclear antigen expression, concomitant with stimulation of Notch signaling, as determined by increased Notch receptor (N1 and N3) and target gene (Hairy-related transcription factor 1–3) mRNA levels. Interaction of the ligand with the Notch receptor initiates proteolytic cleavage by α- and γ-secretase, resulting in the release of the active Notch intracellular domain. Neither EtOH nor ACT had any significant effect on α-secretase activity. A fluorogenic peptide cleavage assay demonstrated almost complete inhibition by EtOH of Delta-like ligand 4-stimulated γ-secretase activity in solubilized HCASMCs (similar to the effect of the control inhibitor DAPT) but no effect of ACT treatment. EtOH, but not ACT, affected the association and distribution of the γ-secretase catalytic subunit presenilin-1 with lipid rafts, as determined by dual fluorescent labeling and confocal microscopic visualization. In conclusion, ACT stimulates vascular smooth muscle cell Notch signaling and growth, effects opposite to those of EtOH. These differential actions on vascular smooth muscle cells of EtOH and its metabolite ACT may be important in mediating the ultimate effects of drinking on cardiovascular disease. NEW & NOTEWORTHY Acetaldehyde stimulates, in a Notch-dependent manner, the vascular smooth muscle cell growth that contributes to atherogenesis; effects opposite to those of ethanol. These data suggest that in addition to ethanol itself, its metabolite acetaldehyde may also mediate some of the effects of alcohol consumption on vascular cells and, thus, cardiovascular health.

THE ROLE OF NOTCH SIGNALING IN VASCULAR SMOOTH MUSCLE CELL MIGRATION

2004 ◽  
Vol 13 (3) ◽  
pp. 131
Author(s):  
Yvonne A Birney ◽  
Catherine H Sweeney ◽  
David Morrow ◽  
Agniezka Scheller ◽  
Philip M Cummins ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Notch Signaling ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Smooth Muscle Cell Migration

Interpreting HVEM of muscle-cell impulse networks

1992 ◽  
Vol 50 (1) ◽  
pp. 126-127
Author(s):  
Paul DeCosta ◽  
Kyugon Cho ◽  
Stephen Shemlon ◽  
Heesung Jun ◽  
Stanley M. Dunn
Keyword(s):  
Structural Analysis ◽  
Muscle Cell ◽  
Electron Micrographs ◽  
Relative Size ◽  
Automatic Classification ◽  
Nerve Fibers ◽  
Analysis Algorithm ◽  
Structural Networks

Introduction: The analysis and interpretation of electron micrographs of cells and tissues, often requires the accurate extraction of structural networks, which either provide immediate 2D or 3D information, or from which the desired information can be inferred. The images of these structures contain lines and/or curves whose orientation, lengths, and intersections characterize the overall network.Some examples exist of studies that have been done in the analysis of networks of natural structures. In, Sebok and Roemer determine the complexity of nerve structures in an EM formed slide. Here the number of nodes that exist in the image describes how dense nerve fibers are in a particular region of the skin. Hildith proposes a network structural analysis algorithm for the automatic classification of chromosome spreads (type, relative size and orientation).

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