scholarly journals Rapid Imaging of Signaling between the Endothelium and Smooth Muscle; Development of a Rapid Remote Refocusing Epifluorescence Microscope

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Charlotte Buckley ◽  
Penny Lawton ◽  
Calum Wilson ◽  
John Girkin ◽  
John McCarron
Keyword(s):  
Smooth Muscle ◽  
Muscle Development ◽  
Rapid Imaging ◽  
Epifluorescence Microscope

Myosin phosphatase isoform switching in vascular smooth muscle development

2006 ◽  
Vol 40 (2) ◽  
pp. 274-282 ◽  
Author(s):  
M PAYNE ◽  
H ZHANG ◽  
T PROSDOCIMO ◽  
K JOYCE ◽  
Y KOGA ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Development ◽  
Myosin Phosphatase ◽  
Isoform Switching

BMP4 and WNT signaling interact to promote mouse tracheal mesenchyme morphogenesis

2021 ◽  
Author(s):  
Natalia Bottasso Arias ◽  
Lauren Leesman ◽  
Kaulini Burra ◽  
John Snowball ◽  
Ronak M Shah ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Wnt Signaling ◽  
Rna Sequencing ◽  
Muscle Development ◽  
Target Genes ◽  
Bmp Signaling ◽  
Embryonic Mouse ◽  
Tracheal Cartilage ◽  
Cartilage Formation

Tracheobronchomalacia and Complete Tracheal Rings are congenital malformations of the trachea associated with morbidity and mortality for which the etiology remains poorly understood. Epithelial expression of Wls (a cargo receptor mediating Wnt ligand secretion) by tracheal cells is essential for patterning the embryonic mouse trachea's cartilage and muscle. RNA sequencing indicated that Wls differentially modulated the expression of BMP signaling molecules. We tested whether BMP signaling, induced by epithelial Wnt ligands, mediates cartilage formation. Deletion of Bmp4 from respiratory tract mesenchyme impaired tracheal cartilage formation that was replaced by ectopic smooth muscle, recapitulating the phenotype observed after epithelial deletion of Wls in the embryonic trachea. Ectopic muscle was caused in part by anomalous differentiation and proliferation of smooth muscle progenitors rather than tracheal cartilage progenitors. Mesenchymal deletion of Bmp4 impaired expression of Wnt/β-catenin target genes, including targets of WNTsignaling: Notum, and Axin2. In vitro, rBMP4 rescued the expression of Notum in Bmp4 deficient tracheal mesenchymal cells and induced Notum promoter activity via SMAD1/5. RNA sequencing of Bmp4 deficient tracheas identified genes essential for chondrogenesis and muscle development co-regulated by BMP and WNT signaling. During tracheal morphogenesis, WNT signaling induces Bmp4 in mesenchymal progenitors to promote cartilage differentiation and restrict trachealis muscle. In turn, Bmp4 differentially regulates the expression of Wnt/β-catenin targets to attenuate mesenchymal WNT signaling and to further support chondrogenesis.

MESENCHYMAL-EPITHELIAL INTERACTIONS IN BLADDER SMOOTH MUSCLE DEVELOPMENT

1998 ◽  
pp. 1040-1046 ◽  
Author(s):  
MICHAEL J. DiSANDRO ◽  
YINGWU LI ◽  
LAURENCE S. BASKIN ◽  
SIMON HAYWARD ◽  
GERALD CUNHA
Keyword(s):  
Smooth Muscle ◽  
Muscle Development ◽  
Bladder Smooth Muscle

scholarly journals Localization and topography of antigenic domains within the heavy chain of smooth muscle myosin.

1985 ◽  
Vol 101 (1) ◽  
pp. 66-72 ◽  
Author(s):  
M D Schneider ◽  
J R Sellers ◽  
M Vahey ◽  
Y A Preston ◽  
R S Adelstein
Keyword(s):  
Smooth Muscle ◽  
Immunoelectron Microscopy ◽  
Heavy Chain ◽  
Muscle Development ◽  
Solid Phase ◽  
Smooth Muscles ◽  
Smooth Muscle Myosin ◽  
Actin Binding ◽  
Heavy Meromyosin ◽  
Muscle Myosin

We have produced and characterized monoclonal antibodies that label antigenic determinants distributed among three distinct, nonoverlapping peptide domains of the 200-kD heavy chain of avian smooth muscle myosin. Mice were immunized with a partially phosphorylated chymotryptic digest of adult turkey gizzard myosin. Hybridoma antibody specificities were determined by solid-phase indirect radioimmunoassay and immunoreplica techniques. Electron microscopy of rotary-shadowed samples was used to directly visualize the topography of individual [antibody.antigen] complexes. Antibody TGM-1 bound to a 50-kD peptide of subfragment-1 (S-1) previously found to be associated with actin binding and was localized by immunoelectron microscopy to the distal aspect of the myosin head. However, there was no antibody-dependent inhibition of the actin-activated heavy meromyosin ATPase, nor was antibody TGM-1 binding to actin-S-1 complexes inhibited. Antibody TGM-2 detected an epitope of the subfragment-2 (S-2) domain of heavy meromyosin but not the S-2 domain of intact myosin or rod, consistent with recognition of a site exposed by chymotryptic cleavage of the S-2:light meromyosin junction. Localization of TGM-2 to the carboxy-terminus of S-2 was substantiated by immunoelectron microscopy. Antibody TGM-3 recognized an epitope found in the light meromyosin portion of myosin. All three antibodies were specific for avian smooth muscle myosin. Of particular interest is that antibody TGM-1, unlike TGM-3, bound poorly to homogenates of 19-d embryonic smooth muscles. This indicates the expression of different myosin heavy chain epitopes during smooth muscle development.

scholarly journals Epigenetic factors coordinate intestinal development

2018 ◽  
Author(s):  
Julia Ganz ◽  
Ellie Melancon ◽  
Catherine Wilson ◽  
Angel Amores ◽  
Peter Batzel ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Smooth Muscle ◽  
Intestinal Tract ◽  
Muscle Development ◽  
Cell Types ◽  
Epigenetic Modifications ◽  
Neuronal Morphology ◽  
Intestinal Smooth Muscle ◽  
Enteric Neuron ◽  
Neuron Number

AbstractIntestinal epithelium development depends on epigenetic modifications, but whether that is also the case for other intestinal tract cell types remains unclear. We found that functional loss of a DNA methylation machinery component, ubiquitin-like protein containing PHD and RING finger domains 1 (uhrf1), leads to reduced enteric neuron number, changes in neuronal morphology, and severe intestinal smooth muscle disruption. Genetic chimeras revealed that Uhrf1 functions both cell-autonomously in enteric neuron progenitors and cell-non-autonomously in surrounding intestinal cells. Uhrf1 recruits the DNA methyltransferase Dnmt1 to unmethylated DNA during replication. Dnmt1 is also expressed in enteric neuron and smooth muscle progenitors. dnmt1 mutants show a strong reduction in enteric neuron number and disrupted intestinal smooth muscle. Because dnmt1;uhrf1 double mutants have a similar phenotype to dnmt1 and uhrf1 single mutants, Dnmt1 and Uhrf1 must function together during enteric neuron and intestinal muscle development. This work shows that genes controlling epigenetic modifications are important in coordinating intestinal tract development, provides the first demonstration that these genes are important in ENS development, and advances uhrf1 and dnmt1 as potential new Hirschsprung disease candidates.SummaryThis work provides evidence that DNA methylation factors are important in all cell types that contribute to development of a functional intestine.

Smooth muscle development during postnatal growth of distal bronchioles in infant rhesus monkeys

2004 ◽  
Vol 97 (6) ◽  
pp. 2364-2371 ◽  
Author(s):  
Mai-Uyen T. Tran ◽  
Alison J. Weir ◽  
Michelle V. Fanucchi ◽  
April E. Murphy ◽  
Laura S. Van Winkle ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Rhesus Monkeys ◽  
Muscle Development ◽  
Postnatal Growth ◽  
Fetal Life ◽  
Muscle Bundle ◽  
Smooth Muscle Bundle ◽  
Bundle Size ◽  
The Impact ◽  
Infant Rhesus

Development of smooth muscle in conducting airways begins early in fetal life. Whereas the pattern and regulation of smooth muscle differentiation are well-defined, the impact of airway growth on the process is not. To evaluate the transformations in organization during postnatal growth, smooth muscle bundle organization (size, abundance, and orientation) was mapped in five generations of distal airways of infant rhesus monkeys (5 days and 1, 2, 3, and 6 mo old). On the basis of direct measurement of the bronchiole proximal to the terminal bronchiole, length increased by 2-fold, diameter by 1.35-fold, and surface area by 2.8-fold between 5 days and 6 mo of age. Smooth muscle bundle size was greater in proximal bronchioles than in respiratory bronchioles and did not change with age. However, relative bundle size decreased in proportion to airway size as the airways grew. Relative bundle abundance was constant regardless of airway generation or age. The distribution of smooth muscle bundle orientation changed with age in each airway generation, and there were significant changes in the terminal and respiratory bronchioles. We conclude that smooth muscle undergoes marked organizational changes as airways grow during postnatal development.

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