scholarly journals Identification of Cilia in Different Mouse Tissues

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1623
Author(s):  
Xinhua Li ◽  
Shuting Yang ◽  
Vishwa Deepk ◽  
Zahra Chinipardaz ◽  
Shuying Yang
Keyword(s):  
Cell Surface ◽  
Primary Cilia ◽  
Apical Cell ◽  
Extracellular Fluid ◽  
Mouse Tissues ◽  
Dual Reporter ◽  
The Brain ◽  
Postnatal Stage ◽  
Comprehensive Study

Cilia are microtubule-based hair-like organelles that extend from the cell surface. However, the existence and distribution of cilia in each organ and tissue at the postnatal stage in vivo remain largely unknown. In this study, we defined cilia distribution and arrangement and measured the ciliary lengths and the percentage of ciliated cells in different organs and tissues in vivo by using cilium dual reporter-expressing transgenic mice. Cilia were identified by the presence of ARL13B with an mCherry+ signal, and the cilium basal body was identified by the presence of Centrin2 with a GFP+ signal. Here, we provide in vivo evidence that chondrocytes and cells throughout bones have cilia. Most importantly, we reveal that: 1. primary cilia are present in hepatocytes; 2. no cilia but many centrioles are distributed on the apical cell surface in the gallbladder, intestine, and thyroid epithelia; 3. cilia on the cerebral cortex are well oriented, pointing to the center of the brain; 4. ARL13B+ inclusion is evident in the thyroid and islets of Langerhans; and 5. approximately 2% of cilia show irregular movement in nucleus pulposus extracellular fluid. This study reveals the existence and distribution of cilia and centrioles in different tissues and organs, and provides new insights for further comprehensive study of ciliary function in these organs and tissues.

Correlative light and electron microscopy of primary (9+0) cilia: Response of ciliary varicosities to hypotonic treatment in kidney epithelial cells

1992 ◽  
Vol 50 (1) ◽  
pp. 572-573
Author(s):  
Samuel S. Bowser ◽  
Karen E. Roth ◽  
Conly L. Rieder
Keyword(s):  
Electron Microscopy ◽  
Golgi Apparatus ◽  
Cell Surface ◽  
Primary Cilia ◽  
Apical Cell ◽  
Light And Electron Microscopy ◽  
Kidney Tubule ◽  
Hypotonic Treatment ◽  
Structural Association

Primary cilia are centrosomal appendages which in kidney epithelia extend several micrometers from the apical cell surface into the lumen of the kidney tubule. Although considered by some to be “rudimentary appendages” because they are nonmotile, their intimate structural association with the Golgi apparatus and nucleus suggests to others that they mediate interactions between the cell and its environment. Such a sensory role is not without precedence since various photo- and chemoreceptors are highly modified primary cilia. Despite the near-ubiquitous distribution of primary cilia few studies have addressed their function experimentally, and little detailed information is available regarding their behavior in vivo.

scholarly journals CEP55 promotes cilia disassembly through stabilizing Aurora A kinase

2021 ◽  
Vol 220 (2) ◽  
Author(s):  
Yu-Cheng Zhang ◽  
Yun-Feng Bai ◽  
Jin-Feng Yuan ◽  
Xiao-Lin Shen ◽  
Yu-Ling Xu ◽  
...  
Keyword(s):  
Cell Surface ◽  
Primary Cilia ◽  
Perinatal Death ◽  
Clinical Manifestations ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Mammalian Development ◽  
Polycystic Kidneys ◽  
And Control

Primary cilia protrude from the cell surface and have diverse roles during development and disease, which depends on the precise timing and control of cilia assembly and disassembly. Inactivation of assembly often causes cilia defects and underlies ciliopathy, while diseases caused by dysfunction in disassembly remain largely unknown. Here, we demonstrate that CEP55 functions as a cilia disassembly regulator to participate in ciliopathy. Cep55−/− mice display clinical manifestations of Meckel–Gruber syndrome, including perinatal death, polycystic kidneys, and abnormalities in the CNS. Interestingly, Cep55−/− mice exhibit an abnormal elongation of cilia on these tissues. Mechanistically, CEP55 promotes cilia disassembly by interacting with and stabilizing Aurora A kinase, which is achieved through facilitating the chaperonin CCT complex to Aurora A. In addition, CEP55 mutation in Meckel–Gruber syndrome causes the failure of cilia disassembly. Thus, our study establishes a cilia disassembly role for CEP55 in vivo, coupling defects in cilia disassembly to ciliopathy and further suggesting that proper cilia dynamics are critical for mammalian development.

scholarly journals Brain Eicosanoid Formation following Acute Penetration Injury as Studied by in vivo Microdialysis

1990 ◽  
Vol 10 (1) ◽  
pp. 143-146 ◽  
Author(s):  
James A. Yergey ◽  
Melvyn P. Heyes
Keyword(s):  
Time Course ◽  
Brain Injuries ◽  
Extracellular Fluid ◽  
Sampling Period ◽  
In Vivo Microdialysis ◽  
Rat Striatum ◽  
Microdialysis Probe ◽  
The Brain ◽  
Eicosanoid Formation

Formation of eicosanoids has been implicated in the pathological changes that follow brain injuries. In the present study, we used a microdialysis probe to both induce acute penetration injury and also sample extracellular fluid concentrations of eicosanoids. Formation of prostaglandin (PG) D2, PGF2 a, and thromboxane B2 was highest in the first hour following introduction of the probe into rat striatum. In contrast, the level of PGE2 was highest during the sixth hour of collection, while 6-keto-PGF1 a remained stable throughout the sampling period. We conclude that in vivo microdialysis may be useful in the evaluation of the time course of the effects of acute penetration injury of the brain on the local production of eicosanoids.

In Vivo Monitoring of Multiple Trace Metals in the Brain Extracellular Fluid of Anesthetized Rats by Microdialysis−Membrane Desalter−ICPMS

2007 ◽  
Vol 79 (23) ◽  
pp. 8900-8910 ◽  
Author(s):  
Y. T. Chung ◽  
Y. C. Ling ◽  
C. S. Yang ◽  
Y. C. Sun ◽  
P. L. Lee ◽  
...  
Keyword(s):  
Trace Metals ◽  
Extracellular Fluid ◽  
Brain Extracellular Fluid ◽  
In Vivo Monitoring ◽  
Anesthetized Rats ◽  
The Brain

scholarly journals Effect of hyperoxic and hyperbaric conditions on the adenosinergic pathway and CD26 expression in rat

2015 ◽  
Vol 119 (2) ◽  
pp. 140-147 ◽  
Author(s):  
Laurie Bruzzese ◽  
Jean-Claude Rostain ◽  
Laëtitia Née ◽  
Jocelyne Condo ◽  
Giovanna Mottola ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Cell Surface ◽  
Oxygen Supply ◽  
Oxygen Level ◽  
Camp Production ◽  
Hyperbaric Hyperoxia ◽  
High Oxygen Level ◽  
The Brain ◽  
Hyperbaric Conditions

The nucleoside adenosine acts on the nervous and cardiovascular systems via the A2A receptor (A2AR). In response to oxygen level in tissues, adenosine plasma concentration is regulated in particular via its synthesis by CD73 and via its degradation by adenosine deaminase (ADA). The cell-surface endopeptidase CD26 controls the concentration of vasoactive and antioxidant peptides and hence regulates the oxygen supply to tissues and oxidative stress response. Although overexpression of adenosine, CD73, ADA, A2AR, and CD26 in response to hypoxia is well documented, the effects of hyperoxic and hyperbaric conditions on these elements deserve further consideration. Rats and a murine Chem-3 cell line that expresses A2AR were exposed to 0.21 bar O2, 0.79 bar N2 (terrestrial conditions; normoxia); 1 bar O2 (hyperoxia); 2 bar O2 (hyperbaric hyperoxia); 0.21 bar O2, 1.79 bar N2 (hyperbaria). Adenosine plasma concentration, CD73, ADA, A2AR expression, and CD26 activity were addressed in vivo, and cAMP production was addressed in cellulo. For in vivo conditions, 1) hyperoxia decreased adenosine plasma level and T cell surface CD26 activity, whereas it increased CD73 expression and ADA level; 2) hyperbaric hyperoxia tended to amplify the trend; and 3) hyperbaria alone lacked significant influence on these parameters. In the brain and in cellulo, 1) hyperoxia decreased A2AR expression; 2) hyperbaric hyperoxia amplified the trend; and 3) hyperbaria alone exhibited the strongest effect. We found a similar pattern regarding both A2AR mRNA synthesis in the brain and cAMP production in Chem-3 cells. Thus a high oxygen level tended to downregulate the adenosinergic pathway and CD26 activity. Hyperbaria alone affected only A2AR expression and cAMP production. We discuss how such mechanisms triggered by hyperoxygenation can limit, through vasoconstriction, the oxygen supply to tissues and the production of reactive oxygen species.

Propionate enters GABAergic neurons, inhibits GABA transaminase, causes GABA accumulation and lethargy in a model of propionic acidemia

2018 ◽  
Vol 475 (4) ◽  
pp. 749-758 ◽  
Author(s):  
Cecilie Morland ◽  
Anne-Sofie Frøland ◽  
Mi Nguyen Pettersen ◽  
Jon Storm-Mathisen ◽  
Vidar Gundersen ◽  
...  
Keyword(s):  
Motor Impairment ◽  
Extracellular Fluid ◽  
Propionic Acidemia ◽  
Gabaergic Neurons ◽  
Inner Mitochondrial Membrane ◽  
Gaba Transaminase ◽  
Histone H4 Acetylation ◽  
The Brain

Propionic acidemia is the accumulation of propionate in blood due to dysfunction of propionyl-CoA carboxylase. The condition causes lethargy and striatal degeneration with motor impairment in humans. How propionate exerts its toxic effect is unclear. Here, we show that intravenous administration of propionate causes dose-dependent propionate accumulation in the brain and transient lethargy in mice. Propionate, an inhibitor of histone deacetylase, entered GABAergic neurons, as could be seen from increased neuronal histone H4 acetylation in the striatum and neocortex. Propionate caused an increase in GABA (γ-amino butyric acid) levels in the brain, suggesting inhibition of GABA breakdown. In vitro propionate inhibited GABA transaminase with a Ki of ∼1 mmol/l. In isolated nerve endings, propionate caused increased release of GABA to the extracellular fluid. In vivo, propionate reduced cerebral glucose metabolism in both striatum and neocortex. We conclude that propionate-induced inhibition of GABA transaminase causes accumulation of GABA in the brain, leading to increased extracellular GABA concentration, which inhibits neuronal activity and causes lethargy. Propionate-mediated inhibition of neuronal GABA transaminase, an enzyme of the inner mitochondrial membrane, indicates entry of propionate into neuronal mitochondria. However, previous work has shown that neurons are unable to metabolize propionate oxidatively, leading us to conclude that propionyl-CoA synthetase is probably absent from neuronal mitochondria. Propionate-induced inhibition of energy metabolism in GABAergic neurons may render the striatum, in which >90% of the neurons are GABAergic, particularly vulnerable to degeneration in propionic acidemia.

scholarly journals Vascular endothelial cells maintained in the absence of fibroblast growth factor undergo structural and functional alterations that are incompatible with their in vivo differentiated properties.

1979 ◽  
Vol 83 (2) ◽  
pp. 468-486 ◽  
Author(s):  
I Vlodavsky ◽  
L K Johnson ◽  
G Greenburg ◽  
D Gospodarowicz
Keyword(s):  
Endothelial Cells ◽  
Cell Surface ◽  
Vascular Endothelium ◽  
Vascular Endothelial Cells ◽  
Apical Cell ◽  
Cell Monolayer ◽  
Vascular Endothelial ◽  
Morphological Appearance ◽  
A Cell

Vascular endothelial cells cultured in the presence of fibroblast growth factor (FGF) adopt at confluence a morphological appearance similar to that of the vascular endothelium in vivo. Similarly, their apical cell surface is, as in vivo, nonthrombogenic. In contrast, when the cultures are maintained in the absence of FGF, the cells undergo within two to three passages structural and functional alterations that are incompatible with their in vivo morphological appearance and physiological function. Cultures maintained in the absence of FGF no longer adopt, upon reaching confluence, the configuration of a monolayer composed of small closely apposed and nonoverlapping, cuboidal cells. Instead, confluent cultures deprived of FGF consist of large, overlapping cells which have lost the polarity of cell surface characteristic of the vascular endothelium. The apical cell surface becomes thrombogenic, as reflected by its ability to bind platelets, whereas fibronectin, which at confluence is normally associated only with the basal cell surface, can be found both on top of and underneath the cell layer. Among other changes, both sparse and confluent cultures maintained in the absence of FGF showed a greatly increased production of fibronectin. CSP-60, a cell surface protein whose appearance is correlative with the adoption of a cell monolayer configuration, can no longer be detected in cultures maintained in the absence of FGF. Overlapping endothelial cells maintained in the absence of FGF can also no longer function as a protective barrier against the uptake of ligands such as low density lipoprotein. Exposure of the culture to FGF induces a restoration of the normal endothelial characteristics concomitant with the adoption of a flattened cell monolayer morphology. These results demonstrate that, in addition to being a mitogen. FGF is involved in controlling the differentiation and phenotypic expression of the vascular endothelium. This is reflected by its effect on the morphological appearance, polarity of cell surfaces, platelet binding capacity, and barrier function of the vascular endothelium.

Effect of pH and inhibitors on beta-amyloid fibril assembly

1996 ◽  
Vol 54 ◽  
pp. 752-753
Author(s):  
Beverly E. Maleeff ◽  
Timothy K. Hart ◽  
Stephen J. Wood ◽  
Ronald Wetzel
Keyword(s):  
Amyloid Fibril ◽  
Peptide Fragment ◽  
Hydrophobic Peptides ◽  
Amyloid Fibril Formation ◽  
Effects Of Ph ◽  
Severity Of The Disease ◽  
Kinetics Of ◽  
The Brain

Alzheimer's disease is characterized post-mortem in part by abnormal extracellular neuritic plaques found in brain tissue. There appears to be a correlation between the severity of Alzheimer's dementia in vivo and the number of plaques found in particular areas of the brain. These plaques are known to be the deposition sites of fibrils of the protein β-amyloid. It is thought that if the assembly of these plaques could be inhibited, the severity of the disease would be decreased. The peptide fragment Aβ, a precursor of the p-amyloid protein, has a 40 amino acid sequence, and has been shown to be toxic to neuronal cells in culture after an aging process of several days. This toxicity corresponds to the kinetics of in vitro amyloid fibril formation. In this study, we report the biochemical and ultrastructural effects of pH and the inhibitory agent hexadecyl-N-methylpiperidinium (HMP) bromide, one of a class of ionic micellar detergents known to be capable of solubilizing hydrophobic peptides, on the in vitro assembly of the peptide fragment Aβ.

Microvascular features that suggest effectors of blood-flow regulation in the brain: Evidence by SEM of corrosion casts of intracerebral vessels

1990 ◽  
Vol 48 (3) ◽  
pp. 274-275
Author(s):  
Enrico D.F. Motti ◽  
Hans-Georg Imhof ◽  
Gazi M. Yasargil
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Corrosion Casts ◽  
Cerebral Microcirculation ◽  
Pial Arteries ◽  
Random Occurrence ◽  
Brain Arteries ◽  
Homogeneous Network ◽  
The Brain

Physiologists have devoted most attention in the cerebrovascular tree to the arterial side of the circulation which has been subdivided in three levels: 1) major brain arteries which keep microcirculation constant despite changes in perfusion pressure; 2) pial arteries supposed to be effectors regulating microcirculation; 3) intracerebral arteries supposed to be deprived of active cerebral blood flow regulating devices.The morphological search for microvascular effectors in the cerebrovascular bed has been elusive. The opaque substance of the brain confines in vivo investigation to the superficial pial arteries. Most morphologists had to limit their observation to the random occurrence of a favorable site in the practically two-dimensional thickness of diaphanized histological sections. It is then not surprising most investigators of the cerebral microcirculation refer to an homogeneous network of microvessels interposed between arterioles and venules.We have taken advantage of the excellent depth of focus afforded by the scanning electron microscope (SEM) to investigate corrosion casts obtained injecting a range of experimental animals with a modified Batson's acrylic mixture.

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