Teleost Chloride Cell Tight Junctions: Environmental Salinity and Dynamic Structural Changes

2001 ◽  
pp. 463-476
Keyword(s):  
Tight Junctions ◽  
Structural Changes ◽  
Chloride Cell ◽  
Environmental Salinity

Recovery of mucosal barrier function in ischemic porcine ileum and colon is stimulated by a novel agonist of the ClC-2 chloride channel, lubiprostone

2007 ◽  
Vol 292 (2) ◽  
pp. G647-G656 ◽  
Author(s):  
Adam J. Moeser ◽  
Prashant K. Nighot ◽  
Kory J. Engelke ◽  
Ryuji Ueno ◽  
Anthony T. Blikslager
Keyword(s):  
Tight Junctions ◽  
Barrier Function ◽  
Structural Changes ◽  
Ex Vivo ◽  
Short Circuit ◽  
Mucosal Barrier ◽  
Ileal Mucosa ◽  
Signaling Mechanism ◽  
Ussing Chambers ◽  
Mucosal Barrier Function

Previous studies utilizing an ex vivo porcine model of intestinal ischemic injury demonstrated that prostaglandin (PG)E2 stimulates repair of mucosal barrier function via a mechanism involving Cl− secretion and reductions in paracellular permeability. Further experiments revealed that the signaling mechanism for PGE2-induced mucosal recovery was mediated via type-2 Cl− channels (ClC-2). Therefore, the objective of the present study was to directly investigate the role of ClC-2 in mucosal repair by evaluating mucosal recovery in ischemia-injured intestinal mucosa treated with the selective ClC-2 agonist lubiprostone. Ischemia-injured porcine ileal mucosa was mounted in Ussing chambers, and short-circuit current ( Isc) and transepithelial electrical resistance (TER) were measured in response to lubiprostone. Application of 0.01–1 μM lubiprostone to ischemia-injured mucosa induced concentration-dependent increases in TER, with 1 μM lubiprostone stimulating a twofold increase in TER (ΔTER = 26 Ω·cm2; P < 0.01). However, lubiprostone (1 μM) stimulated higher elevations in TER despite lower Isc responses compared with the nonselective secretory agonist PGE2 (1 μM). Furthermore, lubiprostone significantly ( P < 0.05) reduced mucosal-to-serosal fluxes of 3H-labeled mannitol to levels comparable to those of normal control tissues and restored occludin localization to tight junctions. Activation of ClC-2 with the selective agonist lubiprostone stimulated elevations in TER and reductions in mannitol flux in ischemia-injured intestine associated with structural changes in tight junctions. Prostones such as lubiprostone may provide a selective and novel pharmacological mechanism of accelerating recovery of acutely injured intestine compared with the nonselective action of prostaglandins such as PGE2.

scholarly journals Dynamic Changes in Sarcoplasmic Reticulum Structure in Ventricular Myocytes

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Amanda L. Vega ◽  
Can Yuan ◽  
V. Scott Votaw ◽  
Luis F. Santana
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Tight Junctions ◽  
Molecular Motors ◽  
Structural Changes ◽  
Ventricular Myocytes ◽  
Molecular Motor ◽  
Ryanodine Receptors ◽  
Dynamic Changes ◽  
Ec Coupling

The fidelity of excitation-contraction (EC) coupling in ventricular myocytes is remarkable, with each action potential evoking a transient. The prevalent model is that the consistency in EC coupling in ventricular myocytes is due to the formation of fixed, tight junctions between the sarcoplasmic reticulum (SR) and the sarcolemma where release is activated. Here, we tested the hypothesis that the SR is a structurally inert organelle in ventricular myocytes. Our data suggest that rather than being static, the SR undergoes frequent dynamic structural changes. SR boutons expressing functional ryanodine receptors moved throughout the cell, approaching or moving away from the sarcolemma of ventricular myocytes. These changes in SR structure occurred in the absence of changes in during EC coupling. Microtubules and the molecular motors dynein and kinesin 1(Kif5b) were important regulators of SR motility. These findings support a model in which the SR is a motile organelle capable of molecular motor protein-driven structural changes.

Fine-Structural Changes in a Lepidopteran Nervous System During Metamorphosis

1974 ◽  
Vol 14 (2) ◽  
pp. 369-387
Author(s):  
BARBARA J. McLAUGHLIN
Keyword(s):  
Tight Junctions ◽  
Manduca Sexta ◽  
Structural Changes ◽  
Cell Layer ◽  
Adult Emergence ◽  
Cell Junctions ◽  
Type I ◽  
Type Ii ◽  
Type Ii Cell ◽  
I Cells

The fine structure of the metamorphosing abdominal nerve cord of Manduca sexta has been studied. In fifth instar larvae, the connectives are ensheathed by a complex, thickened neural lamella. The underlying perineurium at this stage consists of 2 layers. The outer layer consists of interdigitating type I cells which are attached to the overlying neural lamella by hemidesmosomes, and to each other by occasional gap and tight junctions which persist throughout development. They are attached by desmosomes to a thin underlying type II cell layer, which is joined by gap and tight junctions and which has desmosomal attachments with the underlying glial membranes. The larval axons are surrounded by multiple glial wrappings containing bundles of microtubules. During the first week after larval-pupal ecdysis, the neural lamella degenerates and is phagocytosed by invading haemocytes. The underlying perineurial I cells gradually become hypertrophied and vacuolated. At the same time the type II layer, which does not increase in size, appears to be composed of either one or two cells which form a continuous ‘bracelet’ around each connective. The cellular bracelet is joined at one or two places by extensive gap, tight and septate junctions, and gap junctions are also seen along its perineurial I and glial borders. The underlying axons are embedded in vast amounts of glial cytoplasm containing relatively few microtubules. During the second week after larval-pupal ecdysis, the neural lamella is reformed and the perineurium flattens again. Type I and II cell junctions remain as described in earlier stages. Before adult emergence, the axons are again wrapped by glial cells rich in microtubules.

scholarly journals Obesity-Linked Gut Microbiome Dysbiosis Associated with Derangements in Gut Permeability and Intestinal Cellular Homeostasis Independent of Diet

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ravinder Nagpal ◽  
Tiffany M. Newman ◽  
Shaohua Wang ◽  
Shalini Jain ◽  
James F. Lovato ◽  
...  
Keyword(s):  
Cell Death ◽  
Tight Junctions ◽  
Gut Microbiome ◽  
High Fat Diet ◽  
Structural Changes ◽  
Intestinal Cell ◽  
Gut Permeability ◽  
Microbiome Composition ◽  
Diet Induced Obesity ◽  
Cellular Turnover

This study aimed to determine the association between non-high-fat diet-induced obesity- (non-DIO-) associated gut microbiome dysbiosis with gut abnormalities like cellular turnover of intestinal cells, tight junctions, and mucin formation that can impact gut permeability. We used leptin-deficient (Lepob/ob) mice in comparison to C57BL/6J control mice, which are fed on identical diets, and performed comparative and correlative analyses of gut microbiome composition, gut permeability, intestinal structural changes, tight junction-mucin formation, cellular turnover, and stemness genes. We found that obesity impacted cellular turnover of the intestine with increased cell death and cell survival/proliferation gene expression with enhanced stemness, which are associated with increased intestinal permeability, changes in villi/crypt length, and decreased expression of tight junctions and mucus synthesis genes along with dysbiotic gut microbiome signature. Obesity-induced gut microbiome dysbiosis is also associated with abnormal intestinal organoid formation characterized with decreased budding and higher stemness. Results suggest that non-DIO-associated gut microbiome dysbiosis is associated with changes in the intestinal cell death versus cell proliferation homeostasis and functions to control tight junctions and mucous synthesis-regulating gut permeability.

Fine Structural Changes in the Microvasculature of the Mouse Pinna: Aging and Radiation Injury

1974 ◽  
Vol 32 ◽  
pp. 54-55
Author(s):  
S. Phyllis Steamer ◽  
Rosemarie L. Devine
Keyword(s):  
Structural Changes ◽  
Radiation Treatment ◽  
Arterial Stenosis ◽  
Ultrastructural Changes ◽  
Vascular Effects ◽  
Microvascular Changes ◽  
Surrounding Connective Tissue ◽  
Fission Neutrons ◽  
Total Body

The importance of radiation damage to the skin and its vasculature was recognized by the early radiologists. In more recent studies, vascular effects were shown to involve the endothelium as well as the surrounding connective tissue. Microvascular changes in the mouse pinna were studied in vivo and recorded photographically over a period of 12-18 months. Radiation treatment at 110 days of age was total body exposure to either 240 rad fission neutrons or 855 rad 60Co gamma rays. After in vivo observations in control and irradiated mice, animals were sacrificed for examination of changes in vascular fine structure. Vessels were selected from regions of specific interest that had been identified on photomicrographs. Prominent ultrastructural changes can be attributed to aging as well as to radiation treatment. Of principal concern were determinations of ultrastructural changes associated with venous dilatations, segmental arterial stenosis and tortuosities of both veins and arteries, effects that had been identified on the basis of light microscopic observations. Tortuosities and irregularly dilated vein segments were related to both aging and radiation changes but arterial stenosis was observed only in irradiated animals.

Evaluation of single-electron movies of glutamine synthetase molecules

1983 ◽  
Vol 41 ◽  
pp. 280-281
Author(s):  
W. Kunath ◽  
E. Zeitler ◽  
M. Kessel
Keyword(s):  
Electron Microscope ◽  
Glutamine Synthetase ◽  
Electron Irradiation ◽  
Structural Damage ◽  
Structural Changes ◽  
Single Electron ◽  
Continuous Series ◽  
Digital Recording ◽  
Recording Device ◽  
Low Exposure

The features of digital recording of a continuous series (movie) of singleelectron TV frames are reported. The technique is used to investigate structural changes in negatively stained glutamine synthetase molecules (GS) during electron irradiation and, as an ultimate goal, to look for the molecules' “undamaged” structure, say, after a 1 e/Å2 dose.The TV frame of fig. la shows an image of 5 glutamine synthetase molecules exposed to 1/150 e/Å2. Every single electron is recorded as a unit signal in a 256 ×256 field. The extremely low exposure of a single TV frame as dictated by the single-electron recording device including the electron microscope requires accumulation of 150 TV frames into one frame (fig. lb) thus achieving a reasonable compromise between the conflicting aspects of exposure time per frame of 3 sec. vs. object drift of less than 1 Å, and exposure per frame of 1 e/Å2 vs. rate of structural damage.

Fine Structural Changes in the Adenohypophyses of Rats Following Destruction of the Pituitary Stalk

1977 ◽  
Vol 35 ◽  
pp. 496-497
Author(s):  
K. Kovacs ◽  
E. Horvath ◽  
J. M. Bilbao ◽  
F. A. Laszlo ◽  
I. Domokos
Keyword(s):  
Structural Changes ◽  
Tissue Injury ◽  
Anterior Lobe ◽  
Uranyl Acetate ◽  
Male Rats ◽  
Pituitary Stalk ◽  
Sequence Of Events ◽  
Pituitary Glands ◽  
Electrolytic Lesions ◽  
Ultrathin Sections

Electrolytic lesions of the pituitary stalk in rats interrupt adenohypophysial blood flow and result in massive infarction of the anterior lobe. In order to obtain a deeper insight into the morphogenesis of tissue injury and to reveal the sequence of events, a fine structural investigation was undertaken on adenohypophyses of rats at various intervals following destruction of the pituitary stalk.The pituitary stalk was destroyed electrolytically, with a Horsley-Clarke apparatus on 27 male rats of the R-Amsterdam strain, weighing 180-200 g. Thirty minutes, 1,2,4,6 and 24 hours after surgery the animals were perfused with a glutaraldehyde-formalin solution. The skulls were then opened and the pituitary glands removed. The anterior lobes were fixed in glutaraldehyde-formalin solution, postfixed in osmium tetroxide and embedded in Durcupan. Ultrathin sections were stained with uranyl acetate and lead citrate and investigated with a Philips 300 electron microscope.

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