The Role of Microtubule Organization in Chondrocyte Response to Osmotic Loading

2007 ◽  
Author(s):  
Elizabeth S. Oswald ◽  
Pen-hsiu Grace Chao ◽  
J. Chloe Bulinski ◽  
Gerard A. Ateshian ◽  
Clark T. Hung
Keyword(s):  
Intracellular Transport ◽  
Morphological Changes ◽  
Cellular Responses ◽  
Microtubule Organization ◽  
Osmotic Loading ◽  
Volume Response ◽  
Cytoplasmic Organization

The cytoskeleton, including actin filaments and microtubules, provides chondrocytes with structure, cytoplasmic organization, and intracellular transport. The cytoskeleton is known to be involved in cellular responses to physiologic mechanical and osmotic loading signals, including morphological changes and mechanostransduction [1, 2]. Here, we examine microtubule (MT) involvement in volume response of chondrocytes to osmotic loading, as well as organization of stable MT with hypoosmotic loading. We also explore the hypothesis that chondrocytes from different zones of cartilage possess cytoskeletons with different properties, which help explain variations in their volume response to osmotic loading in situ and in vitro [3].

scholarly journals Chemotherapy-Induced Peripheral Neuropathy and Changes in Cytoskeleton

2019 ◽  
Vol 20 (9) ◽  
pp. 2287 ◽  
Author(s):  
Alessio Malacrida ◽  
Cristina Meregalli ◽  
Virginia Rodriguez-Menendez ◽  
Gabriella Nicolini
Keyword(s):  
Morphological Changes ◽  
Proteasome Inhibitors ◽  
Sensory Nerves ◽  
Microtubule Organization ◽  
Peripheral Neurotoxicity ◽  
Chemotherapy Drugs ◽  
Associated Proteins ◽  
Dying Back

Despite the different antineoplastic mechanisms of action, peripheral neurotoxicity induced by all chemotherapy drugs (anti-tubulin agents, platinum compounds, proteasome inhibitors, thalidomide) is associated with neuron morphological changes ascribable to cytoskeleton modifications. The “dying back” degeneration of distal terminals (sensory nerves) of dorsal root ganglia sensory neurons, observed in animal models, in in vitro cultures and biopsies of patients is the most evident hallmark of the perturbation of the cytoskeleton. On the other hand, in highly polarized cells like neurons, the cytoskeleton carries out its role not only in axons but also has a fundamental role in dendrite plasticity and in the organization of soma. In the literature, there are many studies focused on the antineoplastic-induced alteration of microtubule organization (and consequently, fast axonal transport defects) while very few studies have investigated the effect of the different classes of drugs on microfilaments, intermediate filaments and associated proteins. Therefore, in this review, we will focus on: (1) Highlighting the fundamental role of the crosstalk among the three filamentous subsystems and (2) investigating pivotal cytoskeleton-associated proteins.

scholarly journals The Neuroinflammatory Role of Pericytes in Epilepsy

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 759
Author(s):  
Gaku Yamanaka ◽  
Fuyuko Takata ◽  
Yasufumi Kataoka ◽  
Kanako Kanou ◽  
Shinichiro Morichi ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Current Knowledge ◽  
Morphological Changes ◽  
Cell Damage ◽  
Neurovascular Unit ◽  
Experimental Studies ◽  
Intractable Epilepsy ◽  
In Vivo Studies

Pericytes are a component of the blood–brain barrier (BBB) neurovascular unit, in which they play a crucial role in BBB integrity and are also implicated in neuroinflammation. The association between pericytes, BBB dysfunction, and the pathophysiology of epilepsy has been investigated, and links between epilepsy and pericytes have been identified. Here, we review current knowledge about the role of pericytes in epilepsy. Clinical evidence has shown an accumulation of pericytes with altered morphology in the cerebral vascular territories of patients with intractable epilepsy. In vitro, proinflammatory cytokines, including IL-1β, TNFα, and IL-6, cause morphological changes in human-derived pericytes, where IL-6 leads to cell damage. Experimental studies using epileptic animal models have shown that cerebrovascular pericytes undergo redistribution and remodeling, potentially contributing to BBB permeability. These series of pericyte-related modifications are promoted by proinflammatory cytokines, of which the most pronounced alterations are caused by IL-1β, a cytokine involved in the pathogenesis of epilepsy. Furthermore, the pericyte-glial scarring process in leaky capillaries was detected in the hippocampus during seizure progression. In addition, pericytes respond more sensitively to proinflammatory cytokines than microglia and can also activate microglia. Thus, pericytes may function as sensors of the inflammatory response. Finally, both in vitro and in vivo studies have highlighted the potential of pericytes as a therapeutic target for seizure disorders.

The Role of Microbiology in Models of Dental Caries: Reaction Paper

1995 ◽  
Vol 9 (3) ◽  
pp. 255-269 ◽  
Author(s):  
G.H. Bowden
Keyword(s):  
Process Selection ◽  
Advantages And Disadvantages ◽  
Test Models ◽  
Plaque Development ◽  
In Vitro Systems ◽  
Selection Of

Models of the caries process have made significant contributions toward defining the roles of bacteria in caries. Microbiologists use a variety of in vitro systems to model aspects of the caries process. Also, in situ models in humans provide information on the microbiology of caries in vivo. These models do not involve the entire process leading to natural caries; consequently, the results from such studies are used to deduce the roles of bacteria in natural caries. Therefore, they can be described as Inferential Caries Models. In contrast, animal models and some clinical trials in humans involve natural caries and can be described as Complete Caries Models. Furthermore, these models are used in two distinct ways. They can be used as Exploratory Models to explore different aspects of the caries process, or as Test Models to determine the effects of anticaries agents. This dichotomy in approach to the use of caries models results in modification of the models to suit a particular role. For example, if we consider Exploratory Models, the in situ appliance in humans is superior to others for analyzing the microbiology of plaque development and demineralization in vivo. The chemostat and biofilm models are excellent for exploring factors influencing bacterial interactions. Both models can also be used as Test Models. The in situ model has been used to test the effects of fluoride on the microflora and demineralization, while the chemostat and biofilm models allow for the testing of antibacterial agents. Each model has its advantages and disadvantages and role in analysis of the caries process. Selection of the model depends on the scientific question posed and the limitations imposed by the conditions available for the study.

A Study of Nuclei and Intercellular Ground Substance during the in situ Differentiation of Somites in Taricha torosa

Development ◽  
1961 ◽  
Vol 9 (4) ◽  
pp. 650-660
Author(s):  
Cyril V. Finnegan
Keyword(s):  
Morphological Changes ◽  
Periodic Acid ◽  
Ground Substance ◽  
Tail Bud ◽  
Interphase Nuclei ◽  
Taricha Torosa ◽  
Intercellular Matrix ◽  
Schiff Reagent

In order better to evaluate results obtained in this laboratory concerning the responses of differentiating postneurula somite tissue to other mesoderm tissue placed in its immediate vicinity (Finnegan, unpublished), it was necessary to examine somite differentiation in situ. A qualitative examination of somite interphase nuclei of tail-bud and later stages was performed to note their morphological changes since it was assumed, as suggested by Briggs & King (1955), that such changes indicate cellular differentiation and, conversely, that absence of such changes indicates that the cells are not actively differentiating. Because of the possible role of the intercellular matrix in histogenesis (see Grobstein, 1954, 1959; and Edds, 1958) a study was made of the development in the somite of that portion of the intercellular matrix which is demonstrable histochemically with the periodic acid-Schirf (PAS) technique. The visual clarity of the results has been materially aided by the fluorescent Schiff reagent of Culling & Vassar (1961) which makes possible a fluorescent Feulgen and a fluorescent PAS reaction.

Adaptation to calcium deprivation in the rat: effects of parathyroidectomy.

1977 ◽  
Vol 232 (3) ◽  
pp. E336
Author(s):  
J T Pento ◽  
L C Waite ◽  
P J Tracy ◽  
A D Kenny
Keyword(s):  
Adaptive Response ◽  
Calcium Transport ◽  
Parathyroid Tissue ◽  
Adaptation Period ◽  
Short Term ◽  
High Calcium

The role of parathyroid hormone (PTH) in the adaptive response in gut calcium transport to calcium deprivation has been studied in the rat using both the in vitro everted duodenal sac and the in situ ligated duodenal segment technique. Intact or parathyroidectomized (PTX) young rats were placed on a low calcium (0.01%) diet for 7-, 14-, or 21-day adaptation periods and compared with control rats maintained on a high calcium (1.5%) diet. Prior PTX (3 days before the start of the adaptation period) abolished the adaptive response (enhanced calcium transport) induced by calcium deprivation for a 7-day adaptation period, but did not abolish a response after a 21-day period. A 14-day adaptation period gave equivocal results. It is concluded that PTH appears to be necessary for short-term (7-day) adaptation, but not for long-term (21-day) adaptation to calcium deprivation. However, if accessory parathyroid tissue is present, the data could be interpreted differently: the essentiality of PTH for the adaptive response might be independent of the length of the adaptation period. The data also contribute to a possible resolution of the controversy concerning the involvement of PTH in the regulation of intestinal calcium transport in the rat.

scholarly journals Hepatocyte-tumor cell interaction in vitro. I. Conditions for rosette formation and inhibition by anti-H-2 antibody.

1980 ◽  
Vol 151 (4) ◽  
pp. 984-989 ◽  
Author(s):  
V Schirrmacher ◽  
R Cheingsong-Popov ◽  
H Arnheiter
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Metastatic Tumor ◽  
Cell Interaction ◽  
Rosette Formation ◽  
Normal Cells ◽  
Neuraminidase Treatment

Murine hepatocytes, isolated by an in situ collagenase-perfusion technique and cultured in Petri dishes, were shown to form rosettes with liver-metastasizing syngeneic tumor cells. Pretreatment of the tumor cells with neuraminidase generally increased the binding, whereas pretreatment of the liver cells with neuraminidase abolished the binding completely. The tumor-cell binding may be mediated by the previously described lectin-like receptor of hepatocytes that also was sensitive to neuraminidase treatment and that bound desialylated cells better than normal cells. Anti-H-2 sera could efficiently inhibit the rosette formation of metastatic tumor cells with the hepatocytes, which points to a possible role of H-2 molecules in this interaction of neoplastic and normal cells.

In situobservation of morphological changes of γ′ precipitates in a pre-deformed single-crystal Ni-base superalloy

2011 ◽  
Vol 44 (5) ◽  
pp. 935-944 ◽  
Author(s):  
Pavel Strunz ◽  
Gerhard Schumacher ◽  
Hellmuth Klingelhöffer ◽  
Albrecht Wiedenmann ◽  
Jan Šaroun ◽  
...  
Keyword(s):  
External Load ◽  
Morphological Changes ◽  
The Past ◽  
Subsequent Heating ◽  
Detailed Evaluation ◽  
The Matrix ◽  
Base Superalloy

Exposure of a superalloy to an external load results in anisotropic coarsening of the γ′ precipitates, so-called rafting. It was reported in the past that γ′ rafting can also occur as a result of purely thermal treatment, without the simultaneous presence of an external load, if the specimen has been pre-deformed at relatively low temperature. The evolution of γ′ morphology in pre-deformed specimens of SCA425 Ni-base superalloy was examined in the present study. Unlike in the previous experiments, the compressive stress was used for pre-straining.In situsmall-angle neutron scattering (SANS) was employed, which enabled the determination of the morphology directly at high temperature. Both for strong and for weak pre-straining, rounding of the originally cuboidal precipitates towards an ellipsoidal shape on heating was observed. Weak pre-straining (0.1, 0.5%) does not cause rafting on subsequent heating. On the other hand, the detailed evaluation of SANS data provides some indication of rafting during the subsequent heating after severe compressive pre-straining (2%). The experiment indicates the role of dislocation rearrangement at the matrix/precipitate interface during pre-straining.

Biomechanics of the Lumbar Disc

1997 ◽  
Vol 01 (02) ◽  
pp. 81-94 ◽  
Author(s):  
V. K. Goel ◽  
N. M. Grosland ◽  
J. Scifert
Keyword(s):  
Morphological Changes ◽  
Imaging Techniques ◽  
Lumbar Disc ◽  
Analytical Models ◽  
Clinical Observations ◽  
Disc Bulge ◽  
Mechanical Factors ◽  
Methods Analytical

The human disc and the facets work in unison to transmit loads across a lumbar motion segment. For this reason, if one component is affected by the degenerative process, the other follows. Modern imaging techniques and clinical observations have adequately delineated morphological changes in the spinal structures, while in vitro biomechanical studies have revealed that repetitive complex loads may lead to loosening of spinal structures, annular tears, and herniated discs. In addition to such experimental methods, analytical models have been able to explain the role of mechanical factors in producing disc degeneration and herniation. Furthermore, these techniques are applicable to investigating various surgical stabilization procedures. From a biomechanical perspective, surgical procedures such as discectomy are effective in reducing pain due to a decrease in disc bulge following surgery. Excessive instability across the disc, however, may require the use of bone grafts, cages or other types of interbody spacers to restore disc height. Efforts are currently underway to restore disc mechanics via an artificial disc. The following review is aimed at outlining the role of mechanical foctors in both inducing and stabilizing the degenerated/herniated intervertebral disc.

scholarly journals AL355338 acts as an oncogenic lncRNA by interacting with protein ENO1 to regulate EGFR/AKT pathway in NSCLC

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qian Hua ◽  
Dongliang Wang ◽  
Lin Zhao ◽  
Zhihui Hong ◽  
Kairu Ni ◽  
...  
Keyword(s):  
Aerobic Glycolysis ◽  
Transcript Abundance ◽  
Metabolic Reprogramming ◽  
Clinical Samples ◽  
Abnormal Metabolism ◽  
Considerable Morbidity

Abstract Background Non-small cell lung cancer (NSCLC) is a malignancy with considerable morbidity and mortality. Abnormal metabolism is a hallmark of cancer; however, the mechanism of glycolysis regulation in NSCLC progression is not completely understood. Recent studies suggest that some dysregulated long non-coding RNAs (lncRNAs) play important roles in tumor metabolic reprogramming. Methods To identify glycolysis-associated-lncRNAs in NSCLC, we compared RNA-sequencing results between high 18F-fluorodeoxyglucose (FDG)-uptake NSCLC tissues and paired paratumor tissues. The transcript abundance of AL355338 in 80 pairs of clinical samples was evaluated by quantitative real-time PCR assay and fluorescence in situ hybridization. The biological role of AL355338 on NSCLC cells were evaluated by functional experiments in vitro and in vivo. Moreover, RNA pull-down, mass spectrometry and RNA immunoprecipitation (RIP) assays were used to identify the protein interacted with AL355338. Co-immunoprecipitation, in situ proximity ligation assays and western blotting were applied to define the potential downstream pathways of AL355338. Results AL355338 was an upregulated glycolysis-associated lncRNA in NSCLC. Functional assays revealed that AL355338 was critical for promoting aerobic glycolysis and NSCLC progression. Mechanistic investigations showed that AL355338 directly bound with alpha-enolase (ENO1) and enhanced the protein’s stability by modulating its degradation and ubiquitination. A positive correlation was observed between AL355338 and ENO1 in NSCLC, and ENO1 was subsequently confirmed to be responsible for the oncogenic role of AL355338. Furthermore, AL355338 was capable of modulating ENO1/EGFR complex interaction and further activating EGFR-AKT signaling. Conclusions This study indicates that AL355338 confers an aggressive phenotype to NSCLC, and targeting it might be an effective therapeutic strategy.

scholarly journals LncRNA-URHC Functions as a ceRNA to Regulate Danjb9 Expression by Competitively Binding to miR-5007-3p in Hepatocellular Carcinoma

2021 ◽  
Author(s):  
kunwei niu ◽  
Shibin Qu ◽  
Xuan Zhang ◽  
Jimin Dai ◽  
Jianlin Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Biological Effects ◽  
Luciferase Reporter ◽  
Underlying Mechanisms ◽  
Proliferation In Vitro ◽  
Hcc Cells

Abstract Background: Hepatocellular carcinoma (HCC) is often diagnosed at a late stage, when the prognosis is poor. The regulation of long non-coding RNAs (lncRNAs) plays a crucial role in HCC. However, the precise regulatory mechanisms of lncRNA signaling in HCC remain largely unknown. We study aim to investigate the underlying mechanisms of lncRNA (upregulated in hepatocellular carcinoma) URHC in HCC. Methods: RT-qPCR, fluorescence in situ hybridization (FISH) staining, EdU, colony formation, and tumor xenografts experiments were used to identify localized and biological effects of URHC on HCC cells in vitro and in vivo. The bioinformatics analysis, Dual-luciferase reporter assay, and rescue experiments revealed the potential mechanism of URHC.Results: URHC silencing may inhibit the HCC cells proliferation in vitro and in vivo. We found that URHC was mainly localized in the cytoplasm. The expression of miR-5007-3p was negatively regulated by URHC. And miR-5007-3p could reverse the effect of URHC in HCC cells. The expression of DNAJB9 was negatively regulated by miR-5007-3p but positively regulated by URHC. These suggesting of lncRNA-URHC positively regulated the level of DNAJB9 by sponging miR-5007-3p.Conclusion: Together, our study elucidated the role of URHC as a miRNA sponge in HCC, and shed new light on lncRNA-directed diagnostics and therapeutics in HCC.

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