Distinct effects of cell-cell communication and corticosteroids on the synthesis and distribution of cytokeratins in cultured rat hepatocytes

1991 ◽  
Vol 99 (3) ◽  
pp. 609-615 ◽  
Author(s):  
G. Baffet ◽  
P. Loyer ◽  
D. Glaise ◽  
A. Corlu ◽  
P.L. Etienne ◽  
...  

Cytokeratins CK 8 and CK 18 are the two keratins expressed in the liver. They are known to undergo extensive changes in expression with alteration of the hepatocyte phenotype in vitro. In this study, we have investigated the variation in levels of these two cytokeratins in hepatocytes selected from different situations in vivo. The amounts of corresponding transcripts were compared; cytokeratin 8 and 18 mRNAs were present at similar levels in hepatocytes freshly isolated from adult liver and, unexpectedly, from 17-day-old foetuses and newborn rats, whereas they were markedly higher in regenerating hepatocytes isolated early after partial hepatectomy. In order to investigate whether the different factors that can promote hepatocyte differentiation also produce a similar set of cytoskeletal changes, we have analysed both the expression and the distribution of cytokeratins in hepatocytes under different culture conditions allowing modulation of differentiation. Establishment of cell-cell contacts and addition of glucocorticoids were used as two modulating factors. Coculturing hepatocytes with rat liver epithelial cells (RLEC), which favours active expression of liver-specific genes, resulted in a gradual decline of cytokeratin mRNAs, whereas pure hepatocyte cultures, which exhibit rapid phenotypic changes, expressed increasing levels of CK 8 and CK 18 transcripts. Furthermore, intracellular CK distribution was dramatically modified in parallel: the CK-positive material formed a fine network of fibrils uniformly distributed in the cytoplasm of hepatocytes in pure culture, whereas in cocultured cells CK immunofluorescence appeared principally located at the cellular periphery and it was regularly arranged in long fibrils just beneath the plasma membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Wendy Fitzgerald ◽  
Michael L. Freeman ◽  
Michael M. Lederman ◽  
Elena Vasilieva ◽  
Roberto Romero ◽  
...  

Abstract Cytokines are soluble factors that mediate cell–cell communications in multicellular organisms. Recently, another system of cell–cell communication was discovered, which is mediated by extracellular vesicles (EVs). Here, we demonstrate that these two systems are not strictly separated, as many cytokines in vitro, ex vivo, and in vivo are released in EV-encapsulated forms and are capable of eliciting biological effects upon contact with sensitive cells. Association with EVs is not necessarily a property of a particular cytokine but rather of a biological system and can be changed upon system activation. EV-encapsulated cytokines were not detected by standard cytokine assays. Deciphering the regulatory mechanisms of EV-encapsulation will lead to a better understanding of cell–cell communications in health and disease.


2016 ◽  
Vol 198 (24) ◽  
pp. 3278-3286 ◽  
Author(s):  
Christina C. Saak ◽  
Karine A. Gibbs

ABSTRACT Proteus mirabilis is a social bacterium that is capable of self (kin) versus nonself recognition. Swarming colonies of this bacterium expand outward on surfaces to centimeter-scale distances due to the collective motility of individual cells. Colonies of genetically distinct populations remain separate, while those of identical populations merge. Ids proteins are essential for this recognition behavior. Two of these proteins, IdsD and IdsE, encode identity information for each strain. These two proteins bind in vitro in an allele-restrictive manner. IdsD-IdsE binding is correlated with the merging of populations, whereas a lack of binding is correlated with the separation of populations. Key questions remained about the in vivo interactions of IdsD and IdsE, specifically, whether IdsD and IdsE bind within single cells or whether IdsD-IdsE interactions occur across neighboring cells and, if so, which of the two proteins is exchanged. Here we demonstrate that IdsD must originate from another cell to communicate identity and that this nonresident IdsD interacts with IdsE resident in the recipient cell. Furthermore, we show that unbound IdsD in recipient cells does not cause cell death and instead appears to contribute to a restriction in the expansion radius of the swarming colony. We conclude that P. mirabilis communicates IdsD between neighboring cells for nonlethal kin recognition, which suggests that the Ids proteins constitute a type of cell-cell communication. IMPORTANCE We demonstrate that self (kin) versus nonself recognition in P. mirabilis entails the cell-cell communication of an identity-encoding protein that is exported from one cell and received by another. We further show that this intercellular exchange affects swarm colony expansion in a nonlethal manner, which adds social communication to the list of potential swarm-related regulatory factors.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jun Zhao ◽  
Tao Liu ◽  
Long Ma ◽  
Ming Yan ◽  
Zhengyi Gu ◽  
...  

Nymphaea candidais traditional Uighur medicine that is commonly used to treat head pains, cough, hepatitis and hypertension in Xinjiang of China. In this article, the extract ofN. candidawas measured for antioxidant activity, using 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals scavenging assay and reducing power determination, and compared with those of the positive controls of butylated hydroxytoluene (BHT) and gallic acid (GA). The active extract was further purified by liquid-liquid partition to afford four fractions, of which the ethyl acetate-soluble (EA) fraction (NCE) exhibited the strongest antioxidant capacity with IC50value of 12.6 g/mL for DPPH. Thirteen phenolic compounds were isolated from this fraction, and they all showed significant antioxidant activities in DPPH model system. Furthermore, NCE showed potent antioxidant capacity with IC50value of 59.32 g/mL, 24.48 g/mL and 86.85 g/mL, for ,·OH and H2O2radicals, respectively. Moreover, NCE on BCG plus LPS-induced immunological liver injury was evaluated using primary cultured rat hepatocytes. NCE produced significant hepatoprotective effects as evidenced by decreased supernatant enzyme activities (AST—aspartate transaminase,P<  .01; ALT—alanine transferase,P<  .01) and nitric oxide (NO,P<  .01) production. These results revealed thein vitroantioxidant and hepatoprotective activities of NCE against immunological liver injury. Further investigations are necessary to verify these activitiesin vivo.


2015 ◽  
Vol 93 (4) ◽  
pp. 417-420 ◽  
Author(s):  
Sara M. Molinas ◽  
Leandro R. Soria ◽  
Julieta Marrone ◽  
Mauro Danielli ◽  
Laura Trumper ◽  
...  

It has been proposed that, during metabolic acidosis, the liver downregulates mitochondrial ammonia detoxification via ureagenesis, a bicarbonate-consuming process. Since we previously demonstrated that hepatocyte mitochondrial aquaporin-8 channels (mtAQP8) facilitate the uptake of ammonia and its metabolism into urea, we studied whether mtAQP8 is involved in the liver adaptive response to acidosis. Primary cultured rat hepatocytes were adapted to acidosis by exposing them to culture medium at pH 7.0 for 40 h. Control cells were exposed to pH 7.4. Hepatocytes exposed to acid medium showed a decrease in mtAQP8 protein expression (–30%, p < 0.05). Ureagenesis from ammonia was assessed by incubating the cells with 15N-labeled ammonia and measuring 15N-labeled urea synthesis by nuclear magnetic resonance. Reduced ureagenesis was found in acidified hepatocytes (–31%, p < 0.05). In vivo studies in rats subjected to 7 days acidosis also showed decreased protein expression of hepatic mtAQP8 (–50%, p < 0.05) and reduced liver urea content (–35%; p < 0.05). In conclusion, our in vitro and in vivo data suggest that hepatic mtAQP8 expression is downregulated in acidosis, a mechanism that may contribute to decreased ureagenesis from ammonia in response to acidosis.


2021 ◽  
Vol 13 ◽  
Author(s):  
Luis Alfonso González-Molina ◽  
Juan Villar-Vesga ◽  
Julián Henao-Restrepo ◽  
Andrés Villegas ◽  
Francisco Lopera ◽  
...  

Astrocytes are specialized glial cells that are essential components of the neurovascular unit (NVU) and are involved in neurodevelopment, brain maintenance and repair, and neurodegeneration. Astrocytes mediate these processes by releasing cellular mediators such as extracellular vesicles (EVs). EVs are vehicles of cell-cell communication and have been proposed as mediators of damage in AD. However, the transcellular mechanism by which Alzheimer disease (AD) astrocytes impair the function of NVU components is poorly understood. Therefore, we evaluated the effects of adult PS1-KI and 3xTg-AD astrocyte conditioned media (CM) and EVs on NVU components (neuroglia and endothelium) in vitro. Additionally, SAD and FAD astrocyte-derived EVs (A-EVs) were characterized, and we evaluated their effects on NVU in cocultured cells in vitro and on intrahippocampal CA1 cells in vivo. Surprisingly, cultured 3xTg-AD astrocytes showed increased glial fibrillary acidic protein (GFAP) reactivity compared to PS1-KI astrocytes, which denotes astrocytic hyperreactivity. CM from adult mice 3xTg-AD astrocytes increased cell-cell gaps between endothelial cells, filopodia-like dendritic protrusions in neurons and neuronal and endothelial cell death. 3xTg-AD A-EVs induced neurotoxicity and increased astrocyte GFAP reactivity. Cultured human postmortem astrocytes from AD patients also increased GFAP reactivity and EVs release. No differences in the size or number of A-EVs were detected between AD and control samples; however, both SAD and FAD A-EVs showed increased expression of the surface marker aquaporin 4. A-EVs induced cytotoxicity and astrocyte hyperactivation: specifically, FAD A-EVs induced neuroglial cytotoxicity and increased gaps between the endothelium, while SAD A-EVs mainly altered the endothelium. Similarly, both AD A-EVs increased astrocyte GS reactivity and vascular deterioration in vivo. We associated this finding with perivascular reactive astrocytes and vascular deterioration in the human AD brain. In summary, these results suggest that AD A-EVs impair neuroglial and vascular components.


1993 ◽  
Vol 295 (1) ◽  
pp. 217-220 ◽  
Author(s):  
T Nishimaki-Mogami ◽  
A Takahashi ◽  
K Toyoda ◽  
Y Hayashi

The capability of (4R)-4-(2,3,4,6,6a beta,7,8,9,9a alpha,9b beta-decahydro-6a beta-methyl-3-oxo-1H-cyclopental[f]quinolin-7 beta-yl)valeric acid (DCQVA), a catabolite of cholic acid produced by enterobacteria, to induce peroxisome proliferation in vivo and in vitro was studied. Rats given 0.3% DCQVA in the diet for 2 weeks showed marked increases in peroxisomal beta-oxidation, mitochondrial 2,4-dienoyl-CoA reductase and microsomal laurate omega-oxidation activities in the liver compared with control rats given the diet without DCQVA. Cultured rat hepatocytes treated with DCQVA for 72 h also exhibited greatly enhanced beta-oxidation activity. The increased activity was concentration-dependent and the effective concentrations were comparable with those of clofibric acid that produced the same degree of induction in the assay. The results demonstrate that DCQVA is a potent peroxisome proliferator that occurs naturally in rat intestine.


Sign in / Sign up

Export Citation Format

Share Document