scholarly journals Vimentin in a cold-water fish, the rainbow trout: highly conserved primary structure but unique assembly properties

1996 ◽  
Vol 109 (3) ◽  
pp. 569-578 ◽  
Author(s):  
H. Herrmann ◽  
M.D. Munick ◽  
M. Brettel ◽  
B. Fouquet ◽  
J. Markl

We have isolated from a rainbow trout (Oncorhynchus mykiss) spleen cDNA library a clone coding for vimentin. The deduced amino acid sequence reveals a high degree of identity with vimentin from carp (81%), frog (71%), chick and human (73% each). Large stretches in the central alpha-helical rod are identical within all four classes of vertebrates, but in 17 residues spread over the entire rod, the two fish differ distinctly from the tetrapod species. In addition, in the more diverged non-helical head domain, a nonapeptide motif previously shown to be important for regular filament formation is conserved. Recombinant trout vimentin assembles into bona fide filaments in vitro, with a temperature optimum between 18 and 24 degrees C. Above 27 degrees C, however, filament assembly is abruptly abolished and short filaments with thickened ends as well as structures without typical intermediate filament appearance are formed. This distinguishes its assembly properties significantly from amphibian, avian and mammalian vimentin. Also in vivo, after cDNA transfection into vimentin-free mammalian epithelial cells, trout vimentin does not form typical intermediate filament arrays at 37 degrees C. At 28 degrees C, and even more pronounced at 22 degrees C, the vimentin-positive material in the transfected cells is reorganized in the perinuclear region with a partial fibrillar appearance, but typical intermediate filament arrays are not formed. Together with immunoblotting and immunolocalization data from trout tissues, where vimentin is predominantly found in glial and white blood cells, we conclude that vimentin is indeed important in its filamentous form in fish and other vertebrates, possibly fulfilling cellular functions not directly evident in gene targeting experiments carried out in mice.

2000 ◽  
Vol 278 (4) ◽  
pp. R956-R963 ◽  
Author(s):  
Jean-Michel Weber ◽  
Deena S. Shanghavi

The rate of hepatic glucose production (Ra glucose) of rainbow trout ( Oncorhynchus mykiss) was measured in vivo by continuous infusion of [6-3H]glucose and in vitro on isolated hepatocytes to examine the role of epinephrine (Epi) in its regulation. By elevating Epi concentration and/or blocking β-adrenoreceptors with propranolol (Prop), our goals were to investigate the mechanism for Epi-induced hyperglycemia to determine the possible role played by basal Epi concentration in maintaining resting Ra glucose and to assess indirect effects of Epi in the intact animal. In vivo infusion of Epi caused hyperglycemia (3.75 ± 0.16 to 8.75 ± 0.54 mM) and a twofold increase in Ra glucose (6.57 ± 0.79 to 13.30 ± 1.78 μmol ⋅ kg− 1 ⋅ min− 1, n = 7), whereas Prop infusion decreased Ra from 7.65 ± 0.92 to 4.10 ± 0.56 μmol ⋅ kg− 1 ⋅ min− 1( n = 10). Isolated hepatocytes increased glucose production when treated with Epi, and this response was abolished in the presence of Prop. We conclude that Epi-induced trout hyperglycemia is entirely caused by an increase in Ra glucose, because the decrease in the rate of glucose disappearance normally seen in mammals does not occur in trout. Basal circulating levels of Epi are involved in maintaining resting Ra glucose. Epi stimulates in vitro glucose production in a dose-dependent manner, and its effects are mainly mediated by β-adrenoreceptors. Isolated trout hepatocytes produce glucose at one-half the basal rate measured in vivo, even when diet, temperature, and body size are standardized, and basal circulating Epi is responsible for part of this discrepancy. The relative increase in Ra glucose after Epi stimulation is similar in vivo and in vitro, suggesting that indirect in vivo effects of Epi, such as changes in hepatic blood flow or in other circulating hormones, do not play an important role in the regulation of glucose production in trout.


2017 ◽  
Vol 98 (2) ◽  
pp. 559-565 ◽  
Author(s):  
Ali Ehsani ◽  
Mohammad Sedigh Jasour ◽  
Naser Agh ◽  
Mohammad Hashemi ◽  
Mahdi Khodadadi

1998 ◽  
Vol 157 (1) ◽  
pp. 63-70 ◽  
Author(s):  
JM Wilson ◽  
MM Vijayan ◽  
CJ Kennedy ◽  
GK Iwama ◽  
TW Moon

We report for the first time that beta-naphthoflavone (BNF) abolishes ACTH stimulation of cortisol production in rainbow trout (Oncorhynchus mykiss). There was significantly higher hepatic cytochrome P450 content and ethoxyresorufin O-de-ethylase and uridine-5'-diphosphoglucuronic acid transferase activities in BNF-treated fish than in sham-treated controls. BNF did not significantly affect either plasma turnover or tissue distribution of [3H]cortisol-derived radioactivity. Hepatic membrane fluidity and hepatocyte capacity for cortisol uptake were not altered by BNF as compared with the sham-treated fish. These results taken together suggest that BNF does not affect cortisol-clearance mechanisms in trout. A 3 min handling disturbance period elicited a plasma cortisol response in the sham-treated fish; however, the response in the BNF-treated fish was muted and significantly lower than in the sham fish. This in vivo response corroborates the lack of interrenal sensitivity to ACTH in vitro in the BNF-treated fish, suggesting that BNF affects the ACTH pathway in trout. Our results suggest the possibility that cytochrome P450-inducing compounds may affect cortisol dynamics by decreasing interrenal responsiveness to ACTH stimulation in fish, thereby impairing the physiological responses that are necessary for the animal to cope with the stressor.


2011 ◽  
Vol 27 (10) ◽  
pp. 573-582 ◽  
Author(s):  
Abigail E. Bartram ◽  
Matthew J. Winter ◽  
Duane B. Huggett ◽  
Paul McCormack ◽  
Lisa A. Constantine ◽  
...  

1993 ◽  
Vol 180 (1) ◽  
pp. 27-37
Author(s):  
S F Perry ◽  
S Thomas

Respiratory variables of rainbow trout (Oncorhynchus mykiss) blood were monitored continuously in vivo using an extracorporeal circulation or in vitro using blood flowing in a semi- closed loop. The experiments were designed to assess the rapid effects of endogenous catecholamines on red blood cell (RBC) O2 and CO2 transport. The addition of catecholamines (nominal final blood concentrations were 250 nmol l-1 adrenaline and 20 nmol l-1 noradrenaline) caused activation of RBC Na+/H+ exchange both in vivo and in vitro as indicated by the reductions in whole-blood pH. In both experimental systems, the activation of Na+/H+ exchange was associated with a rapid reduction of blood PCO2, indicating a sudden net movement of plasma CO2 into the RBC. In vitro the initial reduction of blood PCO2 was followed by a pronounced elevation as a result of the titration of plasma HCO3- by H+ extruded from the RBC. Blood PO2 fell markedly in a transitory manner after the addition of catecholamines. The decreases in PO2 were probably caused by rapid increases in the affinity/capacity of haemoglobin for O2 which, in turn, caused O2 molecules to enter the RBC from the plasma. The results are discussed with reference to the role of circulating catecholamines in rapidly modifying blood O2 and CO2 transport in rainbow trout.


2020 ◽  
Vol 21 (16) ◽  
pp. 5884
Author(s):  
Sara Balbuena-Pecino ◽  
Esmail Lutfi ◽  
Natàlia Riera-Heredia ◽  
Esther Gasch-Navalón ◽  
Emilio J. Vélez ◽  
...  

Soybeans are one of the most used alternative dietary ingredients in aquafeeds. However, they contain phytoestrogens like genistein (GE), which can have an impact on fish metabolism and health. This study aimed to investigate the in vitro and in vivo effects of GE on lipid metabolism, apoptosis, and autophagy in rainbow trout (Oncorhynchus mykiss). Primary cultured preadipocytes were incubated with GE at different concentrations, 10 or 100 μM, and 1 μM 17β-estradiol (E2). Furthermore, juveniles received an intraperitoneal injection of GE at 5 or 50 µg/g body weight, or E2 at 5 µg/g. In vitro, GE 100 μM increased lipid accumulation and reduced cell viability, apparently involving an autophagic process, indicated by the higher LC3-II protein levels, and higher lc3b and cathepsin d transcript levels achieved after GE 10 μM. In vivo, GE 50 µg/g upregulated the gene expression of fatty acid synthase (fas) and glyceraldehyde-3-phosphate dehydrogenase in adipose tissue, suggesting enhanced lipogenesis, whereas it increased hormone-sensitive lipase in liver, indicating a lipolytic response. Besides, autophagy-related genes increased in the tissues analyzed mainly after GE 50 µg/g treatment. Overall, these findings suggest that an elevated GE administration could lead to impaired adipocyte viability and lipid metabolism dysregulation in rainbow trout.


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