scholarly journals Characterization of Nuclear 3,5,3′-Triiodothyronine Receptors in the Developing Rat Lung: Effects of Hypo- and Hyperthyroidism

1982 ◽  
Vol 16 (3) ◽  
pp. 238-242 ◽  
Author(s):  
J Ruel ◽  
P Coulombe ◽  
J H Dussault
Keyword(s):  
Rat Lung ◽  
1984 ◽  
Vol 104 (4_Supplb) ◽  
pp. S91-S92
Author(s):  
G. DAXENBICHLER ◽  
E. H. MOSER
Keyword(s):  
Rat Lung ◽  

Lipids ◽  
1983 ◽  
Vol 18 (1) ◽  
pp. 50-54
Author(s):  
James P. Kehrer ◽  
Anne P. Autor

Toxicology ◽  
1999 ◽  
Vol 133 (1) ◽  
pp. 43-58 ◽  
Author(s):  
B.A. Hart ◽  
C.H. Lee ◽  
G.S. Shukla ◽  
A. Shukla ◽  
M. Osier ◽  
...  

1996 ◽  
Vol 271 (3) ◽  
pp. L392-L399 ◽  
Author(s):  
T. M. Nguyen ◽  
H. Guillozo ◽  
L. Marin ◽  
C. Tordet ◽  
S. Koite ◽  
...  

Rat fetal lung is a target tissue for 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25 (OH)2 D3]. We have identified the cells that respond to the hormone and tested the hypothesis that the lung is also a source of 1 alpha,25(OH)2D3. We found that 1) at the end of pregnancy (days 20-21) alveolar type II cells (ATII) bore 1 alpha,25(OH)2D3 receptors and responded to the hormone. Incubating these cells with 10(-9) M 1 alpha,25(OH)2D3 for 48 h stimulated the synthesis (87.3 +/- 9.1%) and release (61.7 +/- 6.1%) of disaturated phosphatidylcholine; 2) EB-1213, a 1 alpha,25(OH)2D3 analogue with low calcemic activity, had similar effects on ATII; 3) neither fetal lung fibroblasts nor neonatal ATII (day 2 postpartum) expressed 1 alpha,25(OH)2D3 receptors; and 4) in contrast, fetal lung fibroblasts taken on days 19-22 of gestation converted [3H]25(OH)D3 to [3H]1 alpha,25(OH)2D3, whereas ATII and skin fibroblasts did not. These findings suggest that 1 alpha,25(OH)2D3 is a local mediator of epithelial-mesenchymal cell interactions in the developing rat lung and that 1 alpha,25(OH)2D3 or EB-1213 might be therapeutically useful in treating the respiratory distress syndrome of premature neonates.


1995 ◽  
Vol 270 (4) ◽  
pp. 1583-1588 ◽  
Author(s):  
Becky A. Speelman ◽  
Katrina Allen ◽  
Tamara L. Grounds ◽  
Marian R. Neutra ◽  
Tomas Kirchhausen ◽  
...  

1996 ◽  
Vol 39 ◽  
pp. 351-351
Author(s):  
Viswanathan Subramanian ◽  
Walid Al-Jumaily ◽  
Margaret Bruce

1988 ◽  
Vol 66 (5) ◽  
pp. 425-435 ◽  
Author(s):  
Amy Mok ◽  
Tanya Wong ◽  
Octavio Filgueiras ◽  
Paul G. Casola ◽  
Don W. Nicholson ◽  
...  

CDPdiacylglycerol pyrophosphatase (E. C. 3.6.1.26) activity has been examined in rat lung mitochondrial and microsomal fractions. While the mitochondrial hydrolase exhibited a broad pH optimum from pH 6–8, the microsomal activity decreased rapidly above pH 6.5. Apparent Km values of 36.2 and 23.6 μM and Vmax values of 311 and 197 pmol∙min−1∙mg protein−1 were observed for the mitochondrial and microsomal preparations, respectively. Addition of parachloromercuriphenylsulphonic acid led to a marked inhibition of the microsomal fraction but slightly stimulated the mitochondrial activity at low concentrations. Mercuric ions were inhibitory with both fractions. Although biosynthetic reactions utilizing CDPdiacylglycerol require divalent cations, addition of Mg2+, Mn2+, Ca2+, Zn2+, Co2+, and Cu2+ all inhibited the catabolic CDPdiacylglycerol hydrolase activity in both fractions. EDTA and EGTA also produced an inhibitory effect, especially with the mitochondrial fraction. Although addition of either adenine or cytidine nucleotides led to a decrease in activity with both fractions, the marked susceptibility to AMP previously reported for this enzyme in Escherichia coli membranes, guinea pig brain lysosomes, and pig liver mitochondria was not observed. These results indicate that rat lung mitochondria and microsomes contain specific CDPdiacylglycerol hydrolase activities, which could influence the rate of formation of phosphatidylinositol and phosphatidylglycerol for pulmonary surfactant.


1983 ◽  
Vol 234 (1) ◽  
pp. 165-177 ◽  
Author(s):  
Wayne A. Rosenkrans ◽  
John T. Albright ◽  
Robert E. Hausman ◽  
David P. Penney

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