scholarly journals Cytidine monophosphate-dependent synthesis of phosphatidylglycerol in permeabilized type II pneumonocytes

1985 ◽  
Vol 232 (2) ◽  
pp. 539-545 ◽  
Author(s):  
J E Bleasdale ◽  
N R Thakur ◽  
G R Rader ◽  
M Tesan
Keyword(s):  
Lung Surfactant ◽  
Head Group ◽  
Type Ii ◽  
Free Medium ◽  
Rat Serum ◽  
Maximal Stimulation ◽  
Foetal Rat ◽  
Cytidine Monophosphate

Results of previous investigations support the proposition that, in type II pneumonocytes, CMP is involved in integration of the synthesis of phosphatidylcholine and phosphatidylglycerol for lung surfactant. In the present investigation, the amount of CMP in rat type II pneumonocytes was altered directly and resultant changes in the synthesis of phosphatidylglycerol were examined. Type II pneumonocytes were made permeable to CMP by treatment with Ca2+-free medium, and phosphatidylglycerol synthesis was then assessed by measurement of the incorporation of a radiolabelled precursor, [14C]glycerol 3-phosphate, that was not effectively utilized by cells that resisted permeabilization. Incorporation of [14C]glycerol 3-phosphate into phosphatidylglycerol (but not into other lipids) was stimulated greatly by CMP (half-maximal stimulation at approx. 0.1 mM). CMP stimulated the incorporation of [14C]glycerol 3-phosphate into both the phosphatidyl moiety and the head group of phosphatidylglycerol. Incorporation of [14C]palmitate into phosphatidylglycerol was also stimulated by CMP. myo-Inositol, at concentrations found in foetal-rat serum (0.2-2.0 mM), inhibited CMP-dependent incorporation of [14C]glycerol 3-phosphate into phosphatidylglycerol and promoted, instead, CMP-dependent incorporation into phosphatidylinositol. These data, when extrapolated to foetal type II pneumonocytes, are consistent with the view that the developmental increase in the synthesis of phosphatidylglycerol for surfactant by foetal lungs is promoted by the increase in intracellular CMP and the declining availability of myo-inositol that were found previously to be associated with this period of development.

scholarly journals The influence of myo-inositol on phosphatidylglycerol synthesis by rat type II pneumonocytes

1983 ◽  
Vol 212 (3) ◽  
pp. 811-818 ◽  
Author(s):  
J E Bleasdale ◽  
N E Tyler ◽  
F N Busch ◽  
J G Quirk
Keyword(s):  
Incubation Medium ◽  
Bovine Serum ◽  
Total Lipid Extract ◽  
Type Ii ◽  
Rat Serum ◽  
Adult Rat ◽  
Foetal Rat ◽  
Inositol Uptake ◽  
Foetal Bovine Serum

Type II pneumonocytes isolated from adult rat lung were incubated in a serum-free medium containing [14C]glycerol and the incorporation of 14C into glycerophospholipids was measured. After 24 h, more than 80% of the 14C incorporated into total lipids or into phosphatidylcholine and approx. 90% of the 14C incorporated into phosphatidylglycerol after 24 h was recovered in the glycerophosphoester moieties of these molecules. Supplementation of the incubation medium with foetal-bovine serum (10%, v/v) did not alter the incorporation of [14C]glycerol by type II pneumonocytes after 24 h into either a total lipid extract or phosphatidylcholine. In the presence of foetal-bovine serum, however, the incorporation of 14C into phosphatidylglycerol was decreased and the incorporation of 14C into phosphatidylinositol was increased. In the absence of foetal-bovine serum, the incorporation of 14C into phosphatidylglycerol was decreased progressively as the concentration of myo-inositol in the incubation medium was increased. The range of concentration (0.04-0.50 mM) over which myo-inositol had the greatest influence on [14C]glycerol incorporation into phosphatidylglycerol by type II pneumonocytes in vitro encompassed the concentration range measured in foetal-rat serum late in gestation. At 4 days before birth, the concentration of myo-inositol in foetal-rat serum was 0.36 mM and decreased to 0.23 mM 1 day before birth. The concentration of myo-inositol in adult rat serum increased from 0.03 mM to 0.06 mM during pregnancy. Isolated rat type II pneumonocytes were found to take up myo-inositol by a saturable process. A half-maximal rate of myo-inositol uptake occurred at a concentration of myo-inositol of 0.29 mM. The results of this investigation are consistent with the hypothesis that late in gestation there is a decreasing availability of myo-inositol to the foetal lungs and that this favours the biosynthesis of phosphatidylglycerol for surfactant at the expense of phosphatidylinositol biosynthesis.

Uptake of a natural surfactant and increased delivery of small organic anions into type II pneumocytes

2001 ◽  
Vol 281 (1) ◽  
pp. L144-L154 ◽  
Author(s):  
Matthias Griese ◽  
Astrid Baatz ◽  
Julia Beck ◽  
Barbara Deubzer
Keyword(s):  
Sodium Salt ◽  
Targeted Delivery ◽  
Lung Surfactant ◽  
Organic Anions ◽  
Type Ii Cells ◽  
Type Ii ◽  
Natural Surfactant ◽  
Type Ii Pneumocytes ◽  
Acid Sodium Salt

The uptake of natural lung surfactant into differentiated type II cells may be used for the targeted delivery of other molecules. The fluorescent anion pyranine [hydroxypyren-1,3,6-trisulfonic acid, sodium salt (HPTS)] was incorporated into a bovine surfactant labeled with [3H]dipalmitoylphosphatidylcholine ([3H]DPPC). The uptake of [3H]DPPC and of HPTS increased with time of incubation and concentration, decreased with the size of the vesicles used, and was stimulated by 8-bromo-cAMP and partially inhibited by hypertonic sucrose. However, the amount of HPTS uptake was ∼100 times smaller than that of [3H]DPPC. This large difference was due to a more rapid regurgitation of some of the HPTS from the cells but not to leakage from the surfactant before uptake. The acidification of the internalized surfactant increased linearly over 90 min to 7.13, and after 24 h, a pH of 6.83 was measured. In conclusion, after internalization of a double-labeled natural surfactant, the lipid moieties were accumulated in relation to the anions, which were targeted to a compartment not very acidic and in part rapidly expelled from the cells.

scholarly journals Efficacy and adverse reaction to different doses of atorvastatin in the treatment of type II diabetes mellitus

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Hua Jiang ◽  
Hong Zheng
Keyword(s):  
Diabetes Mellitus ◽  
Type Ii Diabetes ◽  
Adverse Reactions ◽  
Density Lipoprotein ◽  
Type Ii Diabetes Mellitus ◽  
Retinol Binding Protein ◽  
Type Ii ◽  
Sprague Dawley ◽  
Rat Serum ◽  
Different Doses

Abstract Background: Type II diabetes mellitus (T2DM), a persistent metabolic disorder, is primarily characterized by insulin resistance, relative insulin deficiency and dyslipidemia. Here, we aimed to investigate whether different doses of atorvastatin (ATV) affect rats with T2DM. A total of 110 Sprague–Dawley rats were successfully established as T2DM models. Methods: First, the total cholesterol, triglyceride (TG), high-/low-/very-low-density lipoprotein cholesterol (HDL-c/LDL-c/VLDL-c), alanine transaminase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine (Cr), apolipoprotein Al (ApoA1) and apolipoprotein B (ApoB) levels in rat serum were analyzed. In addition, cholesteryl ester transfer protein (CETP) and retinol-binding protein 4 (RBP4) were also measured. Then, the incidence of adverse reactions was noted. Finally, the pathological study of liver and pancreatic tissues was performed. Results: Rats administered ATV at the doses of 40 and 80 mg/(kg·day) showed down-regulated TG, LDL-c, ApoB, CETP and RBP4 levels yet up-regulated HDL-c and ApoAl levels. Rats administered ATV at a dose of 80 mg/(kg·day) exhibited a higher incidence of adverse reactions and higher ALT and AST levels but lower BUN and Cr levels, which might affect liver and kidney function. Rats administered ATV at the doses of 40 and 80 mg/(kg·day) demonstrated significantly improved liver injury and pancreatic injury induced by T2DM. Conclusion: These data revealed that ATV could improve the lipid metabolism in T2DM rats and 40 mg/(kg·day) may serve as the optimal dose for the reduction of lipid levels and the incidence of adverse effects.

ROLE OF THE MESENCHYME IN THE INDUCTION OF THE RAT PROSTATE GLAND BY ANDROGENS IN ORGAN CULTURE

1979 ◽  
Vol 82 (1) ◽  
pp. 171-NP ◽  
Author(s):  
ILSE LASNITZKI ◽  
TAKEO MIZUNO
Keyword(s):  
Organ Culture ◽  
De Novo ◽  
Prostate Gland ◽  
Young Male ◽  
Free Medium ◽  
Foetal Rat ◽  
Rat Prostate ◽  
Do So

SUMMARY Rat prostate glands are induced de novo by androgens in 16·5-day-old male and female urogenital sinuses in vitro as epithelial buds projecting into the surrounding mesenchyme. The role of the mesenchyme in this process has been investigated in various epithelial-mesenchymal recombinations in organ culture. Isolated epithelium did not form buds but required the presence of the mesenchyme to do so. This requirement seemed to be specific; in the presence of testosterone or dihydrotestosterone only urogenital mesenchyme increased cell division in the urogenital epithelium and stimulated prostatic bud formation. In contrast, heterotypic mesenchyme did not affect epithelial mitosis and failed to induce buds while heterotypic epithelia did not respond to urogenital mesenchyme. In recombinants of urogenital mesenchyme pretreated with androgen and untreated urogenital epithelium, grown in androgen-free medium, the majority of explants developed prostatic buds while only a few buds were formed from epithelium pretreated with androgen when it was recombined with untreated mesenchyme. The role of the mesenchyme in the loss of androgen responsiveness of the older female sinuses was examined in heterochronic recombinants. It was found that the old female mesenchyme failed to induce buds in young epithelium while young male or female mesenchymes induced them in the old female epithelium. The results suggest that the urogenital mesenchyme is essential for the initiation of the foetal rat prostate gland and that it may be a target for androgens and complement or mediate their effect on the epithelium.

scholarly journals Type II insulin-like growth factor receptor is present in rat serum.

1987 ◽  
Vol 84 (21) ◽  
pp. 7720-7724 ◽  
Author(s):  
W. Kiess ◽  
L. A. Greenstein ◽  
R. M. White ◽  
L. Lee ◽  
M. M. Rechler ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Insulin Like Growth Factor ◽  
Type Ii ◽  
Rat Serum

Insulin and growth hormone act synergistically to stimulate insulin-like growth factor-I production by cultured chicken hepatocytes

1991 ◽  
Vol 128 (3) ◽  
pp. 389-393 ◽  
Author(s):  
B. Houston ◽  
I. E. O'Neill
Keyword(s):  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Free Medium ◽  
In Vitro System ◽  
Factor I ◽  
Maximal Stimulation ◽  
Igf I ◽  
Growth Factor I ◽  
Stimulation Of

ABSTRACT Cultured chicken hepatocytes were used to investigate whether insulin and GH interact to regulate insulin-like growth factor-I (IGF-I) production in vitro. In the first set of experiments hepatocytes were preincubated for 6 h in hormone-free medium, and the effects of various combinations of insulin and GH on IGF-I production over the next 24 h were quantified by radioimmunoassay. Basal IGF-I production was 5·36 pg IGF-I/μg DNA and this was increased 1·31±0·13-fold (mean ± s.e.m.) by insulin, 1·90±0·24-fold by GH and 4·46±0·68-fold by a combination of insulin and GH. These results demonstrate that insulin and GH interact synergistically to stimulate IGF-I production in vitro. The synergism with GH occurred at physiological concentrations of insulin with half-maximal stimulation occurring at an insulin concentration of 6 ng/ml. In hepatocytes which had been exposed to insulin immediately before the start of the experiment, the presence of insulin was no longer required for maximal stimulation of IGF-I production by GH. This in-vitro system will facilitate the study of the molecular basis of the interaction between insulin and GH. Journal of Endocrinology (1991) 128, 389–393

scholarly journals Effect of Hyaluronic Acid on the Differentiation of Mesenchymal Stem Cells into Mature Type II Pneumocytes

Polymers ◽  
2021 ◽  
Vol 13 (17) ◽  
pp. 2928
Author(s):  
Francesca Della Sala ◽  
Mario di Gennaro ◽  
Gianluca Lista ◽  
Francesco Messina ◽  
Luigi Ambrosio ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Lung Surfactant ◽  
Repair Process ◽  
Surfactant Protein ◽  
Alveolar Type ◽  
Type Ii ◽  
Type Ii Pneumocytes ◽  
Mature Type ◽  
Pulmonary Damage ◽  
Msc Differentiation

Hyaluronic acid (HA) is an essential component of the extracellular matrix (ECM) of the healthy lung, playing an important role in the structure of the alveolar surface stabilizing the surfactant proteins. Alveolar type II (ATII) cells are the fundamental element of the alveolus, specializing in surfactant production. ATII cells represent the main target of lung external lesion and a cornerstone in the repair process of pulmonary damage. In this context, knowledge of the factors influencing mesenchymal stem cell (MSC) differentiation in ATII cells is pivotal in fulfilling therapeutic strategies based on MSCs in lung regenerative medicine. To achieve this goal, the role of HA in promoting the differentiation of MSCs in mature Type II pneumocytes capable of secreting pulmonary surfactant was evaluated. Results demonstrated that HA, at a specific molecular weight can greatly increase the expression of lung surfactant protein, indicating the ability of HA to influence MSC differentiation in ATII cells.

scholarly journals MicroRNA-22 enhances the differentiation of mouse induced pluripotent stem cells into alveolar epithelial type II cells

2020 ◽  
Vol 64 (s2) ◽  
Author(s):  
Fan Tao ◽  
Feng Wang ◽  
Weichen Zhang ◽  
Yaming Hao
Keyword(s):  
Stem Cells ◽  
Induced Pluripotent Stem Cells ◽  
Pluripotent Stem Cells ◽  
Lung Surfactant ◽  
Lung Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Cellular Processes ◽  
Cell Based Therapy ◽  
Induced Pluripotent

Considerable evidence has verified that microRNAs (miRNAs) play important roles in various cellular processes including differentiation. However, the regulatory roles of miRNAs involved in the differentiation of induced pluripotent stem cells (iPSC) into lung epithelial cells are still unknown. In this study, we first evaluated the current protocols to differentiate iPSC into alveolar epithelial type II (AEC II) cells, but the efficiency is low. We next identified that miR-22 can efficiently enhance the differentiation of iPSC into AEC II cells under the stimulation of proper growth factors and growing on appropriate matrix. Moreover, the AEC II cells generated from iPSC with miR-22 overexpression can proliferate and secrete lung surfactant. Here, we discovered a previously unknown interaction between miR-22 and iPSC differentiation but also provide a potential target for the effective derivation of AEC II from iPSCs for cell-based therapy.

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