Ignet

Gene Information

Gene symbol: SFTPB

Gene name: surfactant protein B

HGNC ID: 10801

Synonyms: SP-B

Related Genes

#	Gene Symbol	Number of hits
1	INS	1 hits
2	PRPH2	1 hits
3	SFTPA1	1 hits
4	SFTPA2B	1 hits
5	SFTPC	1 hits

Related Sentences

#	PMID	Sentence
1	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
2	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
3	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
4	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
5	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
6	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
7	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
8	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
9	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
10	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
11	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
12	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
13	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
14	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
15	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
16	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
17	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
18	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
19	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
20	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
21	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
22	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
23	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
24	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
25	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
26	1639013	We have previously shown that insulin inhibits the accumulation of surfactant-associated protein A (SP-A), the major surfactant-associated protein, in human fetal lung explants maintained in vitro.
27	1639013	In the present study, we used Northern blot analysis to evaluate the effects of insulin on the content of SP-A messenger RNA (mRNA) as well as on the content of mRNA for the hydrophobic surfactant-associated proteins SP-B and SP-C in human fetal lung explants maintained in vitro.
28	1639013	We observed that insulin, at concentrations of 25-2500 ng/ml, significantly inhibited the accumulation of SP-A mRNA when compared to controls (P less than 0.01).
29	1639013	The inhibitory effect of insulin on SP-A mRNA accumulation was dose dependent with an approximately 75% inhibition observed at 2500 ng/ml.
30	1639013	Insulin, at the concentration of 2500 ng/ml, significantly inhibited the accumulation of SP-B mRNA by approximately 30% when compared to control levels (P less than 0.01) but had no effect at lower concentrations.
31	1639013	Insulin had no significant effect on SP-C mRNA levels at any concentration tested.
32	1639013	Our findings provide evidence that insulin may delay fetal lung development by inhibiting SP-A and SP-B gene expression.
33	1639013	We have previously shown that insulin inhibits the accumulation of surfactant-associated protein A (SP-A), the major surfactant-associated protein, in human fetal lung explants maintained in vitro.
34	1639013	In the present study, we used Northern blot analysis to evaluate the effects of insulin on the content of SP-A messenger RNA (mRNA) as well as on the content of mRNA for the hydrophobic surfactant-associated proteins SP-B and SP-C in human fetal lung explants maintained in vitro.
35	1639013	We observed that insulin, at concentrations of 25-2500 ng/ml, significantly inhibited the accumulation of SP-A mRNA when compared to controls (P less than 0.01).
36	1639013	The inhibitory effect of insulin on SP-A mRNA accumulation was dose dependent with an approximately 75% inhibition observed at 2500 ng/ml.
37	1639013	Insulin, at the concentration of 2500 ng/ml, significantly inhibited the accumulation of SP-B mRNA by approximately 30% when compared to control levels (P less than 0.01) but had no effect at lower concentrations.
38	1639013	Insulin had no significant effect on SP-C mRNA levels at any concentration tested.
39	1639013	Our findings provide evidence that insulin may delay fetal lung development by inhibiting SP-A and SP-B gene expression.
40	1639013	We have previously shown that insulin inhibits the accumulation of surfactant-associated protein A (SP-A), the major surfactant-associated protein, in human fetal lung explants maintained in vitro.
41	1639013	In the present study, we used Northern blot analysis to evaluate the effects of insulin on the content of SP-A messenger RNA (mRNA) as well as on the content of mRNA for the hydrophobic surfactant-associated proteins SP-B and SP-C in human fetal lung explants maintained in vitro.
42	1639013	We observed that insulin, at concentrations of 25-2500 ng/ml, significantly inhibited the accumulation of SP-A mRNA when compared to controls (P less than 0.01).
43	1639013	The inhibitory effect of insulin on SP-A mRNA accumulation was dose dependent with an approximately 75% inhibition observed at 2500 ng/ml.
44	1639013	Insulin, at the concentration of 2500 ng/ml, significantly inhibited the accumulation of SP-B mRNA by approximately 30% when compared to control levels (P less than 0.01) but had no effect at lower concentrations.
45	1639013	Insulin had no significant effect on SP-C mRNA levels at any concentration tested.
46	1639013	Our findings provide evidence that insulin may delay fetal lung development by inhibiting SP-A and SP-B gene expression.
47	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
48	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
49	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
50	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
51	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
52	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
53	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
54	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
55	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
56	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
57	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
58	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
59	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
60	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
61	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
62	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
63	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
64	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
65	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
66	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
67	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
68	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
69	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
70	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
71	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
72	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
73	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
74	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
75	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
76	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
77	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
78	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
79	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
80	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
81	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
82	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
83	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
84	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
85	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
86	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
87	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
88	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
89	1805157	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.
90	1805157	Amniotic fluid SP-A, SP-B, and L/S increased with advancing gestation.
91	1805157	SP-A was a more specific predictor of nonrespiratory distress syndrome (RDS) than L/S or SP-B; however, the sensitivity of SP-A in predicting RDS was less than L/S less than 2.0 (26.3 versus 82.3%, respectively).
92	1805157	In 209 pregnancies assessed within 48 h of delivery, the sensitivity of SP-B in predicting RDS (nondetectable SP-B) was comparable to the L/S, however, SP-B = 0 was frequently observed in mature infants, limiting its specificity for prediction of RDS.
93	1805157	Measurement of SP-A or SP-B did not improve the prediction of RDS.
94	1805157	SP-A, SP-B, and L/S were not affected by infant sex, Apgar score, rupture of membranes, size for gestational age, maternal diabetes, hypertension, or exposure to medications.
95	1805157	SP-A, SP-B, and L/S were significantly elevated in amniotic fluid from black mothers.
96	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
97	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
98	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
99	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
100	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
101	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
102	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
103	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
104	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
105	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
106	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
107	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
108	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
109	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
110	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
111	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
112	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
113	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
114	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
115	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
116	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
117	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
118	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
119	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
120	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
121	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
122	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
123	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
124	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
125	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
126	8048547	Exposure of explants of 18-day fetal rat lung to Na butyrate resulted in a decrease in surfactant protein A (SP-A) mRNA concentration to 7% of control after 6 h and to 18% of control after 24 h.
127	8048547	The effects on SP-B mRNA were similar to those on SP-A, but quantitatively less.
128	8618787	The mRNA levels of SP (SP-A, SP-B, SP-C) were assessed in d 18 and 20 fetuses by Northern blot analysis, and nuclear run-on assays were performed with lung nuclei from d 20 fetuses (term = 22 d).
129	8618787	Our findings indicate: 1) dex causes a greater increase in SP-A and SP-B mRNA levels in d 18 (12-16-fold) compared with day 20 (4-6-fold) fetuses (p < 0.05) in normal and STZ-DB pregnancy; 2) a 2-3-fold increase in SP-C mRNA levels was observed in response to dex in d 18 and 20 fetuses; 3) the increase in transcription of SP-A and SP-B in d 20 fetuses after dex is 68 and 60%, respectively, of the increase in their mRNA levels whereas in STZ-DB, the decrease in transcription compared with mRNA levels is 3.67-fold for SP-A and 2.42 fold SP-B; and 4) changes in SP-C transcription in either in vivo model, dex-treated or STZ-DB, correspond well with changes in mRNA levels.
130	8618787	The mRNA levels of SP (SP-A, SP-B, SP-C) were assessed in d 18 and 20 fetuses by Northern blot analysis, and nuclear run-on assays were performed with lung nuclei from d 20 fetuses (term = 22 d).
131	8618787	Our findings indicate: 1) dex causes a greater increase in SP-A and SP-B mRNA levels in d 18 (12-16-fold) compared with day 20 (4-6-fold) fetuses (p < 0.05) in normal and STZ-DB pregnancy; 2) a 2-3-fold increase in SP-C mRNA levels was observed in response to dex in d 18 and 20 fetuses; 3) the increase in transcription of SP-A and SP-B in d 20 fetuses after dex is 68 and 60%, respectively, of the increase in their mRNA levels whereas in STZ-DB, the decrease in transcription compared with mRNA levels is 3.67-fold for SP-A and 2.42 fold SP-B; and 4) changes in SP-C transcription in either in vivo model, dex-treated or STZ-DB, correspond well with changes in mRNA levels.
132	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
133	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
134	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
135	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
136	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
137	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
138	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
139	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
140	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
141	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
142	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
143	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
144	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
145	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
146	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
147	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
148	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
149	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
150	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
151	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
152	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
153	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
154	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
155	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
156	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
157	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
158	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
159	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
160	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
161	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
162	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
163	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
164	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
165	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
166	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
167	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
168	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
169	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
170	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
171	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
172	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
173	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
174	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
175	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
176	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
177	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
178	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
179	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
180	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
181	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
182	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
183	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
184	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
185	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
186	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
187	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
188	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
189	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
190	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
191	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
192	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
193	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
194	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
195	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
196	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
197	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
198	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
199	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
200	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
201	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
202	10027080	SP mRNA content (SP-A, SP-B, SP-C) was assessed by Northern blot analysis in fetal day 20 lung explants (term = 22 days) cultured for 44 hours in medium containing 10, 25, 50, or 100 mM glucose.
203	10027080	Our findings were (1) No consistent alteration in SP-A mRNA content was observed at different glucose concentrations (P > .05); (2) SP-B and SP-C mRNA content were reduced in a dose-dependent manner when glucose concentration was increased from 10 mM to 100 mM.
204	10027080	These findings indicate that the decrease in SP-B and SP-C mRNA in fetuses of STZ-DB rats may be, in part, due to a direct effect of hyperglycemia, whereas the decrease in SP-A mRNA content in STZ-DB rats appears to be due to other effects of diabetes in pregnancy.
205	10027080	SP mRNA content (SP-A, SP-B, SP-C) was assessed by Northern blot analysis in fetal day 20 lung explants (term = 22 days) cultured for 44 hours in medium containing 10, 25, 50, or 100 mM glucose.
206	10027080	Our findings were (1) No consistent alteration in SP-A mRNA content was observed at different glucose concentrations (P > .05); (2) SP-B and SP-C mRNA content were reduced in a dose-dependent manner when glucose concentration was increased from 10 mM to 100 mM.
207	10027080	These findings indicate that the decrease in SP-B and SP-C mRNA in fetuses of STZ-DB rats may be, in part, due to a direct effect of hyperglycemia, whereas the decrease in SP-A mRNA content in STZ-DB rats appears to be due to other effects of diabetes in pregnancy.
208	10027080	SP mRNA content (SP-A, SP-B, SP-C) was assessed by Northern blot analysis in fetal day 20 lung explants (term = 22 days) cultured for 44 hours in medium containing 10, 25, 50, or 100 mM glucose.
209	10027080	Our findings were (1) No consistent alteration in SP-A mRNA content was observed at different glucose concentrations (P > .05); (2) SP-B and SP-C mRNA content were reduced in a dose-dependent manner when glucose concentration was increased from 10 mM to 100 mM.
210	10027080	These findings indicate that the decrease in SP-B and SP-C mRNA in fetuses of STZ-DB rats may be, in part, due to a direct effect of hyperglycemia, whereas the decrease in SP-A mRNA content in STZ-DB rats appears to be due to other effects of diabetes in pregnancy.