Disease relevance of Sftpc

• CONCLUSION: In this acute lung injury model, the effects of replacement therapy with surfactant consisting of synthetic phospholipids, SP-B and SP-C, were the same as those observed with MNS [1].
• The effects of the surfactant proteins (SP)-A, SP-B, and SP-C on binding and endocytosis of fluorescently labeled lipid vesicles were studied in rat type II epithelial cells and in MLE-12 cells, a pulmonary adenocarcinoma cell line with alveolar cell characteristics [2].

High impact information on Sftpc

• In a perfused rat lung model labeled with [35S]cysteine/methionine, immunoprecipitation of lung homogenate and lamellar body fractions identified early appearances of 35S-labeled 21-, 18-, and 16-kDa SP-C forms in homogenate and a 16-kDa intermediate form in lamellar bodies [3].
• Furthermore, the data imply that the difference between plain PL surfactant preparations and bovine-derived surfactant preparations containing both SP-B and SP-C can be overcome by addition of SP-C [4].
• We have tested two surfactant preparations with the same phospholipid (PL) composition, containing recombinant surfactant protein-C (rSP-C surfactant) and without SP-C (plain PL surfactant) [4].
• Continuous contraction of culture membrane surface area by 25% for a duration of 4 h resulted in an 83% increase in SP-A, a 42% increase in SP-B, and a 230% increase in SP-C, in comparison with controls [5].
• By contrast, SP-C and SP-D mRNAs were maximally increased relative to values in simultaneously air-exposed control rats after 4 d of exposure [6].

Biological context of Sftpc

• Although the lipid and hydrophobic protein components of surfactant are believed to be secreted together by exocytosis of lamellar body contents, regulation of surfactant protein (SP) B and SP-C secretion has not previously been examined [7].
• 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) [8].
• In contrast, mechanical distention resulted in a decrease in mRNA content of two markers of the type II cell phenotype, surfactant protein (SP)-B and SP-C [9].
• We conclude that respiratory distress after bleomycin in rats results from surfactant dysfunction in part secondary to selective downregulation of SP-B and SP-C [10].
• Incorporation of SP-C in lipid vesicles markedly stimulated binding to the cell membrane at 4 degrees C and endocytosis of lipids at 37 degrees C. SP-C enhanced lipid uptake in MLE-12 cells, type II cells, and NIH 3T3 cells [2].

Anatomical context of Sftpc

• Moreover, the number of silver grains representing SP-C mRNA decreased in alveolar type II cells from diabetic lungs compared with controls, and no silver grains for SP-C mRNA were present in bronchiolar epithelial cells from either control or diabetic groups [11].
• Type II cells that were co-cultured with lung fibroblasts showed significant increases in messenger RNA (mRNA) levels of surfactant protein (SP)-A, SP-B, SP-C, and SP-D [12].
• The abundance of mRNAs for SP-B and SP-C also increased in day-17 fetuses after either 1 or 3 d of DEX treatment.(ABSTRACT TRUNCATED AT 250 WORDS)[13]
• Type II cells cultured on EHS matrix in D-GM had a decreased abundance of mRNAs for SP-A and SP-C than cells cultured on EHS matrix in D-5 as determined by Northern analysis [14].
• Disruption of either microfilaments or microtubules significantly affected the half-lives of mRNAs for SP-A, SP-B, and SP-C [15].

Associations of Sftpc with chemical compounds

• To address the question of whether secretion of SP-B and SP-C is stimulated by the same agonists that stimulate phospholipid secretion, we measured secretion of all four SPs under the same conditions used to measure phosphatidylcholine secretion [7].
• Secretion of SP-B and SP-C was stimulated three- to fivefold by terbutaline, 5'-(N-ethylcarboxyamido)adenosine, ATP, 12-O-tetradecanoylphorbol 13-acetate, and ionomycin [7].
• Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats [8].
• Effects of maternal dexamethasone on expression of SP-A, SP-B, and SP-C in the fetal rat lung [13].
• In addition, the stretch- and glucocorticoid-induced alterations in tropoelastin and SP-C mRNA expression were abrogated with 10 microg/ml actinomycin D [16].

Regulatory relationships of Sftpc

• SP-A significantly enhanced the association of SP-C with isolated type II cells [17].
• The entactin mRNA throughout the alveolar walls of neonatal animals was not limited to cells that expressed surfactant-associated protein C mRNA, a marker of alveolar type II cells [18].

Other interactions of Sftpc

• Regulation of SP-B and SP-C secretion in rat type II cells in primary culture [7].
• Peak levels were observed in adult lungs for SP-A, SP-C and CC10 [19].
• Tropoelastin and collagen type I were used as marker genes for fibroblasts, whereas surfactant protein (SP) A and SP-C were used as marker genes for distal epithelial cells [16].

Analytical, diagnostic and therapeutic context of Sftpc

• The abundance of mRNAs for SP-A, SP-B, and SP-C per fixed amount of total cellular RNA was also determined in lungs from treated and control male and female fetal rats by Northern blot analysis [13].
• We used in situ hybridization to identify sites of message expression of the surfactant-associated proteins A, B, and C (SP-A, SP-B, and SP-C) in adult and fetal rat lung [20].
• Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age [8].
• 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].
• The expression of the messages for SP-A, SP-B, and SP-C was assessed by the reverse-transcriptase polymerase chain reaction (RT-PCR) [21].

References