Journal articles: 'Surfactant-Protein System'

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Mason, Robert J., Kelly Greene, and Dennis R. Voelker. "Surfactant protein A and surfactant protein D in health and disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 1 (July 1, 1998): L1—L13. http://dx.doi.org/10.1152/ajplung.1998.275.1.l1.

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Surfactant protein (SP) A and SP-D are collagenous glycoproteins with multiple functions in the lung. Both of these proteins are calcium-dependent lectins and are structurally similar to mannose-binding protein and bovine conglutinin. Both form polyvalent multimeric structures for interactions with pathogens, cells, or other molecules. SP-A is an integral part of the surfactant system, binds phospholipids avidly, and is found in lamellar bodies and tubular myelin. Initially, most research interest focused on its role in surfactant homeostasis. Recently, more attention has been placed on the role of SP-A as a host defense molecule and its interactions with pathogens and phagocytic cells. SP-D is much less involved with the surfactant system. SP-D appears to be primarily a host defense molecule that binds surfactant phospholipids poorly and is not found in lamellar inclusion bodies or tubular myelin. Both SP-A and SP-D bind a wide spectrum of pathogens including viruses, bacteria, fungi, and pneumocystis. In addition, both molecules have been measured in the systemic circulation by immunologic methods and may be useful biomarkers of disease. The current challenges are characterization of the three-dimensional crystal structure of SP-A and SP-D, molecular cloning of their receptors, and determination of their precise physiological functions in vivo.

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TADENUMA, Hirohiko, Ken YAMADA, and Takamitsu TAMURA. "Analysis of Protein-Mixed Surfactant System Interactions ;." Journal of Japan Oil Chemists' Society 48, no. 3 (1999): 207–13. http://dx.doi.org/10.5650/jos1996.48.207.

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Cañadas, Olga, Bárbara Olmeda, Alejandro Alonso, and Jesús Pérez-Gil. "Lipid–Protein and Protein–Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis." International Journal of Molecular Sciences 21, no. 10 (May 25, 2020): 3708. http://dx.doi.org/10.3390/ijms21103708.

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Pulmonary surfactant is a lipid/protein complex synthesized by the alveolar epithelium and secreted into the airspaces, where it coats and protects the large respiratory air–liquid interface. Surfactant, assembled as a complex network of membranous structures, integrates elements in charge of reducing surface tension to a minimum along the breathing cycle, thus maintaining a large surface open to gas exchange and also protecting the lung and the body from the entrance of a myriad of potentially pathogenic entities. Different molecules in the surfactant establish a multivalent crosstalk with the epithelium, the immune system and the lung microbiota, constituting a crucial platform to sustain homeostasis, under health and disease. This review summarizes some of the most important molecules and interactions within lung surfactant and how multiple lipid–protein and protein–protein interactions contribute to the proper maintenance of an operative respiratory surface.

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Tan, Ya-Xin, Shu-Jun Li, Hai-Tao Li, Xiao-Juan Yin, Bo Cheng, Jing-Li Guo, Na Li, Cheng-Zhong Zheng, and Hong-Yu Chang. "Role of surfactant protein C in neonatal genetic disorders of the surfactant system." Medicine 100, no. 50 (December 17, 2021): e28201. http://dx.doi.org/10.1097/md.0000000000028201.

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Ovsyannikov, D. Yu, M. A. Zhestkova, V. A. Strelnikova, A. P. Averin, M. A. Atipaeva, O. Yu Brunova, G. V. Buyanova, et al. "Genetic Dysfunctions of the Surfactant System in Children: Results of a Multicenter Study." Doctor.Ru 22, no. 3 (2023): 22–31. http://dx.doi.org/10.31550/1727-2378-2023-22-3-22-31.

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Aim: Genetic, clinical, laboratory-instrumental and morphological characteristics of genetic dysfunctions of the surfactant system in children, therapy and outcomes of the disease. Design: Multicentre, ambispective, open-label, descriptive pilot longitudinal study. Materials and methods. We observed 17 children from 16 families with identified mutations in the SFTPC, ABCA3, NKX2-1 genes. Methods used: genealogical, Sanger sequencing, clinical exome sequencing, computed tomography and histological examination of the lungs. Results. The study included 8 children with congenital deficiency of surfactant protein C, 8 children with brain-lung-thyroid syndrome and 1 patient with congenital deficiency of protein ABSA3. Based on the results of a genetic examination of patients, nucleotide variants c.218T>C were identified in 2 out of 8 patients with a mutation in the SFTPC gene, which is the most common according to the literature. In 5 children, the mutations were hereditary. Congenital deficiency of surfactant protein C, ABCA3 protein and brain-lung-thyroid syndrome were characterized by clinical, computed tomography, and morphological signs of interstitial lung disease. Despite complex respiratory, anti-inflammatory therapy, the frequency of deaths in congenital deficiency of surfactant protein C was 37.5%. Conclusion. Children with severe respiratory distress syndrome of newborns, interstitial lung disease with the development of severe chronic respiratory failure, burdened with a family history should undergo genetic testing to detect mutations in the genes SFTPB, SFTPC, ABCA3. The patient's combination of respiratory symptoms with congenital hypothyroidism and neurological pathology is the basis for genetic examination for NKX2-1 gene mutations to exclude the brain-lung-thyroid syndrome. Keywords: genetic dysfunctions of the surfactant system, congenital deficiency of surfactant protein C, congenital deficiency of ABCA3 protein, brain-lung-thyroid syndrome, NKX2-1 gene, children.

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Moreira, Leonardo Marmo, and Juliana Pereira Lyon. "Interaction between surfactants and proteins." Pubvet 16, no. 5 (May 2022): 1–8. http://dx.doi.org/10.31533/pubvet.v16n05a1115.1-8.

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Several approaches have been focused on the protein-surfactant interaction. Surfactant-protein interactions are very common in the fields of medicine, chemistry, biology etc. Indeed, many aspects of this interaction have been studied, such as the influence of the aggregation state of the surfactant (monomer, pre-micellar aggregate, micelle, and liposomes) on the protein structure, the properties of the surfactant-protein system, the characterization of the interaction sites on the protein surface, the identification of the intermediate protein conformations etc. The interaction of several types of proteins with the different kind of surfactant can furnish various information to the research of biochemical and biophysical systems, such as the structure-activity relationship of proteins as well as the mechanism of interaction between proteins and amphiphilic molecules. In this context, proteins with prosthetic group are very interesting ones, since the presence of the non-amino acid group can furnishes various information through different instrumental techniques of analysis, acting as a label of all polypeptide chains. The present work analyzes this topic and the potential of these studies.

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Kim, Hugh I., Hyungjun Kim, Young Shik Shin, Luther W. Beegle, Seung Soon Jang, Evan L. Neidholdt, William A. Goddard, James R. Heath, Isik Kanik, and J. L. Beauchamp. "Interfacial Reactions of Ozone with Surfactant Protein B in a Model Lung Surfactant System." Journal of the American Chemical Society 132, no. 7 (February 24, 2010): 2254–63. http://dx.doi.org/10.1021/ja908477w.

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Matalon, S., V. DeMarco, I. Y. Haddad, C. Myles, J. W. Skimming, S. Schurch, S. Cheng, and S. Cassin. "Inhaled nitric oxide injures the pulmonary surfactant system of lambs in vivo." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 2 (February 1, 1996): L273—L280. http://dx.doi.org/10.1152/ajplung.1996.270.2.l273.

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Nitric oxide (.NO) is a free radical, and as such may damage the pulmonary surfactant system. To determine the potential toxicity of .NO in vivo, we exposed 35 newborn lambs to 0, 20, 80 or 200 ppm .NO in either 21 or 60% O2 for 6 h. At the end of the exposure, lambs had normal values of arterial Po2, Pco2, and pH; total protein concentration in the bronchoalveolar lavage was also at normal levels. There were no differences in the surface properties of surfactant among the air or 60% O2 groups. Pulmonary surfactant samples, isolated from the bronchoalveolar lavage of lambs breathing air or 20 ppm .NO and reconstituted at a lipid concentration of 3 mg/ml, reached a low minimum surface tension (Tmin < 3 mN/m) in a pulsating bubble surfactometer. On the other hand, abnormal surface properties were observed in 36 and 60% of surfactant samples isolated from lungs of lambs that breathed 80 or 200 ppm .NO, respectively. These findings were confirmed using a captive bubble surfactometer. Surfactant protein A, isolated from the lungs of lambs that breathed 200 ppm .NO, exhibited decreased ability to aggregate lipids in vitro. These data are consistent with injury to the surfactant apoproteins during inhalation of either 80 or 200 ppm .NO for 6 h.

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Rodriguez-Capote, Karina, Kaushik Nag, Samuel Schürch, and Fred Possmayer. "Surfactant protein interactions with neutral and acidic phospholipid films." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 1 (July 1, 2001): L231—L242. http://dx.doi.org/10.1152/ajplung.2001.281.1.l231.

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The captive bubble tensiometer was employed to study interactions of phospholipid (PL) mixtures of dipalmitoylphosphatidylcholine (DPPC) and 1-palmitoyl-2-oleoyl- sn-glycero-3-phosphocholine (POPC) or 1-palmitoyl-2-oleoyl- sn-glycero-3-[phospho- rac-(1-glycerol)] (POPG) at 50 μg/ml with physiological levels of the surfactant protein (SP) A SP-B, and SP-C alone and in combination at 37°C. All surfactant proteins enhanced lipid adsorption to equilibrium surface tension (γ), with SP-C being most effective. Kinetics were consistent with the presence of two adsorption phases. Under the conditions employed, SP-A did not affect the rate of film formation in the presence of SP-B or SP-C. Little difference in γmin was observed between the acidic POPG and the neutral POPC systems with SP-B or SP-C with and without SP-A. However, γmax was lower with the acidic POPG system during dynamic, but not during quasi-static, cycling. Considerably lower compression ratios were required to generate low γminvalues with SP-B than SP-C. DPPC-POPG-SP-B was superior to the neutral POPC-SP-B system. Although SP-A had little effect on film formation with SP-B, surface activity during compression was enhanced with both PL systems. In the presence of SP-C, lower compression ratios were required with the acidic system, and with this mixture, SP-A addition adversely affected surface activity. The results suggest specific interactions between SP-B and phosphatidylglycerol, and between SP-B and SP-A. These observations are consistent with the presence of a surface-associated surfactant reservoir which is involved in generating low γ during film compression and lipid respreading during film expansion.

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Willems, Coen H. M. P., Luc J. I. Zimmermann, Renate M. R. Langen, Maria J. A. van den Bosch, Nico Kloosterboer, Boris W. Kramer, and J. Freek van Iwaarden. "Surfactant Protein A Influences Reepithelialization in an Alveolocapillary Model System." Lung 190, no. 6 (October 13, 2012): 661–69. http://dx.doi.org/10.1007/s00408-012-9424-6.

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11

Li, F., E. Rosenberg, C. I. Smith, K. Notarfrancesco, S. R. Reisher, H. Shuman, and S. I. Feinstein. "Correlation of expression of transcription factor C/EBP alpha and surfactant protein genes in lung cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 2 (August 1, 1995): L241—L247. http://dx.doi.org/10.1152/ajplung.1995.269.2.l241.

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C/EBP alpha is a transcription factor which can stimulate expression of genes in lipid-metabolizing epithelial cells. We have detected an increase in mRNA for C/EBP alpha in lungs of fetal rats between days 18 and 20 of gestation, correlating with events occurring during the maturation of the surfactant system, such as an increase in the amount of surfactant protein A mRNA. We have found that C/EBP alpha mRNA levels are substantially enriched in type II alveolar epithelial cells purified from adult lung and that the C/EBP alpha protein is present in type II cell nuclei. When the type II cells are removed from the lung and purified, the protein is rapidly lost. However, both surfactant protein gene expression and C/EBP alpha reappear when cells are plated on Matrigel. Levels of C/EBP alpha mRNA from purified cells decline much more slowly than the protein and are still detectable 48 h after cells have been plated on standard tissue culture plastic. We have also detected the C/EBP alpha protein in nuclear extracts of NCI-H441, a lung-derived cell line that expresses surfactant proteins A and B, but not in A549, a lung-derived cell line which does not express the surfactant proteins. Our data suggest that C/EBP alpha is involved in the development and maintenance of the surfactant system in lung type II cells.

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Maikokera, Raymond, and Habauka M. Kwaambwa. "Use of Viscosity to Probe the Interaction of Anionic Surfactants with a Coagulant Protein from Moringa oleifera Seeds." Research Letters in Physical Chemistry 2009 (May 24, 2009): 1–5. http://dx.doi.org/10.1155/2009/927329.

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The intrinsic viscosity of the coagulant protein was evaluated from the flow times of the protein solutions through a capillary viscometer, and the results suggested the coagulant protein to be globular. The interactions of the coagulant protein with anionic surfactant sodium dodecyl sulphate (SDS) and sodium dodecyl benzene sulfonate (SDBS) were also investigated by capillary viscometry. We conclude that there is strong protein-surfactant interaction at very low surfactant concentrations, and the behavior of the anionic surfactants in solutions containing coagulant protein is very similar. The viscometry results of protein-SDS system are compared with surface tension, fluorescence, and circular dichroism reported earlier. Combining the results of the four studies, the four approaches seem to confirm the same picture of the coagulant protein-SDS interaction. All the physical quantities when studied as function of surfactant concentration for 0.05% (w/v) protein solution either exhibited a maximum or minimum at a critical SDS concentration.

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Hawgood, S. "Pulmonary surfactant apoproteins: a review of protein and genomic structure." American Journal of Physiology-Lung Cellular and Molecular Physiology 257, no. 2 (August 1, 1989): L13—L22. http://dx.doi.org/10.1152/ajplung.1989.257.2.l13.

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In recent years, as the complexity of the surfactant system has become more apparent, investigators with an increasingly diverse set of skills have been attracted to the study of this secretory product of the alveolar epithelium. In addition to advancing our knowledge of the mechanisms underlying the mechanical stability of the lung, recent studies of the surfactant system have also contributed information to less organ-specific biological phenomena such as exocytosis, endocytosis, cell differentiation and lipid-protein interactions in biomembranes. Pulmonary surfactant is not composed of a single class of molecules but, rather, is a collection of interrelated macromolecular lipoprotein complexes that differ in composition, structure, and function. The purpose of this review is to describe the structure of the lung-specific proteins that are associated with the phospholipids of surfactant in the alveolar space. The organization of the genes for the surfactant proteins is outlined and the affects of these proteins on the properties of phospholipid membranes are discussed.

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Peca, Donatella, Renato Cutrera, Andrea Masotti, Renata Boldrini, and Olivier Danhaive. "ABCA3, a key player in neonatal respiratory transition and genetic disorders of the surfactant system." Biochemical Society Transactions 43, no. 5 (October 1, 2015): 913–19. http://dx.doi.org/10.1042/bst20150100.

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Genetic disorders of the surfactant system are rare diseases with a broad range of clinical manifestations, from fatal respiratory distress syndrome (RDS) in neonates to chronic interstitial lung disease (ILD) in children and adults. ABCA3 [ATP-binding cassette (ABC), subfamily A, member 3] is a lung-specific phospholipid transporter critical for intracellular surfactant synthesis and storage in lamellar bodies (LBs). Its expression is developmentally regulated, peaking prior to birth under the influence of steroids and transcription factors. Bi-allelic mutations of the ABCA3 gene represent the most frequent cause of congenital surfactant deficiency, indicating its critical role in lung function. Mutations affect surfactant lipid and protein processing and LBs’ morphology, leading to partial or total surfactant deficiency. Approximately 200 mutations have been reported, most of which are unique to individuals and families, which makes diagnosis and prognosis challenging. Various types of mutations, affecting different domains of the protein, account in part for phenotype diversity. Disease-causing mutations have been reported in most coding and some non-coding regions of the gene, but tend to cluster in the first extracellular loop and the second nucleotide-binding domain (NBD), leading to defective glycosylation and trafficking defects and interfering with ATP binding and hydrolysis respectively. Mono-allelic damaging and benign variants are often subclinical but may act as disease modifiers in lung diseases such as RDS of prematurity or associate with mutations in other surfactant-related genes. Diagnosis is complex but essential and should combine pathology and ultrastructure studies on lung biopsy with broad-spectrum genetic testing of surfactant-related genes, made possible by recent technology advances in the massive parallel sequencing technology.

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Harris, J. D., F. Jackson, M. A. Moxley, and W. J. Longmore. "Effect of exogenous surfactant instillation on experimental acute lung injury." Journal of Applied Physiology 66, no. 4 (April 1, 1989): 1846–51. http://dx.doi.org/10.1152/jappl.1989.66.4.1846.

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Pulmonary surfactant replacement has previously been shown to be effective in the human neonatal respiratory distress syndrome. The value of surfactant replacement in models of acute lung injury other than quantitative surfactant deficiency states is, however, uncertain. In this study an acute lung injury model using rats with chronic indwelling arterial catheters, injured with N-nitroso-N-methylurethane (NNNMU), has been developed. The NNNMU injury was found to produce hypoxia, increased mortality, an alveolitis, and alterations in the pulmonary surfactant system. Alterations of surfactant obtained by bronchoalveolar lavage included a reduction in the phospholipid-to-protein ratio, reduced surface activity, and alterations in the relative percentages of the individual phospholipids compared with controls. Treatment of the NNNMU-injured rats with instilled exogenous surfactant (Survanta) improved oxygenation; reduced mortality to control values; and returned the surfactant phospholipid-to-protein ratio, surface activity, and, with the exception of phosphatidylglycerol, the relative percentages of individual surfactant phospholipids to control values.

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Golubinskaya, E. P., T. G. Filonenko, Y. A. Ermola, A. V. Kubishkin, M. A. Kalfa, T. V. Kramar, and A. V. Geraschenko. "Immunohistochemical evaluation of surfactant-associated protein in fibrosis-cavernous pulmonary tuberculosis." Innovative medicine of Kuban, no. 4 (December 28, 2019): 32–39. http://dx.doi.org/10.35401/2500-0268-2019-16-4-32-39.

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Background. Despite the progress and development of scientific directions in various fields of medicine, the problem of tuberculosis and its morphological manifestations remains relevant and is not fully disclosed due to complex pathogenesis, the presence of various clinical forms, therapeutic pathomorphosis, torpid to therapy, the presence of relapses. It is known that a surfactant system occupies a special place in the system of local lung protection.Aim. To study the condition of surfactant-assotiated protein A in the foci of specific destruction and in the surrounding intact lung tissue to assess its functional status, degree of respiratory failure and possible dissemination of tuberculous inflammation.Material and Metods. An analysis of 163 lung fragments of the dead or operated on for cavernous pulmonary tuberculosis with active bacterial excretion of 89 fragments and with clinical abacilation – 74 was carried out. Results A morphological study revealed stereotypical dynamic depression of surfactant-associated protein A in all the samples studied, both in the areas of cavernous destruction and pericavernouse zone, and in intact lung tissue. The maximum intensivity of the immunohistochemical expression of this surfactant protein was recorded in the alveolar macrophages, which indicated intensive recycling and utilization of the components of the surfactant.Conclusion. Minimizing the production of surfactant components and its active utilization in intact lung tissue leads to a collapse of the alveoli with subsequent progression of respiratory failure.

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Turro, Nicholas J., Xue-Gong Lei, K. P. Ananthapadmanabhan, and M. Aronson. "Spectroscopic Probe Analysis of Protein-Surfactant Interactions: The BSA/SDS System." Langmuir 11, no. 7 (July 1995): 2525–33. http://dx.doi.org/10.1021/la00007a035.

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Stenstam, Anna, Ali Khan, and Håkan Wennerström. "The Lysozyme−Dodecyl Sulfate System. An Example of Protein−Surfactant Aggregation." Langmuir 17, no. 24 (November 2001): 7513–20. http://dx.doi.org/10.1021/la011096t.

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Serrano, Alicia G., and Jesús Pérez-Gil. "Protein–lipid interactions and surface activity in the pulmonary surfactant system." Chemistry and Physics of Lipids 141, no. 1-2 (June 2006): 105–18. http://dx.doi.org/10.1016/j.chemphyslip.2006.02.017.

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Johnston, Sonya D., Christopher B. Daniels, David Cenzato, Jeffrey A. Whitsett, and Sandra Orgeig. "The pulmonary surfactant system matures upon pipping in the freshwater turtle Chelydra serpentina." Journal of Experimental Biology 205, no. 3 (February 1, 2002): 415–25. http://dx.doi.org/10.1242/jeb.205.3.415.

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SUMMARY Pulmonary surfactant (PS), a mixture of phospholipids (PL), neutral lipids and surfactant proteins (SP), lowers surface tension within the lung, which increases lung compliance and improves the removal of fluid at birth. Here, we have examined the expression of thyroid transcription factor-1 (TTF-1) and the surfactant protein SP-B, and also the composition of pulmonary surfactant lipids in the developing lung of the turtle Chelydra serpentina. Lavage and lung tissue were collected from late embryonic, pipped and hatchling turtles. TTF-1, a regulator of gene expression of surfactant proteins and cell differentiation in mammals, was detected using immunohistochemistry in epithelia of the gas-exchange area and conducting airways during late development. Expression declined in hatchlings. SP-B was detected in subsets of cells within the respiratory epithelium at all stages sampled. The same cell types also stained for TTF-1. Turtle surfactant lipids matured toward the end of incubation. Maximal secretion of both total phospholipids and disaturated phospholipid (DSP) occurred at the time of pipping, coincident with the onset of breathing. The DSP/PL ratio increased after pipping, whereas cholesterol levels (Chol) increased prior to pipping. This resulted in a decrease in the Chol/PL and Chol/DSP ratios after pipping. Thus, TTF-1 and SP-B appear to be highly conserved within the vertebrates. Maturation of surfactant phospholipid content occurred with the commencement of pulmonary ventilation.

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Osanai, Kazuhiro, Junko Higuchi, Rieko Oikawa, Makoto Kobayashi, Katsuma Tsuchihara, Masaharu Iguchi, Jyongsu Huang, Dennis R. Voelker, and Hirohisa Toga. "Altered lung surfactant system in a Rab38-deficient rat model of Hermansky-Pudlak syndrome." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 2 (February 2010): L243—L251. http://dx.doi.org/10.1152/ajplung.00242.2009.

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Several Long-Evans rat substrains carrying the phenotype of oculocutaneous albinism and bleeding diathesis are a rat model of Hermansky-Pudlak syndrome (HPS). The mutation responsible for the phenotype ( Ruby) was identified as a point mutation in the initiation codon of Rab38 small GTPase that regulates intracellular vesicle transport. As patients with HPS often develop life-limiting interstitial pneumonia accompanied by abnormal morphology of alveolar type II cells, we investigated lung surfactant system in Long-Evans Cinnamon rats, one strain of the Ruby rats. The lungs showed conspicuous morphology of type II cells containing markedly enlarged lamellar bodies. Surfactant phosphatidylcholine and surfactant protein B were increased in lung tissues and lamellar bodies but not in alveolar lumen. Expression levels of mRNA for surfactant proteins A, B, C, and D were not altered. Isolated type II cells showed aberrant secretory pattern of newly synthesized [3H]phosphatidylcholine, i.e., decreased basal secretion and remarkably amplified agonist-induced secretion. [3H]phosphatidylcholine synthesis and uptake by type II cells were not altered. Thus Rab38-deficient type II cells appear to carry abnormality in lung surfactant secretion but not in synthesis or uptake. These results suggest that aberrant lung surfactant secretion may be involved in the pathogenesis of interstitial pneumonia in HPS.

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Thiruvenkataramani, Ranga Prasanth, Amal Abdul-Hafez, Ira Gewolb, and Bruce Uhal. "Mas Receptor Agonist AVE0991 increases surfactant protein expression under hyperoxic conditions in human lung epithelial cells." Journal of Lung, Pulmonary & Respiratory Research 7, no. 4 (November 17, 2020): 85–91. http://dx.doi.org/10.15406/jlprr.2020.07.00235.

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Background: Hyperoxia in pre-term neonates is a known risk factor of bronchopulmonary dysplasia (BPD). Hyperoxia is known to cause oxidative stress, inflammatory changes that leads to surfactant deactivation, and decreased surfactant expression. The previous research has shown short term exposure to hyperoxia increases surfactant protein expression but decreased expression in long term exposure. Local tissue renin-angiotensin system (RAS) is associated with tissue injury and repair and it may play a role in BPD. Endogenous peptide angiotensin 1-7 acts on the MAS receptor. The activation of the MAS receptor was previously shown to have protective pulmonary responses. However, the effect of MAS receptor activation on surfactant proteins in hyperoxic conditions has not been tested. Objective: To determine the effects of hyperoxia with or without MAS receptor activation on Surfactant proteins. Methods: Human epithelial cell line A549 and human primary alveolar epithelial cells (AECs) were cultured to sub-confluence (60-75%) and treated with hyperoxia (95% oxygen) and normoxia (21% oxygen) for 72 hours with or without the MAS receptor agonist (AVE0991) in serum-free F-12 nutrient media. Cells were lysed and cell lysates were collected for western blot. The statistical analysis was done using Student-Newman-Keuls Multiple comparison test. Results: Surfactant protein concentration increased in AVE treated group under the hyperoxic condition when compared to the control group in both A549 cells and human primary AECs. Surfactant protein was in higher concentration in AVE0991 treated cells in both hyperoxic and normoxic conditions when compared to the non-treated control group. Conclusions: MAS receptor activation via AVE0991 causes an increase in Surfactant protein concentration in both hyperoxic and normoxic conditions. As per our experiments, hyperoxic conditions decrease the production of surfactant protein when compared to normoxic conditions. These results may reveal a novel potential drug for BPD treatment and decrease its severity.

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Bates, Sandra R., Linda W. Gonzales, Jian-Qin Tao, Peter Rueckert, Philip L. Ballard, and Aron B. Fisher. "Recovery of rat type II cell surfactant components during primary cell culture." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 2 (February 1, 2002): L267—L276. http://dx.doi.org/10.1152/ajplung.00227.2001.

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A culture system designed to maintain the differentiated characteristics of rat type II cells based on protocols used for human fetal lung pneumocytes was investigated. Type II cells were isolated either from adult rats with elastase (adult type II cells) or from young rats (4–11 days postnatal) with collagenase and trypsin (young type II cells) and were incubated with dexamethasone (Dex, 10 nM) and cAMP (0.1 mM). By day 4 of culture with hormone treatment, the mRNA levels in adult type II cells were less than 3% of day 0 values, whereas surfactant protein (SP)-A protein content was 26%. However, young type II cells maintained lamellar bodies and microvilli and secreted phospholipid in response to ATP. SP-A, -B, and -C mRNA levels were elevated to 159, 350, and 39%, respectively, of day 0 values with a synergistic response to Dex and cAMP, whereas SP-A protein content rose to 119%. Surfactant mRNA and protein did not recover in cells cultured without hormones. This cell culture system restored surfactant components in rat type II cells.

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Spragg, Roger G., Paul J. Ponganis, James J. Marsh, Gunnar A. Rau, and Wolfgang Bernhard. "Surfactant from diving aquatic mammals." Journal of Applied Physiology 96, no. 5 (May 2004): 1626–32. http://dx.doi.org/10.1152/japplphysiol.00898.2003.

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Diving mammals that descend to depths of 50-70 m or greater fully collapse the gas exchanging portions of their lungs and then reexpand these areas with ascent. To investigate whether these animals may have evolved a uniquely developed surfactant system to facilitate repetitive alveolar collapse and expansion, we have analyzed surfactant in bronchoalveolar lavage fluid (BAL) obtained from nine pinnipeds and from pigs and humans. In contrast to BAL from terrestrial mammals, BAL from pinnipeds has a higher concentration of phospholipid and relatively more fluidic phosphatidylcholine molecular species, perhaps to facilitate rapid spreading during alveolar reexpansion. Normalized concentrations of hydrophobic surfactant proteins B and C were not significantly different among pinnipeds and terrestrial mammals by immunologic assay, but separation of proteins by gel electrophoresis indicated a greater content of surfactant protein B in elephant seal surfactant than in human surfactant. Remarkably, surfactant from the deepest diving pinnipeds produced moderately elevated in vitro minimum surface tension measurements, a finding not explained by the presence of protein or neutral lipid inhibitors. Further study of the composition and function of pinniped surfactants may contribute to the design of optimized therapeutic surfactants.

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Roy, Pialee, and Dipankar Sukul. "Protein–surfactant aggregate as a potential corrosion inhibitor for mild steel in sulphuric acid: zein–SDS system." RSC Advances 5, no. 2 (2015): 1359–65. http://dx.doi.org/10.1039/c4ra12821d.

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D'Angio, C. T., J. N. Finkelstein, M. B. Lomonaco, A. Paxhia, S. A. Wright, R. B. Baggs, R. H. Notter, and R. M. Ryan. "Changes in surfactant protein gene expression in a neonatal rabbit model of hyperoxia-induced fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 4 (April 1, 1997): L720—L730. http://dx.doi.org/10.1152/ajplung.1997.272.4.l720.

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Lung injuries, including bronchopulmonary dysplasia, alter the surfactant system. We developed a newborn rabbit model of acute, followed by chronic, hyperoxic injury to study surfactant protein (SP) gene expression. Initial litters were exposed to >95% O2 until 50% died (LD50; 7-11 days old). Subsequent litters were exposed to >95% O2 for 8 days, followed by 60% O2 until 22-36 days. Controls were exposed to room air. LD50 animals displayed acute pulmonary inflammation, edema, protein leak, and surfactant dysfunction. These changes resolved, and fibrosis developed by 22 days. Whole lung SP-A mRNA expression (measured by membrane hybridization) was twice control levels at 4 days of >95% O2, with specific elevations in terminal bronchioles and type II cells at 4 days and the LD50 by in situ hybridization. Whole lung SP-B and SP-C mRNA were unchanged from control throughout exposure. However, in situ hybridization showed elevations in SP-B and SP-C mRNA in type II cells in inflamed areas at the LD50. SP mRNA alterations resolved by 22-36 days. The surfactant system recovers from acute hyperoxic injury, despite continued 60% O2 exposure.

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Nag, Kaushik, Karina Rodriguez-Capote, Amiya Kumar Panda, Laura Frederick, Stephen A. Hearn, Nils O. Petersen, Samuel Schürch, and Fred Possmayer. "Disparate effects of two phosphatidylcholine binding proteins, C-reactive protein and surfactant protein A, on pulmonary surfactant structure and function." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 6 (December 2004): L1145—L1153. http://dx.doi.org/10.1152/ajplung.00408.2003.

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C-reactive protein (CRP) and surfactant protein A (SP-A) are phosphatidylcholine (PC) binding proteins that function in the innate host defense system. We examined the effects of CRP and SP-A on the surface activity of bovine lipid extract surfactant (BLES), a clinically applied modified natural surfactant. CRP inhibited BLES adsorption to form a surface-active film and the film's ability to lower surface tension (γ) to low values near 0 mN/m during surface area reduction. The inhibitory effects of CRP were reversed by phosphorylcholine, a water-soluble CRP ligand. SP-A enhanced BLES adsorption and its ability to lower γ to low values. Small amounts of SP-A blocked the inhibitory effects of CRP. Electron microscopy showed CRP has little effect on the lipid structure of BLES. SP-A altered BLES multilamellar vesicular structure by generating large, loose bilayer structures that were separated by a fuzzy amorphous material, likely SP-A. These studies indicate that although SP-A and CRP both bind PC, there is a difference in the manner in which they interact with surface films.

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Purevdorj, Erkhembulgan, Katja Zscheppang, Heinz G. Hoymann, Armin Braun, Dietlinde von Mayersbach, Maria-Jantje Brinkhaus, Andreas Schmiedl, and Christiane E. L. Dammann. "ErbB4 deletion leads to changes in lung function and structure similar to bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 3 (March 2008): L516—L522. http://dx.doi.org/10.1152/ajplung.00423.2007.

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Neuregulin is an important growth factor in fetal surfactant synthesis, and downregulation of its receptor, ErbB4, impairs fetal surfactant synthesis. We hypothesized that pulmonary ErbB4 deletion will affect the developing lung leading to an abnormal postnatal lung function. ErbB4-deleted lungs of 11- to 14-wk-old adult HER4heart mice, rescued from their lethal cardiac defects, were studied for the effect on lung function, alveolarization, and the surfactant system. ErbB4 deletion impairs lung function and structure in HER4heart mice resulting in a hyperreactive airway system and alveolar simplification, as seen in preterm infants with bronchopulmonary dysplasia. It also leads to a downregulation of surfactant protein D expression and an underlying chronic inflammation in these lungs. Our findings suggest that this animal model could be used to further study the pathogenesis of bronchopulmonary dysplasia and might help design protective interventions.

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Atochina, Elena N., Michael F. Beers, Seth T. Scanlon, Angela M. Preston, and James M. Beck. "P. cariniiinduces selective alterations in component expression and biophysical activity of lung surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 3 (March 1, 2000): L599—L609. http://dx.doi.org/10.1152/ajplung.2000.278.3.l599.

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Studies of Pneumocystis carinii pneumonia (PCP) suggest an important role for the surfactant system in the pathogenesis of the hypoxemic respiratory insufficiency associated with this infection. We hypothesized that PCP induces selective alterations in alveolar surfactant component expression and resultant biophysical properties. PCP was induced by intratracheal inoculation of 2 × 105P. carinii organisms into C.B-17 scid/ scid mice. Six weeks after inoculation, large (LA)- and small (SA)-aggregate surfactant fractions were prepared from bronchoalveolar lavage fluids and analyzed for expression of surfactant components and for biophysical activity. Total phospholipid content was significantly reduced in LA surfactant fractions from mice infected with PCP (53 ± 15% of uninfected mice; P < 0.05). Quantitation of hydrophobic surfactant protein (SP) content demonstrated significant reductions of alveolar SP-B and SP-C protein levels in mice with PCP compared with those in uninfected mice (46 ± 7 and 19 ± 6%, respectively; P < 0.05 for both). The reductions in phospholipid, SP-B, and SP-C in LA fractions measured during PCP were associated with an increase in the minimum surface tension of LAs as measured by pulsating bubble surfactometer (13.1 ± 1.1 vs. 5.4 ± 1.8 mN/m; P < 0.05). In contrast to decreases in the hydrophobic SPs, SP-D content in the SA fraction was markedly increased (343 ± 30% of control value; P < 0.05) and SP-A levels in LA surfactant were maintained (93 ± 26% of control value) during P. carinii infection. In all cases, the changes in SP content were reflected by commensurate changes in the levels of mRNA. We conclude that PCP induces selective alterations in surfactant component expression, including profound decreases in hydrophobic protein contents and resultant increases in surface tension. These changes, demonstrated in an immunologically relevant animal model, suggest that alterations in surfactant could contribute to the hypoxemic respiratory insufficiency observed in PCP.

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Lock, Mitchell C., Erin V. McGillick, Sandra Orgeig, Song Zhang, I. Caroline McMillen, and Janna L. Morrison. "Mature Surfactant Protein-B Expression by Immunohistochemistry as a Marker for Surfactant System Development in the Fetal Sheep Lung." Journal of Histochemistry & Cytochemistry 63, no. 11 (August 21, 2015): 866–78. http://dx.doi.org/10.1369/0022155415600201.

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Hilgendorff, Anne, Martin Doerner, Daniel Rawer, Jürgen Leick, Andreas Trotter, Michael Ebsen, Clemens Ruppert, Andreas Günther, Ludwig Gortner, and Irwin Reiss. "Effects of a recombinant surfactant protein-C-based surfactant on lung function and the pulmonary surfactant system in a model of meconium aspiration syndrome*." Critical Care Medicine 34, no. 1 (January 2006): 203–10. http://dx.doi.org/10.1097/01.ccm.0000190624.77908.e2.

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Watford, Wendy T., Andrew J. Ghio, and Jo Rae Wright. "Complement-mediated host defense in the lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 5 (November 1, 2000): L790—L798. http://dx.doi.org/10.1152/ajplung.2000.279.5.l790.

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Complement is a system of plasma proteins that aids in the elimination of pathogens from the body. We hypothesized that there is a functional complement system present in the lung that aids in the removal of pathogens. Western blot analysis revealed complement proteins of the alternative and classical pathways of complement in bronchoalveolar lavage fluids (BALF) from healthy volunteers. Functional classical pathway activity was detected in human BALF, but there was no significant alternative pathway activity in lavage fluid, a finding that correlates with the low level of the alternative pathway protein, factor B, in these samples. Although the classical pathway of complement was functional in lavage fluid, the level of the classical pathway activator C1q was very low. We tested the ability of the lung- specific surfactant proteins, surfactant protein A (SP-A) and surfactant protein D (SP-D), to substitute for C1q in classical pathway activation, since they have structural homology to C1q. However, neither SP-A nor SP-D restored classical pathway activity to C1q-depleted serum. These data suggest that the classical pathway of complement is functionally active in the lung where it may play a role in the recognition and clearance of bacteria.

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Mulugeta, Surafel, Shin-Ichi Nureki, and Michael F. Beers. "Lost after translation: insights from pulmonary surfactant for understanding the role of alveolar epithelial dysfunction and cellular quality control in fibrotic lung disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 6 (September 15, 2015): L507—L525. http://dx.doi.org/10.1152/ajplung.00139.2015.

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Dating back nearly 35 years ago to the Witschi hypothesis, epithelial cell dysfunction and abnormal wound healing have reemerged as central concepts in the pathophysiology of idiopathic pulmonary fibrosis (IPF) in adults and in interstitial lung disease in children. Alveolar type 2 (AT2) cells represent a metabolically active compartment in the distal air spaces responsible for pulmonary surfactant biosynthesis and function as a progenitor population required for maintenance of alveolar integrity. Rare mutations in surfactant system components have provided new clues to understanding broader questions regarding the role of AT2 cell dysfunction in the pathophysiology of fibrotic lung diseases. Drawing on data generated from a variety of model systems expressing disease-related surfactant component mutations [surfactant proteins A and C (SP-A and SP-C); the lipid transporter ABCA3], this review will examine the concept of epithelial dysfunction in fibrotic lung disease, provide an update on AT2 cell and surfactant biology, summarize cellular responses to mutant surfactant components [including endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and intrinsic apoptosis], and examine quality control pathways (unfolded protein response, the ubiquitin-proteasome system, macroautophagy) that can be utilized to restore AT2 homeostasis. This integrated response and its derangement will be placed in the context of cell stress and quality control signatures found in patients with familial or sporadic IPF as well as non-surfactant-related AT2 cell dysfunction syndromes associated with a fibrotic lung phenotype. Finally, the need for targeted therapeutic strategies for pulmonary fibrosis that address epithelial ER stress, its downstream signaling, and cell quality control are discussed.

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George, Caroline L. S., Misty L. White, Marsha E. O'Neill, Peter S. Thorne, David A. Schwartz, and Jeanne M. Snyder. "Altered surfactant protein A gene expression and protein metabolism associated with repeat exposure to inhaled endotoxin." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 6 (December 2003): L1337—L1344. http://dx.doi.org/10.1152/ajplung.00064.2003.

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Chronically inhaled endotoxin, which is ubiquitous in many occupational and domestic environments, can adversely affect the respiratory system resulting in an inflammatory response and decreased lung function. Surfactant-associated protein A (SP-A) is part of the lung innate immune system and may attenuate the inflammatory response in various types of lung injury. Using a murine model to mimic occupational exposures to endotoxin, we hypothesized that SP-A gene expression and protein would be elevated in response to repeat exposure to inhaled grain dust and to purified lipopolysaccharide (LPS). Our results demonstrate that repeat exposure to inhaled endotoxin, either in the form of grain dust or purified LPS, results in increased whole lung SP-A gene expression and type II alveolar epithelial cell hyperplasia, whereas SP-A protein levels in lung lavage fluid are decreased. Furthermore, these alterations in SP-A gene activity and protein metabolism are dependent on an intact endotoxin signaling system.

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Yamashita, Cory, Amy Forbes, Jenna M. Tessolini, Li-Juan Yao, James F. Lewis, and Ruud A. W. Veldhuizen. "Protective effects of elevated endogenous surfactant pools to injurious mechanical ventilation." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 4 (April 2008): L724—L732. http://dx.doi.org/10.1152/ajplung.00389.2007.

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Depletion of alveolar macrophages (AM) leads to an increase in endogenous surfactant that lasts several days beyond the repletion of AM. Furthermore, impairment to the endogenous pulmonary surfactant system contributes to ventilation-induced lung injury. The objective of the current study was to determine whether increased endogenous surfactant pools induced via AM depletion was protective against ventilation-induced lung injury. Adult rats were intratracheally instilled with either control or dichloromethylene diphosphonic acid (DMDP) containing liposomes to deplete AMs and thereby increase endogenous surfactant pools. Either 3 or 7 days following instillation, rats were exposed to 2 h of injurious ventilation using either an ex vivo or in vivo ventilation protocol and were compared with nonventilated controls. The measured outcomes were oxygenation, lung compliance, lavage protein, and inflammatory cytokine concentrations. Compared with controls, the DMDP-treated animals had significantly reduced AM numbers and increased surfactant pools 3 days after instillation. Seven days after instillation, AM numbers had returned to normal, but surfactant pools were still elevated. DMDP-treated animals at both time points exhibited protection against ventilation-induced lung injury, which included superior physiological parameters, lower protein leakage, and lower inflammatory mediator release into the air space, compared with animals not receiving DMDP. It is concluded that DMDP-liposome administration protects against ventilation-induced lung injury. This effect appears to be due to the presence of elevated endogenous surfactant pools.

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Orgeig, Sandra, Tamara A. Crittenden, Ceilidh Marchant, I. Caroline McMillen, and Janna L. Morrison. "Intrauterine growth restriction delays surfactant protein maturation in the sheep fetus." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 4 (April 2010): L575—L583. http://dx.doi.org/10.1152/ajplung.00226.2009.

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Pulmonary surfactant is synthesized by type II alveolar epithelial cells to regulate the surface tension at the air-liquid interface of the air-breathing lung. Developmental maturation of the surfactant system is controlled by many factors including oxygen, glucose, catecholamines, and cortisol. The intrauterine growth-restricted (IUGR) fetus is hypoxemic and hypoglycemic, with elevated plasma catecholamine and cortisol concentrations. The impact of IUGR on surfactant maturation is unclear. Here we investigate the expression of surfactant protein (SP) A, B, and C in lung tissue of fetal sheep at 133 and 141 days of gestation (term 150 ± 3 days) from control and carunclectomized Merino ewes. Placentally restricted (PR) fetuses had a body weight <2 SD from the mean of control fetuses and a mean gestational PaO2<17 mmHg. PR fetuses had reduced absolute, but not relative, lung weight, decreased plasma glucose concentration, and increased plasma cortisol concentration. Lung SP-A, -B, and -C protein and mRNA expression was reduced in PR compared with control fetuses at both ages. SP-B and -C but not SP-A mRNA expression and SP-A but not SP-B or -C protein expression increased with gestational age. Mean gestational PaO2was positively correlated with SP-A, -B, and -C protein and SP-B and -C mRNA expression in the younger cohort. SP-A and -B gene expression was inversely related to plasma cortisol concentration. Placental restriction, leading to chronic hypoxemia and hypercortisolemia in the carunclectomy model, results in significant inhibition of surfactant maturation. These data suggest that IUGR fetuses are at significant risk of lung complications, especially if born prematurely.

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Dziura, Maksymilian, Basel Mansour, Mitchell DiPasquale, P. Charukeshi Chandrasekera, James W. Gauld, and Drew Marquardt. "Simulated Breathing: Application of Molecular Dynamics Simulations to Pulmonary Lung Surfactant." Symmetry 13, no. 7 (July 14, 2021): 1259. http://dx.doi.org/10.3390/sym13071259.

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In this review, we delve into the topic of the pulmonary surfactant (PS) system, which is present in the respiratory system. The total composition of the PS has been presented and explored, from the types of cells involved in its synthesis and secretion, down to the specific building blocks used, such as the various lipid and protein components. The lipid and protein composition varies across species and between individuals, but ultimately produces a PS monolayer with the same role. As such, the composition has been investigated for the ways in which it imposes function and confers peculiar biophysical characteristics to the system as a whole. Moreover, a couple of theories/models that are associated with the functions of PS have been addressed. Finally, molecular dynamic (MD) simulations of pulmonary surfactant have been emphasized to not only showcase various group’s findings, but also to demonstrate the validity and importance that MD simulations can have in future research exploring the PS monolayer system.

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38

Jugg, B., J. Jenner, J. N. Hughes, and P. Rice. "The efect of hexafluorocyclobutene on rat bronchoalveolar lavage fluid surfactant phospholipids and alveolar type II cells." Human & Experimental Toxicology 20, no. 5 (May 2001): 267–76. http://dx.doi.org/10.1191/096032701678227686.

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Hexafluorocyclobutene (HFCB), a reactive organohalogen gas, causes overwhelming pulmonary oedema. We investigated its effect on the rat lung surfactant system, comparing its action on type II pneumocytes with airexposed rats. The inflammatory cell population and protein content of bronchoalveolar lavage fluid was analysed following exposure to air or HFCB (LCt30). Six rat lung phospholipids were measured by high-performance liquid chromatography, following solid phase extraction (SPE) from lavage fluid. Transmission electron microscopy (TEM) was used to visualise effects on alveolar type II cell ultrastructure. HFCB caused changes in cell populations and increased lavage fluid protein compared to controls, suggesting a permeability oedema. Changes in the total amount and percentage composition (sustained decrease in phosphatidylglycerol and phosphatidylcholine) of surfactant phospholipids also occurred. TEM observations indicated no direct ultrastructural damage to the type II cells, but showed initial, rapid release of surfactant into the alveolar space. HFCB altered the surfactant system in a manner similar to that shown following another reactive organohalogen gas, perfluoroisobutene (PFIB), but differently to that after phosgene. These differences suggest different mechanisms of action even though pulmonary oedema is the final injury for all gases. Better knowledge of the mechanisms involved will improve prospects for prophylactic/therapeutic intervention.

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Bazaziyan, Behnaz, Mohammad Reza Bozorgmehr, Mohammad Momen-Heravi, and S. Ali Beyramabadi. "Flavodoxin in a binary surfactant system consisting of the nonionic 1-decanoyl-rac-glycerol and the zwitterionic lauryldimethylamine-N-oxide: molecular dynamics simulation approach." Papers in Physics 12 (August 21, 2020): 120004. http://dx.doi.org/10.4279/pip.120004.

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Due to the short time constant of the spin-spin relaxation process, there is a limitation in the preparation of NMR sample solution for large proteins. To overcome this problem, reverse micelle systems are used. Here, molecular dynamics simulation was used to study the structure of flavodoxin in a quaternary mixture of 1-decanoyl-rac-glycerol, lauryldimethylamine-N-oxide, pentane and hexanol. Hexanol was used as co-solvent. Simulations were performed at three different co-solvent concentrations. The proportion of components in the mixture was selected according to experimental conditions. For comparison, simulation of flavodoxin in water was also performed. The simulation results show that the C$$\alpha$$-RMSD for the protein in water is less than for the surfactant mixture. Also, the radius of gyration of flavodoxin increased in the presence of surfactants. The distance between the two residues trp-57 and phe-94, as a measure of protein activity, was obtained from the simulations. The results showed that in the surfactant mixtures this distance increases. Analysis of the secondary structure of the protein shows that the N-terminal part of the flavodoxin is more affected by surfactants. The flavodoxin diffusion coefficient in the surfactant mixture decreased in relation to its diffusion coefficient in water.

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Stenstam, Anna, Daniel Topgaard, and Håkan Wennerström. "Aggregation in a Protein−Surfactant System. The Interplay between Hydrophobic and Electrostatic Interactions." Journal of Physical Chemistry B 107, no. 32 (August 2003): 7987–92. http://dx.doi.org/10.1021/jp0224158.

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Romaní-Pérez, Marina, Verónica Outeiriño-Iglesias, Christian M. Moya, Pilar Santisteban, Lucas C. González-Matías, Eva Vigo, and Federico Mallo. "Activation of the GLP-1 Receptor by Liraglutide Increases ACE2 Expression, Reversing Right Ventricle Hypertrophy, and Improving the Production of SP-A and SP-B in the Lungs of Type 1 Diabetes Rats." Endocrinology 156, no. 10 (July 21, 2015): 3559–69. http://dx.doi.org/10.1210/en.2014-1685.

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Diabetes alters microvascular function in the vascular beds of organs, including the lungs. Cardiovascular complications of pulmonary vascular affectation may be a consequence of the overactivation of the vasoconstrictive and proliferative components of the renin-angiotensin system. We previously reported that pulmonary physiology and surfactant production is improved by the glucagon-like peptide 1 receptor (GLP-1R) agonist liraglutide (LIR) in a rat model of lung hypoplasia. Because we hypothesized that streptozotocin-induced diabetes rats would show deficiencies in lung function, including surfactant proteins, and develop an imbalance of the renin-angiotensin system in the lungs. This effect would in turn be prevented by long-acting agonists of the GLP-1R, such as LIR. The induction of diabetes reduced the surfactant protein A and B in the lungs and caused the vasoconstrictor component of the renin-angiotensin system to predominate, which in turn increased angiotensin II levels, and ultimately being associated with right ventricle hypertrophy. LIR restored surfactant protein levels and reversed the imbalance in the renin-angiotensin system in this type 1 diabetes mellitus rat model. Moreover, LIR provoked a strong increase in angiotensin-converting enzyme 2 expression in the lungs of both diabetic and control rats, and in the circulating angiotensin(1–7) in diabetic animals. These effects prompted complete reversion of right ventricle hypertrophy. The consequences of LIR administration were independent of glycemic control and of glucocorticoids, and they involved NK2 homeobox 1 signaling. This study demonstrates by first time that GLP-1R agonists, such as LIR, might improve the cardiopulmonary complications associated with diabetes.

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Kumari, Santosh, Suvarcha Chauhan, Kuldeep Singh, Ahmad Umar, Hassan Fouad, and Mohammad Shaheer Akhtar. "Study on Volumetric, Compressibility and Viscometric Behavior of Cationic Surfactants (CTAB and DTAB) in Aqueous Glycyl Dipeptide: A Thermo-Acoustic Approach." Molecules 27, no. 24 (December 10, 2022): 8767. http://dx.doi.org/10.3390/molecules27248767.

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This study aims to understand how glycyl dipeptide affected the compressibility, volumetric behavior and viscometric behavior of the cationic surfactants CTAB (Cetyltrimethylammonium bromide) and DTAB (dodecyltrimethylammonium bromide). Information on solute–solute, solute–solvent, and solvent–solvent interactions has been inferred using the quantification of density (ρ), speed of sound (u) and viscosity in aqueous media containing glycyl dipeptide in the temperature range 293.15–313.15 K at an interval of 5 K. The data from the aforementioned research have been used to enumerate numerous volumetric and compressibility metrics that aid in the collection of information about the interactional behavior of the system under consideration. The study suggests that CTAB interacts strongly compared to DTAB with dipeptide, and it also significantly dehydrates glycyl dipeptide. The difference in water–water interactions caused by the loss of hydrophobic hydration of the surfactant molecules upon the addition of cationic surfactants may be the cause of the variation in determined parameters with surfactant concentration. Consideration of the structural rearrangement of molecules that may occur in the system has been used to explain the results of viscosity and computed factors related to viscosity. The patterns of competitive intermolecular interactions in the ternary (dipeptide + water + surfactant) system have been used to analyze the trends of all the parameters. The study may be helpful to understand the stability and structural changes in protein–surfactant systems mediated through various interactions that may be present in the system.

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Bikmetova, Kristina. "Mammalian Surfactant Protein Homology by Domain Collagen Type IV: Evolutionary and Functional Analysis." Natural Systems and Resources, no. 2 (February 2020): 19–23. http://dx.doi.org/10.15688/nsr.jvolsu.2019.2.3.

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The changes in the primary structures of proteins are strongly character due to evolution process. Some changes are beneficial and remain in the process of evolution, some ones are negatively affected to properties of the protein. Neutral changes in amino acid sequences can also occur, without affecting the protein and the body as a whole. Pulmonary surfactant is a surface-active lipoprotein complex (phospho-lipoprotein) formed by type II alveolar cells. The proteins and lipids that make up the surfactant have both hydrophilic and hydrophobic regions. As a medication, pulmonary surfactant is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system. The object of this study is surfactant-associated proteins. The aim of the study was to identify the relationship between the amino acid composition of the protein and its functions. The study of the structure of proteins was carried out using multiple alignment and building a phylogenetic tree. Proteins SP-A and SP-D are members of the C-type collectin family and consist of four domains: N-terminal sequence, collagen-like domain, carbohydrate recognition domain (CRD), “neck” between collagen-like and carbohydraterecognizing domains. Functionally, the most important are the C4 and CRD domains. Point mutations in these domains affect the change in the properties of proteins.

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Johnston, Sonya D., Sandra Orgeig, Olga V. Lopatko, and Christopher B. Daniels. "Development of the pulmonary surfactant system in two oviparous vertebrates." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 2 (February 1, 2000): R486—R493. http://dx.doi.org/10.1152/ajpregu.2000.278.2.r486.

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In birds and oviparous reptiles, hatching is often a lengthy and exhausting process, which commences with pipping followed by lung clearance and pulmonary ventilation. We examined the composition of pulmonary surfactant in the developing lungs of the chicken, Gallus gallus, and of the bearded dragon, Pogona vitticeps. Lung tissue was collected from chicken embryos at days 14, 16, 18 (prepipped), and 20(postpipped) of incubation and from 1 day and 3 wk posthatch and adult animals. In chickens, surfactant protein A mRNA was detected using Northern blot analysis in lung tissue at all stages sampled, appearing relatively earlier in development compared with placental mammals. Chickens were lavaged at days 16, 18, and 20 of incubation and 1 day posthatch, whereas bearded dragons were lavaged at day 55, days 57–60 (postpipped), and days 58–61 (posthatched). In both species, total phospholipid (PL) from the lavage increased throughout incubation. Disaturated PL (DSP) was not measurable before 16 days of incubation in the chick embryo nor before 55 days in bearded dragons. However, the percentage of DSP/PL increased markedly throughout late development in both species. Because cholesterol (Chol) remained unchanged, the Chol/PL and Chol/DSP ratios decreased in both species. Thus the Chol and PL components are differentially regulated. The lizard surfactant system develops and matures over a relatively shorter time than that of birds and mammals. This probably reflects the highly precocial nature of hatchling reptiles.

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Veldhuizen, R. A. W., K. Inchley, S. A. Hearn, J. F. Lewis, and F. Possmayer. "Degradation of surfactant-associated protein B (SP-B) during in vitro conversion of large to small surfactant aggregates." Biochemical Journal 295, no. 1 (October 1, 1993): 141–47. http://dx.doi.org/10.1042/bj2950141.

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Pulmonary surfactant obtained from lung lavages can be separated by differential centrifugation into two distinct subfractions known as large surfactant aggregates and small surfactant aggregates. The large-aggregate fraction is the precursor of the small-aggregate fraction. The ratio of the small non-surface-active to large surface-active surfactant aggregates increases after birth and in several types of lung injury. We have utilized an in vitro system, surface area cycling, to study the conversion of large into small aggregates. Small aggregates generated by surface area cycling were separated from large aggregates by centrifugation at 40,000 g for 15 min rather than by the normal sucrose gradient centrifugation. This new separation method was validated by morphological studies. Surface-tension-reducing activity of total surfactant extracts, as measured with a pulsating-bubble surfactometer, was impaired after surface area cycling. This impairment was related to the generation of small aggregates. Immunoblot analysis of large and small aggregates separated by sucrose gradient centrifugation revealed the presence of detectable amounts of surfactant-associated protein B (SP-B) in large aggregates but not in small aggregates. SP-A was detectable in both large and small aggregates. PAGE of cycled and non-cycled surfactant showed a reduction in SP-B after surface area cycling. We conclude that SP-B is degraded during the formation of small aggregates in vitro and that a change in surface area appears to be necessary for exposing SP-B to protease activity.

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Orioni, Barbara, Mauro Roversi, Camillo La Mesa, Fioretta Asaro, Giorgio Pellizer, and Gerardino D'Errico. "Polymorphic Behavior in Protein−Surfactant Mixtures: The Water−Bovine Serum Albumin−Sodium Taurodeoxycholate System." Journal of Physical Chemistry B 110, no. 24 (June 2006): 12129–40. http://dx.doi.org/10.1021/jp055950r.

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Liu, Hongmei, Xueting Huang, Haifeng Xiong, Miaomiao Liu, Dongmei Hu, Changqing Wei, Guijun Wang, and Kezong Qi. "Co-expression of surfactant protein A and chicken lung lectin in chicken respiratory system." Molecular Immunology 122 (June 2020): 49–53. http://dx.doi.org/10.1016/j.molimm.2020.03.018.

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Zhang, Wan-Guang, Li He, Hua-qing Su, Xue-mei Shi, Bo Zhang, Si-si Wu, Li Mei, et al. "Establishment of surfactant-associated protein a suicide gene system and analysis of its activity." Journal of Huazhong University of Science and Technology [Medical Sciences] 34, no. 3 (June 2014): 337–42. http://dx.doi.org/10.1007/s11596-014-1279-z.

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Keller, A., H. R. Eistetter, T. Voss, and K. P. Schäfer. "The pulmonary surfactant protein C (SP-C) precursor is a type II transmembrane protein." Biochemical Journal 277, no. 2 (July 15, 1991): 493–99. http://dx.doi.org/10.1042/bj2770493.

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Human pulmonary-surfactant-associated protein C (SP-C) is an extremely hydrophobic peptide comprising 34-35 amino acids. It is involved in the reduction of surface tension at the air/liquid in the lung. In order to understand the mechanism by which this molecule is generated from its 197-amino-acid-residues-long precursor and secreted into the alveolar space, we analysed the biosynthesis and processing of this precursor in an ‘in vitro’ system. Our results show that the SP-C precursor is a 21 kDa integral membrane protein. It is anchored in the membrane by a hydrophobic domain that comprises the 20-amino-acid-residues-long hydrophobic core of the mature SP-C peptide. The N-terminus remains in the cytoplasm, which leads to a type II transmembrane orientation of the precursor. Membrane integration occurs in a signal-peptidase-independent manner. The hydrophobic domain acts as both signal sequence and membrane-anchoring domain. We suggest that correct membrane insertion of the SP-C precursor, which is strictly dependent on the hydrophobic-amino-acid sequence represented by the hydrophobic core of the mature SP-C, is itself a prerequisite for further processing and intracellular transport of the mature SP-C.

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Vockeroth, Dan, Lasantha Gunasekara, Matthias Amrein, Fred Possmayer, James F. Lewis, and Ruud A. W. Veldhuizen. "Role of cholesterol in the biophysical dysfunction of surfactant in ventilator-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 1 (January 2010): L117—L125. http://dx.doi.org/10.1152/ajplung.00218.2009.

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Abstract:

Mechanical ventilation may lead to an impairment of the endogenous surfactant system, which is one of the mechanisms by which this intervention contributes to the progression of acute lung injury. The most extensively studied mechanism of surfactant dysfunction is serum protein inhibition. However, recent studies indicate that hydrophobic components of surfactant may also contribute. It was hypothesized that elevated levels of cholesterol significantly contribute to surfactant dysfunction in ventilation-induced lung injury. Sprague-Dawley rats ( n = 30) were randomized to either high-tidal volume or low-tidal volume ventilation and monitored for 2 h. Subsequently, the lungs were lavaged, surfactant was isolated, and the biophysical properties of this isolated surfactant were analyzed on a captive bubble surfactometer with and without the removal of cholesterol using methyl-β-cyclodextrin. The results showed lower oxygenation values in the high-tidal volume group during the last 30 min of ventilation compared with the low-tidal volume group. Surfactant obtained from the high-tidal volume animals had a significant impairment in function compared with material from the low-tidal volume group. Removal of cholesterol from the high-tidal volume group improved the ability of the surfactant to reduce the surface tension to low values. Subsequent reconstitution of high-cholesterol values led to an impairment in surface activity. It is concluded that increased levels of cholesterol associated with endogenous surfactant represent a major contributor to the inhibition of surfactant function in ventilation-induced lung injury.

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Journal articles on the topic 'Surfactant-Protein System'

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