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Gene Review

Sftpa1  -  surfactant protein A1

Rattus norvegicus

Synonyms: PSAP, PSP-A, Pulmonary surfactant-associated protein A, SP-A, Sftp-1, ...
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Disease relevance of Sftpa1

  • The appearance of this surface suggests a putative binding region for membrane-derived SP-A ligands such as phosphatidylcholine and lipid A, the endotoxic lipid component of bacterial lipopolysaccharide that mediates the potentially lethal effects of Gram-negative bacterial infection [1].
  • BACKGROUND: Declining levels of surfactant protein A (SP-A) after lung transplantation are suggested to indicate progression of ischemia/reperfusion (IR) injury [2].
  • In the present study we mapped the epitopes for monoclonal antibodies 1D6 and 6E3 by enzyme-linked immunoassay of recombinant proteins expressed using the baculovirus system, and investigated the domain that is responsible for the SP-A interactions with lipid [3].
  • We constructed replication-deficient, recombinant adenovirus vectors in which a constitutive viral promoter drives the expression of the DNAs for the surfactant-associated proteins, SP-B (AdCMV.SP-B) and SP-A (AdCMV.SP-A) [4].
  • Liposomes composed of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoethanolamine (POPE), with or without rough Escherichia coli LPS (J5), smooth E. coli LPS (B5), or cholesterol, were loaded with self-quenching probes and exposed to native or oxidatively modified SP-A [5].

Psychiatry related information on Sftpa1


High impact information on Sftpa1

  • SP-A also inhibited IAV hemagglutination activity [7].
  • SP-A is shown to bind P. carinii in vivo, and a putative binding site for SP-A on P. carinii is demonstrated to be the mannoserich surface membrane glycoprotein gp120 [8].
  • Alveolar macrophages also exhibit high-affinity binding of SP-A, but rat lung fibroblasts and the alveolar epithelial cell line L2 exhibit only nonspecific binding [9].
  • SP-A inhibited PLA(2) activity non-competitively with K(i) 10 mug/ml and was Ca(2+) -independent [10].
  • These studies provide further evidence that SP-A produced in the lung plays a role in modulating macrophage biology, thereby contributing to the alternative activation state of the alveolar macrophage [11].

Chemical compound and disease context of Sftpa1


Biological context of Sftpa1


Anatomical context of Sftpa1

  • Preincubation of macrophages with SP-A at 37 degrees C but not at 4 degrees C stimulated the phagocytosis [17].
  • Surfactant protein A (SP-A), one of four proteins associated with pulmonary surfactant, binds with high affinity to alveolar phospholipid membranes, positioning the protein at the first line of defense against inhaled pathogens [1].
  • RESULTS: After IR, labelling of tubular myelin for intraalveolar SP-A was significantly increased [2].
  • METHODS: Using immuno electron microscopy and design-based stereology, amount and distribution of SP-A, and of intracellular surfactant phospholipids (lamellar bodies) as well as infiltration by polymorphonuclear leukocytes (PMNs) and alveolar macrophages were evaluated in rat lungs after IR and preservation with EuroCollins or Celsior [2].
  • Immunocytochemistry demonstrated that many cells within the induced tracheal epithelium were positive for SP-A and SP-C proteins [19].

Associations of Sftpa1 with chemical compounds

  • The interdomain carbohydrate recognition domain-neck angle is significantly less in SP-A than in the homologous collectins, surfactant protein D, and mannose-binding protein [1].
  • The SP-A-mediated enhanced phagocytosis was not inhibited by the presence of cycloheximide [17].
  • The crystal structure of the trimeric carbohydrate recognition domain and neck domain of SP-A was solved to 2.1-A resolution with multiwavelength anomalous dispersion phasing from samarium [1].
  • Here we report that newborn rats, which can adapt to even higher levels of hyperoxia (100% O(2)) than do adult rats, manifest changes in the lung surfactant proteins (SP), especially SP-A and SP-D [20].
  • In isolated type II pneumocytes of ambroxol-treated animals, SP-C protein and mRNA content were increased, whereas SP-A, -B and -D protein, mRNA, and immunoreactivity remained unaffected [21].

Physical interactions of Sftpa1

  • Mannose and EDTA inhibited SP-D binding to CD14 but did not decrease SP-A binding [22].
  • Footprinting analysis indicated that SP-A-induced protein binding to SP-B promoter was greater in amount, but not different in location, from that seen in control cells, which normally transcribe SP-B [23].
  • SP-A increased protein binding to HNF-3 and TTF-1 consensus recognition elements [23].

Regulatory relationships of Sftpa1

  • In this report, we have examined the hormonal regulation of the rat surfactant protein B (SP-B) mRNA to determine whether SP-B expression is coordinately regulated with the surfactant phospholipids or with SP-A [24].
  • SP-A significantly enhanced the association of SP-C with isolated type II cells [25].

Other interactions of Sftpa1


Analytical, diagnostic and therapeutic context of Sftpa1

  • Both SP-A and SP-D proteins were increased in lung lavage samples taken from hyperoxia-exposed newborns, relative to those taken from air-exposed controls, with the greatest increases occurring on Days 6 and 8 of exposure [20].
  • METHODS: We studied the mRNA expression of surfactant proteins (SP) A, -B, -C and -D and Clara cell secretory protein (CC10) with RT-PCR and in situ hybridization and protein expression of CC10, SP-A and -D with immunohistochemistry in the lungs of a preterm rat model, in which experimental BPD was induced by prolonged oxidative stress [26].
  • SP-A and SP-D levels in lavage fluid were significantly elevated at 72 h [12].
  • SP-A content was determined in lung homogenates from treated and control male and female fetal rats by an enzyme-linked in lung homogenates from treated and control male and female fetal rats by an enzyme-linked immunosorbent assay [28].
  • 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 [29].


  1. Crystal structure of trimeric carbohydrate recognition and neck domains of surfactant protein A. Head, J.F., Mealy, T.R., McCormack, F.X., Seaton, B.A. J. Biol. Chem. (2003) [Pubmed]
  2. Improved lung preservation relates to an increase in tubular myelin-associated surfactant protein A. Fehrenbach, H., Tews, S., Fehrenbach, A., Ochs, M., Wittwer, T., Wahlers, T., Richter, J. Respir. Res. (2005) [Pubmed]
  3. Epitope mapping for monoclonal antibodies identifies functional domains of pulmonary surfactant protein A that interact with lipids. Kuroki, Y., McCormack, F.X., Ogasawara, Y., Mason, R.J., Voelker, D.R. J. Biol. Chem. (1994) [Pubmed]
  4. In vitro and in vivo transfer and expression of human surfactant SP-A- and SP-B-associated protein cDNAs mediated by replication-deficient, recombinant adenoviral vectors. Korst, R.J., Bewig, B., Crystal, R.G. Hum. Gene Ther. (1995) [Pubmed]
  5. Pulmonary collectins selectively permeabilize model bacterial membranes containing rough lipopolysaccharide. Kuzmenko, A.I., Wu, H., McCormack, F.X. Biochemistry (2006) [Pubmed]
  6. Action of substance P and an SP-hexapeptide analogue on avoidance learning in rats. Hecht, K., Oehme, P., Poppei, M. Die Pharmazie. (1982) [Pubmed]
  7. Evidence for a protective role of pulmonary surfactant protein D (SP-D) against influenza A viruses. Hartshorn, K.L., Crouch, E.C., White, M.R., Eggleton, P., Tauber, A.I., Chang, D., Sastry, K. J. Clin. Invest. (1994) [Pubmed]
  8. 120-kD surface glycoprotein of Pneumocystis carinii is a ligand for surfactant protein A. Zimmerman, P.E., Voelker, D.R., McCormack, F.X., Paulsrud, J.R., Martin, W.J. J. Clin. Invest. (1992) [Pubmed]
  9. Alveolar type II cells express a high-affinity receptor for pulmonary surfactant protein A. Kuroki, Y., Mason, R.J., Voelker, D.R. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  10. Interaction of surfactant protein a with peroxiredoxin 6 regulates phospholipase A2 activity. Wu, Y.Z., Manevich, Y., Baldwin, J.L., Dodia, C., Yu, K., Feinstein, S.I., Fisher, A.B. J. Biol. Chem. (2006) [Pubmed]
  11. Pulmonary surfactant protein A activates a phosphatidylinositol 3-kinase/calcium signal transduction pathway in human macrophages: participation in the up-regulation of mannose receptor activity. Beharka, A.A., Crowther, J.E., McCormack, F.X., Denning, G.M., Lees, J., Tibesar, E., Schlesinger, L.S. J. Immunol. (2005) [Pubmed]
  12. Surfactant proteins A and D increase in response to intratracheal lipopolysaccharide. McIntosh, J.C., Swyers, A.H., Fisher, J.H., Wright, J.R. Am. J. Respir. Cell Mol. Biol. (1996) [Pubmed]
  13. Opsonic activities of surfactant proteins A and D in phagocytosis of gram-negative bacteria by alveolar macrophages. Pikaar, J.C., Voorhout, W.F., van Golde, L.M., Verhoef, J., Van Strijp, J.A., van Iwaarden, J.F. J. Infect. Dis. (1995) [Pubmed]
  14. Surfactant protein A binds Mycoplasma pneumoniae with high affinity and attenuates its growth by recognition of disaturated phosphatidylglycerols. Piboonpocanun, S., Chiba, H., Mitsuzawa, H., Martin, W., Murphy, R.C., Harbeck, R.J., Voelker, D.R. J. Biol. Chem. (2005) [Pubmed]
  15. Surfactant protein A is decreased in a rat model of congenital diaphragmatic hernia. Mysore, M.R., Margraf, L.R., Jaramillo, M.A., Breed, D.R., Chau, V.L., Arévalo, M., Moya, F.R. Am. J. Respir. Crit. Care Med. (1998) [Pubmed]
  16. Internalization of surfactant protein A (SP-A) into lamellar bodies of rat alveolar type II cells in vitro. Kalina, M., McCormack, F.X., Crowley, H., Voelker, D.R., Mason, R.J. J. Histochem. Cytochem. (1993) [Pubmed]
  17. Pulmonary surfactant protein A augments the phagocytosis of Streptococcus pneumoniae by alveolar macrophages through a casein kinase 2-dependent increase of cell surface localization of scavenger receptor A. Kuronuma, K., Sano, H., Kato, K., Kudo, K., Hyakushima, N., Yokota, S., Takahashi, H., Fujii, N., Suzuki, H., Kodama, T., Abe, S., Kuroki, Y. J. Biol. Chem. (2004) [Pubmed]
  18. Isolation and sequence of a cDNA clone for the rat pulmonary surfactant-associated protein (PSP-A). Sano, K., Fisher, J., Mason, R.J., Kuroki, Y., Schilling, J., Benson, B., Voelker, D. Biochem. Biophys. Res. Commun. (1987) [Pubmed]
  19. Induction of alveolar type II cell differentiation in fetal tracheal epithelium by grafted distal lung mesenchyme. Shannon, J.M. Dev. Biol. (1994) [Pubmed]
  20. Elevated expression of surfactant proteins in newborn rats during adaptation to hyperoxia. White, C.W., Greene, K.E., Allen, C.B., Shannon, J.M. Am. J. Respir. Cell Mol. Biol. (2001) [Pubmed]
  21. Cell-specific modulation of surfactant proteins by ambroxol treatment. Seifart, C., Clostermann, U., Seifart, U., Müller, B., Vogelmeier, C., von Wichert, P., Fehrenbach, H. Toxicol. Appl. Pharmacol. (2005) [Pubmed]
  22. Surfactant proteins A and D bind CD14 by different mechanisms. Sano, H., Chiba, H., Iwaki, D., Sohma, H., Voelker, D.R., Kuroki, Y. J. Biol. Chem. (2000) [Pubmed]
  23. Activation of surfactant protein-B transcription: signaling through the SP-A receptor utilizing the PI3 kinase pathway. Strayer, D.S., Korutla, L. J. Cell. Physiol. (2000) [Pubmed]
  24. Hormonal effects on the surfactant protein B (SP-B) mRNA in cultured fetal rat lung. Floros, J., Gross, I., Nichols, K.V., Veletza, S.V., Dynia, D., Lu, H.W., Wilson, C.M., Peterec, S.M. Am. J. Respir. Cell Mol. Biol. (1991) [Pubmed]
  25. Association of surfactant protein C with isolated alveolar type II cells. Pinto, R.A., Hawgood, S., Clements, J.A., Benson, B.J., Naidu, A., Hamilton, R.L., Wright, J.R. Biochim. Biophys. Acta (1995) [Pubmed]
  26. Spatial and temporal expression of surfactant proteins in hyperoxia-induced neonatal rat lung injury. ter Horst, S.A., Fijlstra, M., Sengupta, S., Walther, F.J., Wagenaar, G.T. BMC pulmonary medicine [electronic resource]. (2006) [Pubmed]
  27. Maintenance of surfactant protein A and D secretion by rat alveolar type II cells in vitro. Mason, R.J., Lewis, M.C., Edeen, K.E., McCormick-Shannon, K., Nielsen, L.D., Shannon, J.M. Am. J. Physiol. Lung Cell Mol. Physiol. (2002) [Pubmed]
  28. Effects of maternal dexamethasone on expression of SP-A, SP-B, and SP-C in the fetal rat lung. Schellhase, D.E., Shannon, J.M. Am. J. Respir. Cell Mol. Biol. (1991) [Pubmed]
  29. Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization. Sugahara, K., Iyama, K., Sano, K., Morioka, T. Am. J. Respir. Cell Mol. Biol. (1994) [Pubmed]
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