Surfactant Protein C
Surfactant Protein C - Related Videos
09:34
Extraction and Characterization of Surfactants from Atmospheric Aerosols
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Cited by 26 •
2017
Methods are presented for the targeted extraction of surfactants present in atmospheric aerosols and the determination of their absolute concentrations and surface tension curves in water, including their Critical Micelle Concentration (CMC).
07:20
Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)
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Cited by 21 •
2016
Repeated pulmonary lavages in anesthetized pigs induce lung injury resembling major aspects of human acute respiratory distress syndrome (ARDS). For this purpose the lungs are repeatedly lavaged with 0.9% saline at 37 °C. The goal of the protocol is a reproducible mitigation of gas exchange and hemodynamics for research in ARDS.
10:28
Experimental Measurement of Settling Velocity of Spherical Particles in Unconfined and Confined Surfactant-based Shear Thinning Viscoelastic Fluids
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Cited by 15 •
2014
This paper demonstrates the experimental procedure to measure terminal settling velocities of spherical particles in surfactant-based shear thinning viscoelastic fluids. Fluids over a wide range of rheological properties are prepared and settling velocities are measured for a range of particle sizes in unbounded fluids and fluids between parallel walls.
08:46
Green Fluorescent Protein-based Expression Screening of Membrane Proteins in Escherichia coli
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Cited by 34 •
2015
A streamlined approach to screening for the expression of recombinant membrane proteins in Escherichia coli based on fusion to green fluorescent protein is presented.
06:22
Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
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Cited by 5 •
2021
A combination of surfactant washout using 0.9% saline (35 mL/kg body weight, 37 °C) and high tidal volume ventilation with low PEEP to cause moderate ventilator induced lung injury (VILI) results in experimental acute respiratory distress syndrome (ARDS). This method provides a model of lung injury with low/limited recruitability to study the effect of various ventilation strategies for extended periods.
FAQs
SP-C maturation follows an ordered intracellular route: alveolar type II cells synthesize the precursor proSP-C, direct it through the secretory pathway, and package the processed material with phospholipids in lamellar bodies. This organization prepares the protein for later release into the alveoli and connects intracellular processing with the formation of a functional pulmonary surfactant system.
SP-C’s hydrophobic character helps it function within the lipid-rich surfactant film rather than remaining in the surrounding fluid. At the air-liquid interface, this property supports rapid spreading of the film, allowing newly released surfactant to distribute efficiently. That behavior is important because film organization determines how effectively the surface-tension-reducing layer supports open lung spaces.
Changes in the synthesis, processing, packaging, or release of SP-C can disrupt the coordinated production of pulmonary surfactant. During development, such disruption may impair the establishment of an effective air-liquid interface and compromise lung function after surfactant release. Studying these steps therefore links cellular maturation in type II cells with respiratory outcomes in developing and mature lungs.
Expression and processing provide different information about SP-C biology. Expression indicates whether cells are producing the protein, whereas processing shows whether the precursor is being prepared for packaging and release. Examining both levels can distinguish a production problem from a maturation or trafficking problem, giving developmental biologists a clearer view of where surfactant metabolism may be disrupted.
A study can follow SP-C from production to function by examining its expression in alveolar type II cells, tracing precursor processing through the secretory pathway, evaluating packaging with phospholipids in lamellar bodies, and relating release to surfactant-film behavior. This sequence preserves the biological connection between cellular development, intracellular handling, and respiratory performance.
SP-C studies provide context for neonatal respiratory distress, interstitial lung disease, and genetic disorders of surfactant metabolism. These conditions can be investigated by asking how altered expression or intracellular processing affects packaging, release, or film performance. The resulting connection between molecular defects and surfactant function helps explain why disruptions in this pathway produce respiratory disease.