Graphene oxide (GO) has been widely
used in biological sensing
studies because of its excellent physical and chemical properties.
In particular, the rich functional groups on the surface of GO can
effectively enhance the bonding of biomolecules and serve as an efficient
sensing substrate. However, when biomolecules are labeled with fluorescence,
the GO interface affects the biomolecules by reducing the fluorescence
properties and limiting their applications in biosensing. Here, we
establish an annealed GO (aGO) substrate through the annealing process,
which can effectively increase the bonding amount of a DNA probe because
of the accumulation of oxygen atoms on the surface without significantly
damaging the nanosheet structure. Furthermore, we prove that the aGO
substrate can effectively maintain its fluorescence performance and
stability by exposing more graphic domains. Overall, this study successfully
verifies that GO’s interface annealing modification can be
used as an alternative innovative interface application in biosensing.
Chronic obstructive pulmonary disease (COPD) is one of the most lethal chronic disease worldwide; however, the establishment of reliable
in vitro
models for exploring the biological mechanisms of COPD remains challenging. Here, we determined the differences in the expression and characteristics of the autophagic protein LC3B in normal and COPD human small airway epithelial cells and found that the nucleus of COPD cells obviously accumulated LC3B. We next established 3D human small airway tissues with distinct disease characteristics by regulating the biological microenvironment, extracellular matrix, and air-liquid interface culture methods. Using this biomimetic model, we found that LC3B affects the differentiation of COPD cells into basal, secretory, mucous, and ciliated cells. Moreover, although chloroquine and ivermectin effectively inhibited the expression of LC3B in the nucleus, chloroquine specifically maintained the performance of LC3B in cytoplasm, thereby contributing to the differentiation of ciliated cells and subsequent improvement in the beating functions of the cilia, whereas ivermectin only facilitated differentiation of goblet cells. We demonstrated that the autophagic mechanism of LC3B in the nucleus is one factor regulating the ciliary differentiation and function of COPD cells. Our innovative model can be used to further analyze the physiological mechanisms in the
in vitro
airway environment.
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