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Background
ADRP is a marker of lung lipofibroblasts. Lipofibroblasts play an important role in assist type 2 alveolar epithelial cells function in peripheral lung tissue. Pulmonary fibrosis is characterized by continuous irreversible destruction of peripheral lung tissue. The expression of ADRP and the role of ADRP+ cells in pulmonary fibrosis are of interest to us.
Methods
Quantitative PCR as well as immunohistochemical multiplex staining were used to analyze the expression of ADRP during lung development, bleomycin-induced pulmonary fibrosis, and identify the type and function of ADRP+ cells during pulmonary fibrosis lesions.
Results
ADRP+ cells were found to decrease gradually from birth to adulthood. During pulmonary fibrosis, the expression of ADRP increased gradually, while another marker of lipofibroblast, the expression of PDGFRα decreased. There was a co-localization relationship between macrophage marker CD68 and ADRP. Both M1-type and M2-type macrophages can express ADRP in the early stage of pulmonary fibrosis. While in the subsequent pulmonary fibrosis process, M1-type ADRP+ macrophages gradually decrease, while the ADRP+ cells were mainly M2-type macrophages. ADRP+ M2-type macrophages can release S100A4 and distribute around the lesion area of pulmonary fibrosis. Pulmonary fibrosis gradually developed as M2-polarized macrophages replaced M1 to become the main population of pulmonary ADRP+ macrophages
Conclusion
In the process of pulmonary fibrosis, a large number of ADRP+ cells are macrophages, including M1 and M2 types successively. The aggregation site of ADRP+ M2-type macrophages indicates that fibrosis damage is about to or has already occurred. This study may provide a new research direction for the treatment of pulmonary fibrosis.
Keywords
Idiopathic pulmonary fibrosis, ADRP, Macrophage, Lipofibroblast
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A new preprint design is coming!
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 08 May, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Pulmonology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
ADRP is a marker of lung lipofibroblasts. Lipofibroblasts play an important role in assist type 2 alveolar epithelial cells function in peripheral lung tissue. Pulmonary fibrosis is characterized by continuous irreversible destruction of peripheral lung tissue. The expression of ADRP and the role of ADRP+ cells in pulmonary fibrosis are of interest to us.
Methods
Quantitative PCR as well as immunohistochemical multiplex staining were used to analyze the expression of ADRP during lung development, bleomycin-induced pulmonary fibrosis, and identify the type and function of ADRP+ cells during pulmonary fibrosis lesions.
Results
ADRP+ cells were found to decrease gradually from birth to adulthood. During pulmonary fibrosis, the expression of ADRP increased gradually, while another marker of lipofibroblast, the expression of PDGFRα decreased. There was a co-localization relationship between macrophage marker CD68 and ADRP. Both M1-type and M2-type macrophages can express ADRP in the early stage of pulmonary fibrosis. While in the subsequent pulmonary fibrosis process, M1-type ADRP+ macrophages gradually decrease, while the ADRP+ cells were mainly M2-type macrophages. ADRP+ M2-type macrophages can release S100A4 and distribute around the lesion area of pulmonary fibrosis. Pulmonary fibrosis gradually developed as M2-polarized macrophages replaced M1 to become the main population of pulmonary ADRP+ macrophages
Conclusion
In the process of pulmonary fibrosis, a large number of ADRP+ cells are macrophages, including M1 and M2 types successively. The aggregation site of ADRP+ M2-type macrophages indicates that fibrosis damage is about to or has already occurred. This study may provide a new research direction for the treatment of pulmonary fibrosis.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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