CD248 and integrin alpha-8 are candidate markers for differentiating lung fibroblast subtypes
Sayomi Matsushima1,2, Yoichiro Aoshima1,2, Taisuke Akamatsu3
1Department of Regenerative and Infectious Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu City, Shizuoka, 431-3192, Japan.
BMC Pulmonary Medicine
|January 23, 2020
Summary
Researchers identified two human lung fibroblast subtypes, CD248highITGA8low and CD248lowITGA8high, using cell surface markers. This classification aids understanding of lung development and fibrotic diseases.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Fibrosis Research
Background:
- Lung fibrosis is a fatal condition with variable fibroblast characteristics.
- Understanding fibroblast heterogeneity is crucial for diagnosing and treating lung fibrosis.
- Identifying specific markers for human lung fibroblast subtypes is necessary.
Purpose of the Study:
- To classify distinct mouse lung fibroblast subpopulations.
- To identify molecular markers for human lung fibroblast classification.
- To evaluate the localization of fibroblast subtypes in normal and fibrotic human lungs.
Main Methods:
- Fluorescence-activated cell sorting (FACS) to isolate mouse lung fibroblast subpopulations.
- Microarray analysis to identify cell surface markers.
- Localization studies in normal and idiopathic pulmonary fibrosis (IPF) human lung samples.
Main Results:
- Mouse lung fibroblasts were classified into Sca-1high and Sca-1low subtypes.
- CD248 and integrin alpha-8 (ITGA8) were identified as markers for Sca-1high and Sca-1low fibroblasts, respectively.
- Two human fibroblast subtypes, CD248highITGA8low and CD248lowITGA8high, were identified and localized in specific connective tissues.
Conclusions:
- CD248highITGA8low and CD248lowITGA8high fibroblast subtypes are distinctly localized in human lungs.
- This classification using CD248 and ITGA8 offers a method for studying lung fibroblast functions.
- Findings provide insights into lung development and fibrotic disease pathogenesis.


