Hypercapnia alters Wnt production from PDGFR+ lung fibroblasts

Hypercapnia has deleterious effects on cell function, including inhibition of alveolar epithelial cells (AEC) and fibroblast proliferation without causing cell death. Classical studies and lineage-trace models demonstrated that fibroblast cells can affect the structurally and functionally distinct alveolar type 1 cells (AT1) and alveolar type 2 cells. This fibroblast cells reprogramming depends on certain signaling pathways that plays critical roles in tissue development and homeostasis throughout the organism lifespan. Transcriptomic profiles of flow sorted PDGFR alpha+ fibroblast cells from C57Bl/6 mice exposed to 10% CO2 undernormoxic conditions for 0, and 10 days were generated by standard illumina RNA-Seq protocols.

高碳酸血症（Hypercapnia）对细胞功能具有有害影响，可抑制肺泡上皮细胞（alveolar epithelial cells, AEC）与成纤维细胞的增殖，且不会引发细胞死亡。经典研究与谱系示踪模型均证实，成纤维细胞能够影响结构与功能均存在显著差异的肺泡Ⅰ型细胞（alveolar type 1 cells, AT1）与肺泡Ⅱ型细胞（alveolar type 2 cells, AT2）。此种成纤维细胞重编程过程依赖于特定信号通路，该通路在生物体整个生命周期的组织发育与内环境稳态维持中发挥关键调控作用。本数据集通过标准Illumina RNA测序（Illumina RNA-Seq）实验流程，获取了常氧条件下暴露于10%二氧化碳环境0天及10天的C57BL/6小鼠流式分选得到的血小板源性生长因子受体α阳性（PDGFR alpha+）成纤维细胞的转录组图谱。