Alveolar epithelial cells: differentiation and lung injury

Abstract

Alveolar epithelial cells: differentiation and lung injury SUGAHARA K, TOKUMINE J, TERUYA K, OSHIRO T. Respirology 2006; 11 : S28-S31 Abstract: Re-epithelialization of alveolar epithelial cells is one of the important repair processes in many types of lung injury. The major functions of alveolar type II cells are synthesis and secretion of surfactant, hyperplasia in reaction to alveolar epithelial injury, and serving as progenitor cells for alveolar type I cells. The authors have examined the effects of several soluble factors on cultured alveolar type II cells in vitro , and also examined the histopathology and gene expression of surfactant proteins in the rat lungs with LPS, bleomycin and/or treated with keratinocyte growth factor. The authors next examined the effects of bone marrow stromal cells (BMSC) implanted transvenously into bleomycin-induced lungs. The authors found that keratinocyte growth factor (KGF) is a strong growth factor for alveolar type II cells, and that KGF instillation prevents bleomycin-induced lung injury. Furthermore, the authors showed the possibility of differentiation of implanted BMSC into alveolar epithelial cells. KGF and BMSC may play an important role in maintaining the alveolar epithelium and repairing the damaged epithelium after injury, and may well provide potential therapeutic alternatives.

Pulmonary and extrapulmonary acute respiratory distress syndrome: myth or reality?

“…The conciliating concept to determine the outcome may be the balance between alveolar epithelial inflammation or vascular endothelial injuries and their repair mechanisms [39] (Table 1). …”

Induction of epithelial-mesenchymal transition by flagellin in cultured lung epithelial cells

“…13) (28,30). It has been reported that fibroblasts isolated from IPF lungs have heterogenous phenotypes, suggesting that fibroblasts are derived from multiple cell types, including bone marrow and alveolar epithelial cells (13,24).…”

Genetic disruption of the Nrf2 compromises cell-cycle progression by impairing GSH-induced redox signaling

“…Alveolar epithelial cells are critical for maintaining lung tissue homeostasis and are also important in host defense and innate immunity (Qian et al, 2006;Sugahara et al, 2006;Serrano-Mollar et al, 2007). We have recently demonstrated that disruption of Nrf2 leads to alveolar epithelial cell growth arrest accompanied by oxidative stress (diminished levels of GSH and increased levels of ROS; Reddy et al, 2007a), which is correlated with diminished mRNA expression levels of genes encoding Gclc and Gclm enzymes and dysregulation of networks of transcriptional programs involved in cell proliferation (Reddy et al, 2007b).…”