Ask about this productRelated genes to: SFTPC antibody
- Gene:
- SFTPC NIH gene
- Name:
- surfactant protein C
- Previous symbol:
- SFTP2
- Synonyms:
- SP-C, PSP-C, SMDP2, BRICD6
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2016-10-05
Related products to: SFTPC antibody
Related articles to: SFTPC antibody
- Idiopathic pulmonary fibrosis (IPF) is driven not only by fibroblast activation but also by loss of epithelial identity in alveolar type II (AT2) cells. In fibrotic regions of IPF lungs, AT2 cells frequently transition into cytokeratin 17 (KRT17)-positive alveolar-basal intermediate cells; however, the intracellular mechanisms regulating this fate change remain poorly understood. Although transforming growth factor-β1 (TGF-β1) signaling is a major driver of epithelial remodeling, the regulatory pathways that counterbalance this process in AT2 cells have not been clearly defined. Here, we investigated the interaction between the Rho-associated coiled-coil-containing protein kinase (ROCK) pathway and TGF-β1 signaling using human distal lung-derived alveolar organoids and human IPF lung tissues. ROCK activity was assessed by phosphorylated ezrin/radixin/moesin (pERM), whereas TGF-β1 signaling activity was evaluated by phosphorylated Smad2 (pSmad2). Under basal conditions, AT2 organoids displayed strong pERM expression with minimal pSmad2 activation. TGF-β1 stimulation induced trans-differentiation toward KRT17-positive alveolar-basal intermediate cells, accompanied by loss of surfactant protein C (SFTPC) expression. Inhibition or knockdown of ROCK markedly enhanced this TGF-β1-induced transition, whereas ROCK activation suppressed it. Consistently, human IPF tissues showed pERM-positive/pSmad2-negative AT2 cells in non-fibrotic regions, whereas fibrotic regions were enriched with pSmad2-positive/pERM-negative alveolar-basal intermediate cells. These findings identify ROCK signaling as a key mechanism that preserves AT2 cell identity and antagonizes TGF-β1-driven epithelial remodeling, suggesting epithelial ROCK activity as a potential therapeutic target in IPF. Overall, our results establish ROCK signaling as a gatekeeper of AT2 cell identity during fibrotic lung remodeling. - Source: PubMed
Publication date: 2026/05/06
Feng ZhaozuTakashima TsuyoshiNagata HidekiShintani YasushiMorii Eiichi - Silicosis is a progressive inflammatory and fibrotic lung disease with no effective treatments beyond symptom management. While global NLRP3 inflammasome deficiency attenuates silica-induced pathology, myeloid-specific Nlrp3 deletion provides no protection, suggesting that other cellular sources drive disease. Given that epithelial cells directly encounter inhaled silica particles and express NLRP3, we investigated the functional contribution of epithelial Nlrp3 to silicosis pathogenesis. - Source: PubMed
Publication date: 2026/05/03
Lam MaggieBarry Kristian THodges Christopher JWest Alison CHarpur Christopher MMansell AshleyTate Michelle D - Although stimulation of erythropoietin receptor (EPOR) signaling demonstrates cytoprotective effects-including anti-apoptosis, pro-proliferation, and promotion of inflammation resolution-in various disease models, its alterations and specific role in the process of pulmonary fibrosis are still not well understood. The study aimed at investigating the changes of lung EPOR signal in pulmonary fibrosis and the effect of different cell EPOR signal on pulmonary fibrosis. - Source: PubMed
Wu PengfeiJia JialinJin TianrongLuo BangweiZhang ZhirenWang Guansong - Due to the global obesity crisis, increasing numbers of women enter pregnancy with overweight or obesity. Their offspring are at greater risk of respiratory complications at birth due to metabolic changes that impact lung development that may reduce capacity for surfactant production. We hypothesize that a high-fat-high-energy diet (HF-HED) negatively impacts late gestation fetal lung development. - Source: PubMed
Publication date: 2026/04/27
Lock Mitchell CHuber Hillary FLi CunOrgeig SandraNathanielsz Peter WMorrison Janna L - Silicosis is the most severe occupational disease, with complex fibrotic mechanisms and a lack of effective therapies. Macrophage CX3CR1 has recently been found to play an important role in fibrosis diseases, and our previous studies have revealed that silica induced epithelial-mesenchymal transition (EMT) via macrophages and EMT was closely related to silicosis fibrosis. However, whether macrophage CX3CR1 is involved in silica-induced EMT and pulmonary fibrosis remains unclear. This study aimed to clarify the role and mechanism of macrophage CX3CR1 in silica-induced EMT and pulmonary fibrosis. A silicosis model was established in two types of transgenic mice (Cx3cr1-knockout and Sftpc-EGFP mice), and CX3CR1 was inhibited via gene knockout and pharmacological intervention. Results showed that silica up-regulated CX3CR1 and induced EMT in alveolar epithelial cells while inhibiting CX3CR1 significantly alleviated EMT and fibrosis. In vitro two types of Cx3cr1 siRNA were used in RAW264.7 cells, and it showed that targeting CX3CR1 suppressed silica-induced EMT in MLE-12 cells. Transcriptomic analysis revealed enrichment of the NF-κB pathway in vivo. In vitro experiments further confirmed that combined inhibition of CX3CR1 and NF-κB synergistically alleviated silica-induced EMT. These findings indicate that the CX3CR1-NF-κB axis plays an important role in silica-induced EMT and pulmonary fibrosis, and targeting CX3CR1 inhibits silica-induced epithelial-mesenchymal transition and pulmonary fibrosis in mice via the NF-κB signaling pathway, providing new insights for the prevention and treatment of silicosis. - Source: PubMed
Publication date: 2026/04/23
Zhang JiaxinWang YuhuaHuo ChuanyiJiao XukunZeng XinyingLi JingyaZhu ZhonghuiWang YifeiTian LinWang Yan