Ask about this productRelated genes to: SFTPD antibody
- Gene:
- SFTPD NIH gene
- Name:
- surfactant protein D
- Previous symbol:
- SFTP4
- Synonyms:
- SP-D, COLEC7
- Chromosome:
- 10q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-26
- Date modifiied:
- 2016-10-05
Related products to: SFTPD antibody
Related articles to: SFTPD antibody
- 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 - The lnc-RNA, miRNA, and mRNA networks have been extensively studied for cancer regulation. Furthermore, ceRNA network analysis has proved as an effective candidate for identifying potential diagnostic biomarkers in a variety of cancers. In this study, we described a novel axis of serum Surfactant protein D ()/miR-335-5p/lnc-HNRNPUL2 proposed by bioinformatics analysis and validated in a pilot human study of CRC versus control & in vitro assay to explore its role in the CRC pathogenesis. - Source: PubMed
Publication date: 2026/03/26
Matboli MarwaElanwar AlyIbrahim WalaaHassan Mohamed KamelAli MarwaKhaled RadwaMontaser ShadyKeshk SaraMedhat HadeelShafei Marwa MMohamed Reham AtefFouad Manar Ahmed - Pulmonary surfactant protein D (SP-D) is an innate immune molecule implicated in lung cancer, where its expression correlates with improved survival and reduced tumor growth. Despite its relevance to lung pathobiology, the transcriptional programs regulated by SP-D and their role in cancer progression and metastasis remain poorly understood. Through integrative analysis of multimodal human data we demonstrate that the SP-D gene (SFTPD) expression is reduced to near absence in metastatic non-small cell lung cancer (NSCLC) tissue, linking its loss to metastatic progression. SFTPD overexpression in A549 lung adenocarcinoma cells significantly decreased tumor growth and metastasis in vivo, and intranasal SP-D protein administration reduced lung tumor burden. Mechanistically, SP-D suppressed several signaling pathways, including IL-4/STAT6 signaling. Analysis of clinical lung tumor samples confirmed that SFTPD expression is associated with reduced IL-4/STAT6 signaling, and patients with low SFTPD expression and elevated IL-4 signaling in their tumors showed the poorest disease-free survival. Our findings demonstrate that SP-D interacts with NSCLC cells to suppress lung cancer progression, in part by blocking of the IL-4/STAT6 signaling pathway. - Source: PubMed
Publication date: 2026/03/08
Mohammadi AliInayatullah MohammedSchlosser AndersPilecki BartoszMarcussen NielsÜnsal SeydaMansoori BehzadBaradaran BehzadTallouzi YousefGjerstorff Morten FrierGraversen JonasRavnskjær KimTiwari Vijay KTerp Mikkel GSorensen Grith Lykke - Cancer patients are highly vulnerable to severe COVID-19, requiring models that capture tumor-virus interactions. We investigated tumor- and variant-specific effects of SARS-CoV-2 Gamma and Delta infections using patient-derived organoids (PDOs) from metastatic breast, lung, and colorectal cancers. Viral infection was quantified by Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR) 24 h post-infection, and morphological changes and immune mediators were profiled. Genomic analysis using whole-exome sequencing was performed to identify contributing host-related gene alterations. The Delta variant produced consistently higher viral loads in lung and breast PDOs, while colorectal PDOs showed variable susceptibility. Infection led to reduced area and perimeter and increased circularity across all tumor types. Immune profiling revealed distinct responses: Gamma decreased Interferon alpha (IFNα) in lung PDOs and increased E-selectin in colorectal PDOs. Delta broadly reduced inflammatory mediators in lung [10 kDa interferon gamma-induced protein (IP-10) and Intercellular adhesion molecule 1 (ICAM-1)] and breast [Interleukin-6 (IL-6), Interleukin-13 (IL-13), and Interleukin-17A (IL-17A)] PDOs, while increasing Macrophage inflammatory protein 1-beta (MIP-1β) in colorectal PDOs. Host gene variants involved in trafficking ( and ) and immune signaling (, , , and ) were associated with differential infection profiles. These findings show that SARS-CoV-2 induces variant- and tumor-specific morphological and immunological changes in cancer PDOs, highlighting the potential of this model to unravel host-virus interactions and identify genetic factors that shape infection outcomes in cancer. - Source: PubMed
Publication date: 2026/01/23
Ferreira DanielleSassaro TayanneAlberto Anael Viana Pintode Melo MaríliaAndrade Audrien AlvesFerreira Beatriz IandraMoreira Otacílio CMoreira DanielParente ThiagoBordim Brunade Abreu JúliaRondão FabianaCanedo JorgeFerreira Carlos Gilde Souza ElenMoreira AlineWaghabi MarianaZalis Mariano GustavoTilli Tatiana - Alveolar regeneration requires coordinated alveolar type 1 (AT1)/alveolar type 2 (AT2) responses and an intact epithelial barrier. In vitro systems, however, rarely couple lineage control with high resistance. Here we establish a concise workflow in which human AT2-like progenitors are expanded in a medium containing a small-molecule cocktail (Y-27632/A-83-01/CHIR99021; YAC), followed by air-liquid interface (ALI) culture in medium without the YAC cocktail (hereafter referred to as the YAC(-) condition). Compared with submerged culture, ALI increased AT1(AQP5, AGER, and PDPN) and AT2 (SFTPB, SFTPC, and SFTPD) markers. Within ALI, β-catenin inhibition by XAV939 elevated AT1 features while retaining AT2 protein expression, but was accompanied by reduced AT2 marker expression at the transcriptional level compared with the YAC(-) condition. Transepithelial electrical resistance entered the kΩ range by ALI day 10 and remained high across ALI conditions, with hematoxylin and eosin staining confirming a continuous single-layer epithelium. Passage reduced absolute marker levels and resistance but preserved the rank order across conditions. In scratch assays, ALI monolayers closed wounds over 24-48 h, and spatial immunofluorescence staining showed surfactant protein-C enrichment at the leading edge and podoplanin predominantly behind the front. Collectively, these findings demonstrate that β-catenin modulation within ALI biases the alveolar epithelial profile toward AT1-like features, whereas the YAC(-) condition sustains a balanced AT1/AT2 state with superior epithelial barrier performance and repair capacity. This platform provides a single-monolayer system suitable for dissecting alveolar epithelial differentiation and functional maintenance. - Source: PubMed
Publication date: 2026/02/05
Lin Yu-CheIgarashi MikiSakai YasuyukiNishikawa MasakiIshikawa ShinkichiTanabe Ikuya