NPNT

Last update 08 May 2025

Basic Info

Synonyms

EGFL6L, nephronectin, NPNT

+ [3]

Introduction

Functional ligand of integrin alpha-8/beta-1 in kidney development. Regulates the expression of GDNF with integrin alpha-8/beta-1 which is essential for kidney development. May also play a role in the development and function of various tissues, regulating cell adhesion, spreading and survival through the binding of several integrins (By similarity).

100 Clinical Results associated with NPNT

100 Translational Medicine associated with NPNT

0 Patents (Medical) associated with NPNT

135

Literatures (Medical) associated with NPNT

08 Apr 2025·JCI Insight

Transcriptomic responses of lung mesenchymal cells during pneumonia

Article

Author: Crossland, Nicholas A ; Soucy, Alicia M ; Beach, Thomas G ; Jayaraman, Archana ; Shenoy, Anukul T ; Korkmaz, Filiz T ; Campbell, Joshua D ; Etesami, Neelou S ; Bosmann, Markus ; Mizgerd, Joseph P ; Quinton, Lee J ; Martin, Ian Mc ; Hiller, Bradley E ; Goltry, Wesley N ; Ha, Catherine T ; Frevert, Charles W ; Brune, Jourdan E ; Jones, Matthew R ; Traber, Katrina E

The role of mesenchymal cells during respiratory infection is not well defined, including whether, which, and how the different types of mesenchymal cells respond. We collected all mesenchymal cells from lung single-cell suspensions of mice that were naive (after receiving only saline vehicle), pneumonic (after intratracheal instillation of pneumococcus 24 hours previously), or resolved from infection (after nonlethal pneumococcal infections 6 weeks previously) and performed single-cell RNA sequencing. Cells clustered into 5 well-separated groups based on their transcriptomes: matrix fibroblasts, myofibroblasts, pericytes, smooth muscle cells, and mesothelial cells. Fibroblasts were the most abundant and could be further segregated into Pdgfra+Npnt+Ces1d+Col13a1+ alveolar fibroblasts and Cd9+Pi16+Sca1+Col14a1+ adventitial fibroblasts. The cells from naive and resolved groups overlapped in dimension reduction plots, suggesting the mesenchymal cells returned to baseline transcriptomes after resolution. During pneumonia, all mesenchymal cells responded with altered transcriptomes, revealing a core response that had been conserved across cell types as well as distinct mesenchymal cell type-specific responses. The different subsets of fibroblasts induced similar gene sets, but the alveolar fibroblasts responded more strongly than the adventitial fibroblasts. These data demonstrated diverse and specialized immune activities of lung mesenchymal cells during pneumonia.

01 Apr 2025·European Respiratory Journal

Characterisation of a COPD-associated nephronectin (NPNT) functional splicing genetic variant in human lung tissuevialong-read sequencing

Article

Author: Cho, Michael H ; Silverman, Edwin K ; Castaldi, Peter J ; Wilson, Carole L ; Wienecke, Anastacia N ; Laederach, Alain ; Hersh, Craig P ; Saferali, Aabida ; Ramos, Silvia B V ; Vollmers, Christopher ; Randell, Scott H ; Zhou, Xiaobo ; Liu, Tao ; Sheynkman, Gloria M ; Xu, Zhonghui ; Schnapp, Lynn M

BackgroundIdentification of COPD disease-causing genes is an important tool for understanding why COPD develops, who is at highest COPD risk and how new COPD treatments can be developed. Previous COPD genetic studies have identified a highly significant genetic association nearNPNT(nephronectin), a gene involved in tissue repair, but the biological mechanisms underlying this association are unknown.MethodsSplicing quantitative trait locus (sQTL) analysis was performed to identify common genetic variants that alter RNA splicing in lung tissues. These lung sQTL signals were compared to COPD genetic association results near theNPNTgene using colocalisation analysis to determine whether genetic risk for COPD in this region may act through altered splicing. Long-read sequencing characterised COPD-associated splicing events at isoform-level resolution andin silicoprotein structural analysis identified likely functional effects of this alternative splicing.ResultsAn established COPD genetic risk variant, rs34712979-A, creates a cryptic splice acceptor site that causes four separate splicing changes inNPNT. The only one of these splicing changes that was associated with COPD phenotypes involved a cassette exon (exon 3). Long-read RNA sequencing demonstrated that the COPD risk allele causes a shift in isoform usage away from the dominantNPNTisoform B precursor, which excludes exon 3, to the isoform A precursor, which splices-in exon 3. AlphaFold protein structural analysis reveals that inclusion of this exon disrupts an epidermal growth factor-like functional domain in NPNT.ConclusionGenetic variants in theNPNTgene increase COPD risk by changing RNA splicing ofNPNTin the lung.

01 Apr 2025·European Respiratory Journal

How nephronectin gene splicing shapes the risk of COPD

Communications

Author: Hernández Cordero, Ana I

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