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Voss, C.

Publications and source records attributed to Voss, C..

10 recordsLinked to original sources

Establishing toxicologically relevant primary alveolar macrophage models to enable a realistic assessment of nanomaterials safety

Alveolar macrophages (AMs) are key sentinels of the distal lung, maintaining surfactant homeostasis and clearing inhaled particles through continuous surveillance and phagocytosis. Mechanistic studies of particle-cell interactions, important to assess the respiratory safety or toxicity of particles, however, are limited by the lack of suitable in vitro models that preserve the core features of resident AMs. Here, we benchmarked six murine AM models, including short-term cultured primary AMs (AMs 3 h, AMs 24 h), primary AMs maintained with GM-CSF, TGF-{beta}, and the PPAR-{gamma} agonist rosiglitazone (AMs GTR), bone marrow-derived AM-like cells (BM-AMs), the immortalized AM cell line MH-S, and the non-transformed fetal liver-derived AM-like cell line MPI, against in vivo AMs based on surface phenotype, transcriptomic identity, and their responses to three carbon-based nanomaterials (CBNs). Both cell lines showed limited AM identity, characterized by low CD11c and SiglecF but high CD11b surface expression. In contrast, AMs GTR and BM-AMs more closely preserved resident AM-like surface marker profiles. Transcriptomic features, although differing for alterations in metabolism-related pathways, particularly oxidative phosphorylation, revealed most in vivo-like for the primary AM models. Functional, toxicological assessment using soot-like carbon nanoparticles (CNP), double-walled carbon nanotubes (DWCNT) and multi-walled carbon nanotubes (MWCNT) demonstrated strong model-dependent responses. Consistent with MWCNT-induced reduction in AM numbers observed in vivo, AMs GTR and BM-AMs exhibited the strongest in vitro responses, including cytotoxicity and inflammatory cytokine release. MH-S cells in contrast stood out for their cytotoxic sensitivity supporting their use for high throughput cytotoxicity tests. Overall, these findings identify AMs GTR and BM-AMs as the closest models for studying AMs biology and AM-intrinsic responses to poorly soluble nanoparticles like CBNs, and with regard to availability of higher cell numbers, BM-AMs might provide a scalable platform for mechanistic and higher-throughput nanotoxicology studies.

pharmacology and toxicology↗

Lifespan Analysis of the Lung Epithelium Reveals Inflammatory Reprogramming and Regenerative Decline

Aging is a major risk factor for chronic lung diseases, associated with chronic low-grade inflammation (inflammaging) and impaired epithelial regeneration. How epithelial-intrinsic aging intersects with inflammaging across the lifespan remains poorly understood. Here, we systematically analyzed lung epithelial cells from neonatal, young adult, and aged mice to define age-dependent changes in regenerative capacity. RNA sequencing revealed lifespan-associated shifts characterized by early repression of developmental and WNT/{beta}-catenin programs and progressive activation of DNA damage, inflammation, and senescence signatures. Functionally, neonatal epithelial cells exhibited markedly enhanced organoid-forming capacity compared with young and aged cells. Aged organoids maintained a pro-inflammatory secretory profile indicative of cell-intrinsic inflammaging, and transfer of the aged secretome or TNF- to young cultures significantly impaired regeneration. Comparison of freshly isolated cells and long-term organoid cultures revealed sustained repression of regenerative pathways with age, consistent with stable epigenetic imprinting. Pharmacological inhibition of DNA methylation and WNT signalling partially restored regenerative capacity in adult organoids. Together, these findings identify epigenetic reprogramming and epithelial-intrinsic inflammaging as key determinants of age-dependent regenerative decline.

cell biology↗

iPSC modeling of pulmonary arterial hypertension to uncover pathomechanisms and unrecognized modes of action of sotatercept

Pulmonary arterial hypertension (PAH) is a potentially fatal disease characterized by obliterative remodeling of distal pulmonary arteries, commonly associated with bone morphogenetic receptor type 2 (BMPR2) gene mutations. In patients with PAH, sotatercept, an activin signaling inhibitor, improves hemodynamics and outcomes, but clinical responses vary and sometimes occur within weeks, suggesting additional mechanisms beyond its anti-proliferative, pro-apoptotic and anti-remodeling effects. Using patient-specific induced pluripotent stem cell-derived smooth muscle cells (iSMCs) with BMPR2 extracellular- or kinase-domain mutations, we were able to reproduce Activin A-driven PAH traits, including hyperproliferation, reduced apoptosis, enhanced contraction and excessive matrix production. We identified smooth muscle cell-to-myofibroblast transition as a previously unknown contributor to pulmonary vascular remodeling and demonstrate that it is blocked by sotatercept. Beyond its established effects, sotatercept rapidly reduced contractility, collagen-integrin mechanotransduction and TGF{beta} receptor expression, disrupting a pathological positive feedback loop, reflected by lower levels of circulating TGF{beta}1 in patients on sotatercept. Taken together, our patient-derived iSMC platform links mutation-dependent mechanisms of pulmonary vascular remodeling to variable drug responsiveness and reveals previously unrecognized, potentially rapid-acting modes of sotatercept in PAH. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/711267v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@18d5e53org.highwire.dtl.DTLVardef@2bc80dorg.highwire.dtl.DTLVardef@5ace98org.highwire.dtl.DTLVardef@1b16171_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Post-Domestication selection of MKK3 Shaped Seed Dormancy and End-Use Traits in Barley

Anthropogenic selection of grain traits such as dormancy has shaped the developmental trajectories of crop plants (1). In cereals, shortening dormancy provides rapid and even post-harvest germination, but increases the risk of weather-induced pre-harvest sprouting (PHS) with harvest losses estimated at beyond 1 billion USD a year (2, 3, 4). Our understanding of how, why, when and where diversification of cereal dormancy arose is fragmentary. Here, we show in the founder cereal crop barley (Hordeum vulgare) that the Mitogen-Activated Protein Kinase (MAPK) pathway regulates dormancy primarily through a mosaic of locus haplotypes comprising copy-number variation and inherent kinase activity of Mitogen-activated protein kinase kinase 3 (MKK3). We provide evidence supporting the historical selection of specific MKK3 haplotypes that shape dormancy levels according to changing climatic pressures. Understanding the regulatory landscape of MKK3 provides a genetic framework to balance short grain dormancy and PHS-avoidance during a period of rapid climate change.

plant biology↗

LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance

Chronic myeloid leukemia (CML) resistance to BCR-ABL tyrosine kinase inhibitors (TKIs) can arise from ABL kinase domain mutations, BCR-ABL fusion gene amplification, or kinase-independent mechanisms. To investigate imatinib-resistance, we performed quantitative mass spectrometry comparing the proteome and phosphoproteome of K562 cells (a standard CML model) and ImR cells, an imatinib-resistant K562 derivative that also exhibits cross-resistance to second- and third-generation BCR-ABL TKIs. In addition to revealing global proteome and phosphoproteome changes associated with drug resistance, we identified LIN28A--a multi-functional RNA-binding protein--as a critical mediator of imatinib resistance. LIN28A was significantly overexpressed and hyperphosphorylated in ImR cells. Depleting LIN28A via shRNA restored imatinib sensitivity, while its ectopic expression in parental K562 cells induced imatinib resistance. Mechanistically, LIN28A coordinates an extensive kinase-substrate network regulating proliferation, survival, and metabolism to drive resistance. Notably, pharmacological inhibition of LIN28A-dependent kinases (PKC, AKT, SGK1, and RPS6K) suppressed ImR proliferation. Midostaurin, a clinical PKC/FLT3 inhibitor used in FLT3-ITD--positive AML, potently re-sensitized ImR cells to imatinib. Our findings suggest that targeting LIN28A and its downstream effectors, particularly PKC, could overcome resistance to imatinib and next-generation BCR-ABL inhibitors.

cancer biology↗

Cell circuits underlying nanomaterial specific respiratory toxicology

Nanomaterials emerged as boundless resource of innovation, but their shape and biopersistence related to respiratory toxicology raise longstanding concerns. The development of predictive safety tests for inhaled nanomaterials, however, is hampered by limited understanding of cell type-specific responses. To advance this knowledge, we used single-cell RNA-sequencing to longitudinally analyze cellular perturbations in mice, caused by three carbonaceous nanomaterials of different shape and toxicity upon pulmonary delivery. Focusing on nanomaterial-specific dynamics of lung inflammation, we found persistent depletion of alveolar macrophages by fiber-shaped nanotubes. While only little involvement was observed for alveolar macrophages during the initiation phase, they emerged, together with infiltrating monocyte-derived macrophages, as decisive factors in shifting inflammation towards resolution for spherical nanomaterials, or chronic inflammation for fibers. Fibroblasts, central for fibrosis, sensed macrophage and epithelial signals and emerged as orchestrators of nanomaterial-induced inflammation. Thus, the mode of actions identified in this study will significantly inspire the precision of future in vitro testing. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/579746v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@1d6f061org.highwire.dtl.DTLVardef@3fabb1org.highwire.dtl.DTLVardef@21040eorg.highwire.dtl.DTLVardef@1915c3b_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

Cytokine signaling converging on IL11 in ILD fibroblasts provokes aberrant epithelial differentiation signatures

Interstitial lung disease (ILD) is a heterogenous group of lung disorders where destruction and incomplete regeneration of the lung parenchyma often results in persistent architectural distortion of the pulmonary scaffold. Continuous mesenchyme-centered, disease-relevant signaling likely initiates and perpetuates the fibrotic remodeling process, specifically targeting the epithelial cell compartment, thereby destroying the gas exchange area. With the aim of identifying functionally relevant mediators of the lung mesenchymal-epithelial crosstalk that hold potential as new targets for therapeutic strategies, we developed a 3D organoid co-culture model based on human induced pluripotent stem cell-derived alveolar epithelial type 2 cells that form alveolar organoids in presence of lung fibroblasts from ILD patients as well as a control cell line (IMR-90). While organoid formation capacity and size was comparable in the presence of ILD or control lung fibroblasts, metabolic activity was significantly increased in ILD co-cultures. Alveolar organoids cultured with ILD fibroblasts further demonstrated reduced stem cell function as reflected by reduced Surfactant Protein C gene expression together with an aberrant basaloid-prone differentiation program indicated by elevated Cadherin 2, Bone Morphogenic Protein 4 and Vimentin transcription. In order to screen for key mediators of the misguided mesenchymal-to-epithelial crosstalk with a focus on disease-relevant inflammatory processes, we used mass spectrometry and characterized the secretome of end stage ILD lung fibroblasts in comparison to non-chronic lung disease (CLD) patient fibroblasts. Out of the over 2000 proteins detected by this experimental approach, 47 proteins were differentially abundant comparing ILD and non-CLD fibroblast secretome. The ILD secretome profile was dominated by chemokines, including CXCL1, CXCL3, and CXCL8, interfering with growth factor signaling orchestrated by Interleukin 11 (IL11), steering fibrogenic cell-cell communication, and proteins regulating extracellular matrix remodeling including epithelial-to-mesenchymal transition. When in turn treating alveolar organoids with IL11, we recapitulated the co-culture results obtained with primary ILD fibroblasts including changes in metabolic activity. In summary, we identified mediators likely contributing to the disease-perpetuating mesenchymal-to-epithelial crosstalk in ILD. In our alveolar organoid co-cultures, we were able to highlight the importance of fibroblast-initiated aberrant epithelial differentiation and confirmed IL11 as a key player in ILD pathogenesis by unbiased ILD fibroblast secretome analysis. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=192 SRC="FIGDIR/small/521114v2_ufig1.gif" ALT="Figure 1"> View larger version (59K): org.highwire.dtl.DTLVardef@187500org.highwire.dtl.DTLVardef@1a98b78org.highwire.dtl.DTLVardef@37736org.highwire.dtl.DTLVardef@1878063_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

FIND-IT: Ultrafast mining of genome diversity

Novel crop improvement methodologies, including the exploitation of natural genetic variation, are urgently required to feed our rapidly growing human population in the context of global climate change. Here we describe a Fast Identification of Nucleotide variants by DigITal PCR (FIND-IT) method for the rapid identification of pre-targeted genetic variants or rare alleles in large genomic populations. Libraries of 500,000 individuals can be screened and desired variants isolated within two weeks. FIND-IT is widely applicable for mining valuable diversity in any genomic population, including elite breeding and wild germplasm collections. The method provides single nucleotide resolution that has been validated by identifying and isolating knockout lines, non-synonymous codon changes and variants of miRNA and transcription factor binding sites in the agronomically important crop barley. In contrast to existing methods, FIND-IT does not require transformation, cloning or enzymatic steps, and is exempt from GMO regulations. Thus, FIND-IT can be applied immediately to elite crop cultivars and can be tailored to minimize or eliminate time-consuming backcrossing requirements.

genetics↗

Towards predictive nanotoxicology: from roundabout of molecular events to chronic inflammation prediction

Nanomaterial-induced diseases cannot be reliably predicted because of the lack of clearly identified causal relationships, in particular between acute exposures and chronic symptoms. By applying advanced microscopies and omics to in vitro and in vivo systems, together with in silico molecular modelling, we have here determined that the long-lasting response to a single exposure originates in the counteracting of a newly discovered nanomaterial quarantining and nanomaterial cycling among different lung cell types. This allows us to predict the nanomaterial-induced spectrum of lung inflammation using only in vitro measurements and in silico modelling. Besides its profound implications for cost-efficient animal-free predictive toxicology, our work also paves the way to a better mechanistic understanding of nanomaterial- induced cancer, fibrosis, and other chronic diseases.

molecular biology↗

Longitudinal single cell transcriptomics reveals Krt8+ alveolar epithelial progenitors in lung regeneration

Lung injury activates quiescent stem and progenitor cells to regenerate alveolar structures. The sequence and coordination of transcriptional programs during this process has largely remained elusive. Using single cell RNA-seq, we first generated a whole-organ birds-eye view on cellular dynamics and cell-cell communication networks during mouse lung regeneration from [~]30,000 cells at six timepoints. We discovered an injury-specific progenitor cell state characterized by Krt8 in flat epithelial cells covering alveolar surfaces. The number of these cells peaked during fibrogenesis in independent mouse models, as well as in human acute lung injury and fibrosis. Krt8+ progenitors featured a highly distinct connectome of receptor-ligand pairs with endothelial cells, fibroblasts, and macrophages. To sky dive into epithelial differentiation dynamics, we sequenced >30,000 sorted epithelial cells at 18 timepoints and computationally derived cell state trajectories that were validated by lineage tracing genetic reporter mice. Airway stem cells within the club cell lineage and alveolar type-2 cells underwent transcriptional convergence onto the same Krt8+ progenitor cell state, which later resolved by terminal differentiation into alveolar type-1 cells. We derived distinct transcriptional regulators as key switch points in this process and show that induction of TNF-alpha/NFkappaB, p53, and hypoxia driven gene expression programs precede a Sox4, Ctnnb1, and Wwtr1 driven switch towards alveolar type-1 cell fate. We show that epithelial cell plasticity can induce non-gradual transdifferentiation, involving intermediate progenitor cell states that may persist and promote disease if checkpoint signals for terminal differentiation are perturbed.

systems biology↗