Biology subjects

Merten, M.

Publications and source records attributed to Merten, M..

5 recordsLinked to original sources

bioRxiv2026

Autonomous sampling and eDNA metabarcoding for offshore biodiversity monitoring: a pilot study around an FPSO in the Southwestern Atlantic

Characterizing biodiversity around offshore infrastructure is necessary to assess possible influences of industrial activities on marine communities and distinguish persistent ecological change from short-term variability. Combining environmental DNA (eDNA) metabarcoding with autonomous sampling offers a way to expand biological, spatial and temporal coverage while reducing dependence on crewed field operations. We evaluated this approach around a floating production, storage and offloading unit (FPSO) in the Santos Basin, Brazil, to establish an initial biodiversity reference and inform subsequent monitoring. A third-generation Environmental Sample Processor integrated into the W Tupan II uncrewed surface vessel enabled autonomous water sampling at coastal sites, transit locations and the FPSO area, yielding 64 biological samples. We used mitochondrial 12S and 16S metabarcoding to assess taxonomic diversity, sampling completeness and spatial and short-term temporal variation. Around the FPSO, 47 samples from 21 points detected 34 species with 12S and 28 with 16S, representing 74.3% and 65.4% of the respective estimated species richness. Local analyses showed weak radial differentiation across 300-1,500 m around the FPSO, with no near-far taxonomic indicators remaining significant after multiple-testing corrections. Samples collected at the same point approximately 1-2 h apart were almost as dissimilar as samples from different points, whereas technical replicates of post-extraction processing closely matched their source DNA profiles. Taxon turnover accounted for approximately 73% and 80% of temporal Jaccard dissimilarity for 12S and 16S, respectively. Regional analyses recovered a coastal-offshore compositional contrast, with geography and sampling date jointly represented. This pilot supports autonomous eDNA sampling as an operational approach to offshore biodiversity monitoring. The findings favour repeated sampling across campaigns to distinguish transient detections from recurrent patterns and persistent compositional changes.

molecular biology↗

bioRxiv2025

STAT3 expression is reduced in cardiac pericytes in HFpEF and its loss reduces cellular adhesion and induces pericyte senescence

Heart failure with preserved ejection fraction (HFpEF) accounts for half of heart failure cases and is characterised by reduced pericyte coverage. While the contributions of other cardiac cell types to HFpEF are well-studied, the role of pericytes remains less understood. Using murine single-nucleus RNA sequencing to study cardiac pericytes in HFpEF, we identified reduced STAT3 expression as a hallmark of HFpEF pericytes. Mechanistic studies in vitro revealed that STAT3 deletion induces cellular senescence and impairs pericyte adhesion, recapitulating HFpEF-like characteristics. These findings suggest that STAT3 is crucial for maintaining pericyte homeostasis and highlight its reduction as a potential driver of pericyte loss, a defining feature of HFpEF.

cell biology↗

bioRxiv2023

Age-dependent RGS5 loss in pericytes induces cardiac dysfunction and fibrosis in the heart

BackgroundPericytes are capillary-associated mural cells involved in the maintenance and stability of the vascular network. Although ageing is one of the main risk factors for cardiovascular disease, the consequences of ageing on cardiac pericytes are unknown. MethodsIn this study, we have combined single-nucleus RNA sequencing and histological analysis to determine the effects of ageing on cardiac pericytes. Furthermore, we have conducted in vivo and in vitro analysis of Regulator of G protein signalling 5 (RGS5) loss of function and finally have performed pericytes-fibroblasts co-culture studies to understand the effect of RGS5 deletion in pericytes on the neighbouring fibroblasts. ResultsAgeing reduced the pericyte area and capillary coverage in the murine heart. Single nucleus RNA sequencing analysis further revealed that the expression of Rgs5 was reduced in cardiac pericytes from aged mice. In vivo and in vitro studies showed that the deletion of RGS5 impaired cardiac function, fibrosis, and induced morphological changes and a pro-fibrotic gene expression signature in pericytes characterized by the expression of different extracellular matrix components and growth factors e.g. TGFB2 and PDGFB. Indeed, culturing fibroblasts with the supernatant of RGS5 deficient pericytes induced their activation as evidenced by the increased expression of smooth muscle actin in a TGF{beta}2-dependent mechanism. ConclusionsOur results have identified RGS5 as a crucial regulator of pericyte function during cardiac ageing. The deletion of RGS5 causes cardiac dysfunction and induces myocardial fibrosis, one of the hallmarks of cardiac ageing.

physiology↗

bioRxiv2021

Human Sex Matters: Y-linked lysine demethylase 5D drives accelerated male osteogenic differentiation

Female sex is increasingly associated to a loss of bone mass during aging and an increased risk for fractures developing nonunion. Hormonal factors and cell-intrinsic mechanisms are suggested to drive these sexual dimorphisms, although underlying molecular mechanisms are still a matter of debate. Here, we observed a decreased capacity of calvarial bone recovery in female rats and a profound sexually dimorphic osteogenic differentiation human adult neural crest-derived stem cells (NCSCs). Next to an elevated expression of pro-osteogenic regulators, global trancriptomics revealed Lysine Demethylase 5D (KDM5D) to be highly upregulated in differentiating male NCSCs. Loss of function by siRNA or pharmacological inhibition of KDM5D significantly reduced the osteogenic differentiation capacity of male NCSCs. In summary, we demonstrate craniofacial osteogenic differentiation to be sexually dimorphic with the expression of KDM5D as a prerequisite for accelerated male osteogenic differentiation, emphasizing the analysis of sex-specific differences as a crucial parameter for treating bone defects.

cell biology↗

bioRxiv2019

Identification of a human adult cardiac stem cell population with neural crest origin

Cardiovascular diseases are the major cause of death worldwide, emphasizing the necessity to better understand adult human cardiac cell biology and development. Although the adult heart was considered as a terminally differentiated organ, rare populations of cardiac stem cells (CSCs) have been described so far, with their developmental origin and endogenous function still being a matter of debate.\n\nHere, we identified a Nestin+/S100+/CD105+/Sca1+/cKit- population of CSCs in the myocardium of the adult human heart auricle. Isolated cells showed expression of characteristic neural crest-derived stem cell (NCSC) markers and kept their genetic stability during cultivation in vitro. Cultivated hCSCs efficiently gave rise to functional, beating cardiomyocytes, osteoblasts, adipocytes and neurons. Global transcriptome analysis via RNAseq showed a high similarity between the expression profiles of Nestin+/S100+/CD105+/Sca1+/cKit- hCSCs and adult human NCSCs from the nasal cavity (inferior turbinate stem cells, ITSCs). In detail, 88.1 % of all genes were significantly expressed in both stem cell populations particularly including common NCSC-markers. Based on these observations, we suggest a similar developmental origin of both stem cell populations.\n\nIn summary, we identified a human adult cardiac stem cell population with neural crest-origin, which may also contribute to endogenous cardiac tissue homeostasis and tissue repair in vivo.

cell biology↗