Identifying main interactions in marine predator-prey networks of the Bay of Biscay

Identifying the role that environmental factors and biotic interactions play in species distribution can be essential to better understand and predict how ecosystems will respond to changing environmental conditions. This study aimed at disentangling the assemblage of the pelagic predator–prey community by identifying interspecific associations and their main drivers. For this purpose, we applied the joint species distribution modelling approach, JSDM, to the co-occurrence patterns of both prey and top predator communities obtained from JUVENA surveys during 2013–2016 in the Bay of Biscay. Results showed that the co-occurrence patterns of top predators and prey were driven by a combination of environmental and biotic factors, which highlighted the importance of considering both components to fully understand the community structure. In addition, results also revealed that many biotic interactions, such as schooling in prey (e.g. anchovy–sardine), local enhancement/facilitation in predators (e.g. Cory’s shearwater–fin whale), and predation between predator–prey species (e.g. northern gannet–horse mackerel), were led by positive associations, although predator avoidance behaviour was also suggested between negatively associated species (e.g. striped dolphin–blue whiting). The identification of interspecific associations can therefore provide insights on the functioning of predators–prey network and help advance towards an ecosystem-based managementThis research was funded by the Basque Government (Department of Agriculture, Fishing, and Food Policy) and the Spanish Ministry of Economy, Industry, and Competitiveness through the CHALLENGES project (CTM2013-47032-R). A. Astarloa has benefited from a Basque Government scholarship (PRE_2016_1_0134) and M. Louzao was funded by the Ramo´n y Cajal (RYC-2012-09897) researcher programme of the Spanish Ministry of Economy, Industry, and Competitiveness. JUVENA survey series was sponsored since 2003 by the “Viceconsejerı´a de Agricultura, Pesca y Polı´ticas Alimentarias—Departamento de Desarrollo Econo´mico y Competitividad” of the Basque Government and the “Secretarı´a General de Pesca, Ministerio de Agricultura, Alimentacio´ n y Medio Ambiente” of the Spanish Government

Endothelial loss of Fzd5 stimulates PKC/Ets1-mediated transcription of Angpt2 and Flt1

Aims: Formation of a functional vascular system is essential and its formation is a highly regulated process initiated during embryogenesis, which continues to play important roles throughout life in both health and disease. In previous studies, Fzd5 was shown to be critically involved in this process and here we investigated the molecular mechanism by which endothelial loss of this receptor attenuates angiogenesis. Methods and results: Using short interference RNA-mediated loss-of-function assays, the function and mechanism of signaling via Fzd5 was studied in human endothelial cells (ECs). Our findings indicate that Fzd5 signaling promotes neovessel formation in vitro in a collagen matrix-based 3D co-culture of primary vascular cells. Silencing of Fzd5 reduced EC proliferation, as a result of G0/G1 cell cycle arrest, and decreased cell migration. Furthermore, Fzd5 knockdown resulted in enhanced expression of the factors Angpt2 and Flt1, which are mainly known for their destabilizing effects on the vasculature. In Fzd5-silenced ECs, Angpt2 and Flt1 upregulation was induced by enhanced PKC signaling, without the involvement of canonical Wnt signaling, non-canonical Wnt/Ca2+-mediated activation of NFAT, and non-canonical Wnt/PCP-mediated activation of JNK. We demonstrated that PKC-induced transcription of Angpt2 and Flt1 involved the transcription factor Ets1. Conclusions: The current study demonstrates a pro-angiogenic role of Fzd5, which was shown to be involved in endothelial tubule formation, cell cycle progression and migration, and partly does so by repression of PKC/Ets1-mediated transcription of Flt1 and Angpt2

Use of Biosensors as Alternatives to Current Regulatory Methods for Marine Biotoxins

Marine toxins are currently monitored by means of a bioassay that requires the use of many mice, which poses a technical and ethical problem in many countries. With the exception of domoic acid, there is a legal requirement for the presence of other toxins (yessotoxin, saxitoxin and analogs, okadaic acid and analogs, pectenotoxins and azaspiracids) in seafood to be controlled by bioassay, but other toxins, such as palytoxin, cyclic imines, ciguatera and tetrodotoxin are potentially present in European food and there are no legal requirements or technical approaches available to identify their presence. The need for alternative methods to the bioassay is clearly important, and biosensors have become in recent years a feasible alternative to animal sacrifice. This review will discuss the advantages and disadvantages of using biosensors as alternatives to animal assays for marine toxins, with particular focus on surface plasmon resonance (SPR) technology

Extracellular matrix analysis of human renal arteries in both quiescent and active vascular state

In vascular tissue engineering strategies, the addition of vascular-specific extracellular matrix (ECM) components may better mimic the in vivo microenvironment and potentially enhance cell–matrix interactions and subsequent tissue growth. For this purpose, the exact composition of the human vascular ECM first needs to be fully characterized. Most research has focused on characterizing ECM components in mature vascular tissue; however, the developing fetal ECM matches the active environment required in vascular tissue engineering more closely. Consequently, we characterized the ECM protein composition of active (fetal) and quiescent (mature) renal arteries using a proteome analysis of decellularized tissue. The obtained human fetal renal artery ECM proteome dataset contains higher levels of 15 ECM proteins versus the mature renal artery ECM proteome, whereas 16 ECM proteins showed higher levels in the mature tissue compared to fetal. Elastic EC

Distribution maps of cetacean and seabird populations in the North‐East Atlantic

1. Distribution maps of cetaceans and seabirds at basin and monthly scales are needed for conservation and marine management. These are usually created from standardized and systematic aerial and vessel surveys, with recorded animal den- sities interpolated across study areas. However, distribution maps at basin and monthly scales have previously not been possible because individual surveys have restricted spatial and temporal coverage. 2. This study develops an alternative approach consisting of: (a) collating diverse survey data to maximize spatial and temporal coverage, (b) using detection func- tions to estimate variation in the surface area covered (km2) among these surveys, standardizing measurements of effort and animal densities, and (c) developing species distribution models (SDM) that overcome issues with heterogeneous and uneven coverage. 3. 2.68 million km of survey data in the North-East Atlantic between 1980 and 2018 were collated and standardized. SDM using Generalized Linear Models and General Estimating Equations in a hurdle approach were developed. Distribution maps were then created for 12 cetacean and 12 seabird species at 10 km and monthly resolution. Qualitative and quantitative assessment indicated good model performance. 4. Synthesis and applications. This study provides the largest ever collation and standardization of diverse survey data for cetaceans and seabirds, and the most comprehensive distribution maps of these taxa in the North-East Atlantic. These distribution maps have numerous applications including the identification of im- portant areas needing protection, and the quantification of overlap between vul- nerable species and anthropogenic activities. This study demonstrates how the analysis of existing and diverse survey data can meet conservation and marine management needs.Versión del editor4,7

The extracellular matrix and angiogenesis : Two aspects that define cardiovascular health and disease

Two aspects that define cardiovascular health and disease are the extracellular matrix and angiogenesis. The extracellular matrix   During development, ECM remodeling accompanies the formation of distinct tissues. This impact makes the ECM an ideal scaffold to mimic in tissue constructs for 3D cell models or for transplantation. Here, selection of the appropriate matrix is crucial, as it will profoundly affect cell behavior. In order to this, it is necessary to fully characterize the unique ECM composition of specific tissues during development. In this thesis, the differences between the fetal and mature human ECM was characterized in both the kidney and renal artery. This comparison revealed a specific ECM niche during renal development. This is valuable knowledge for improving current constructs to better mimic renal tissue. A critical difference found is the abundance of EMILIN1 in the fetal ECM of both tissues. This thesis shows that EMILIN1 is important for the degree of renal cell adhesion and thus has potential for the use in renal constructs.   Dysregulation of ECM remodeling is associated with many diseases, including dilated cardiomyopathy (DCM). Myocardial fibrosis is a major feature of DCM and therefore it is inevitable that complex ECM remodeling is involved. This thesis describes the changes in ECM composition and associated remodeling pathways during DCM and it is likely that among these components are novel diagnostic markers or therapeutic targets.   Angiogenesis  VE-cadherin is indispensable for proper angiogenesis, as the amount of VE-cadherin at the plasma membrane is directly linked to endothelial barrier function. This bioavailability is regulated by endocytosis; however, little is known about the exact contribution of endocytic regulators. This thesis reports two novel proteins involved in regulating endocytosis during angiogenesis: CMTM3 and CMTM4. These proteins are involved in regulating the bioavailability of VE-cadherin on the plasma membrane by either stimulating the uptake from or recycling to the cell membrane. This novel fundamental finding holds promising therapeutic perspectives for angiogenic diseases. Dysregulation of angiogenesis contributes to many disorders, including chronic kidney disease (CKD). Genetic alterations have been linked to CKD and recent GWAS studies identified ±100 SNPs associated with CKD traits. Unfortunately, ±90% of these SNPs lie within the non-coding genome, including DNA regulatory regions (DREs). This thesis has linked DREs containing a CKD-associated SNP with their target genes using 4C-sequencing. These results further our understanding of the molecular mechanisms underlying CKD that can aid in the development of future biomarkers or therapies

The extracellular matrix and angiogenesis : Two aspects that define cardiovascular health and disease

Two aspects that define cardiovascular health and disease are the extracellular matrix and angiogenesis. The extracellular matrix   During development, ECM remodeling accompanies the formation of distinct tissues. This impact makes the ECM an ideal scaffold to mimic in tissue constructs for 3D cell models or for transplantation. Here, selection of the appropriate matrix is crucial, as it will profoundly affect cell behavior. In order to this, it is necessary to fully characterize the unique ECM composition of specific tissues during development. In this thesis, the differences between the fetal and mature human ECM was characterized in both the kidney and renal artery. This comparison revealed a specific ECM niche during renal development. This is valuable knowledge for improving current constructs to better mimic renal tissue. A critical difference found is the abundance of EMILIN1 in the fetal ECM of both tissues. This thesis shows that EMILIN1 is important for the degree of renal cell adhesion and thus has potential for the use in renal constructs.   Dysregulation of ECM remodeling is associated with many diseases, including dilated cardiomyopathy (DCM). Myocardial fibrosis is a major feature of DCM and therefore it is inevitable that complex ECM remodeling is involved. This thesis describes the changes in ECM composition and associated remodeling pathways during DCM and it is likely that among these components are novel diagnostic markers or therapeutic targets.   Angiogenesis  VE-cadherin is indispensable for proper angiogenesis, as the amount of VE-cadherin at the plasma membrane is directly linked to endothelial barrier function. This bioavailability is regulated by endocytosis; however, little is known about the exact contribution of endocytic regulators. This thesis reports two novel proteins involved in regulating endocytosis during angiogenesis: CMTM3 and CMTM4. These proteins are involved in regulating the bioavailability of VE-cadherin on the plasma membrane by either stimulating the uptake from or recycling to the cell membrane. This novel fundamental finding holds promising therapeutic perspectives for angiogenic diseases. Dysregulation of angiogenesis contributes to many disorders, including chronic kidney disease (CKD). Genetic alterations have been linked to CKD and recent GWAS studies identified ±100 SNPs associated with CKD traits. Unfortunately, ±90% of these SNPs lie within the non-coding genome, including DNA regulatory regions (DREs). This thesis has linked DREs containing a CKD-associated SNP with their target genes using 4C-sequencing. These results further our understanding of the molecular mechanisms underlying CKD that can aid in the development of future biomarkers or therapies

The extracellular matrix and angiogenesis : Two aspects that define cardiovascular health and disease

Two aspects that define cardiovascular health and disease are the extracellular matrix and angiogenesis. The extracellular matrix   During development, ECM remodeling accompanies the formation of distinct tissues. This impact makes the ECM an ideal scaffold to mimic in tissue constructs for 3D cell models or for transplantation. Here, selection of the appropriate matrix is crucial, as it will profoundly affect cell behavior. In order to this, it is necessary to fully characterize the unique ECM composition of specific tissues during development. In this thesis, the differences between the fetal and mature human ECM was characterized in both the kidney and renal artery. This comparison revealed a specific ECM niche during renal development. This is valuable knowledge for improving current constructs to better mimic renal tissue. A critical difference found is the abundance of EMILIN1 in the fetal ECM of both tissues. This thesis shows that EMILIN1 is important for the degree of renal cell adhesion and thus has potential for the use in renal constructs.   Dysregulation of ECM remodeling is associated with many diseases, including dilated cardiomyopathy (DCM). Myocardial fibrosis is a major feature of DCM and therefore it is inevitable that complex ECM remodeling is involved. This thesis describes the changes in ECM composition and associated remodeling pathways during DCM and it is likely that among these components are novel diagnostic markers or therapeutic targets.   Angiogenesis  VE-cadherin is indispensable for proper angiogenesis, as the amount of VE-cadherin at the plasma membrane is directly linked to endothelial barrier function. This bioavailability is regulated by endocytosis; however, little is known about the exact contribution of endocytic regulators. This thesis reports two novel proteins involved in regulating endocytosis during angiogenesis: CMTM3 and CMTM4. These proteins are involved in regulating the bioavailability of VE-cadherin on the plasma membrane by either stimulating the uptake from or recycling to the cell membrane. This novel fundamental finding holds promising therapeutic perspectives for angiogenic diseases. Dysregulation of angiogenesis contributes to many disorders, including chronic kidney disease (CKD). Genetic alterations have been linked to CKD and recent GWAS studies identified ±100 SNPs associated with CKD traits. Unfortunately, ±90% of these SNPs lie within the non-coding genome, including DNA regulatory regions (DREs). This thesis has linked DREs containing a CKD-associated SNP with their target genes using 4C-sequencing. These results further our understanding of the molecular mechanisms underlying CKD that can aid in the development of future biomarkers or therapies

Characteristic adaptations of the extracellular matrix in dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is a relatively common heart muscle disease characterized by the dilation and thinning of the left ventricle accompanied with left ventricular systolic dysfunction. Myocardial fibrosis is a major feature in DCM and therefore it is inevitable that corresponding extracellular matrix (ECM) changes are involved in DCM onset and progression. Increasing our understanding of how ECM adaptations are involved in DCM could be important for the development of future interventions. This review article discusses the molecular adaptations in ECM composition and structure that have been reported in both animal and human studies of DCM. Furthermore, we provide a transcriptome-based catalogue of ECM genes that are associated with DCM, generated by using NCBI Gene Expression Omnibus database sets for DCM. Based on this in silico analysis, many novel ECM components involved in DCM are identified and discussed in this review. With the information gathered, we propose putative pathways of ECM adaptations in onset and progression of DCM

Characteristic adaptations of the extracellular matrix in dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is a relatively common heart muscle disease characterized by the dilation and thinning of the left ventricle accompanied with left ventricular systolic dysfunction. Myocardial fibrosis is a major feature in DCM and therefore it is inevitable that corresponding extracellular matrix (ECM) changes are involved in DCM onset and progression. Increasing our understanding of how ECM adaptations are involved in DCM could be important for the development of future interventions. This review article discusses the molecular adaptations in ECM composition and structure that have been reported in both animal and human studies of DCM. Furthermore, we provide a transcriptome-based catalogue of ECM genes that are associated with DCM, generated by using NCBI Gene Expression Omnibus database sets for DCM. Based on this in silico analysis, many novel ECM components involved in DCM are identified and discussed in this review. With the information gathered, we propose putative pathways of ECM adaptations in onset and progression of DCM