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Article ; Online: Organ-Specific Endothelial Cell Differentiation and Impact of Microenvironmental Cues on Endothelial Heterogeneity.

Gifre-Renom, Laia / Daems, Margo / Luttun, Aernout / Jones, Elizabeth A V

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Endothelial cells throughout the body are heterogeneous, and this is tightly linked to the specific functions of organs and tissues. Heterogeneity is already determined from development onwards and ranges from arterial/venous specification to ... ...

Abstract	Endothelial cells throughout the body are heterogeneous, and this is tightly linked to the specific functions of organs and tissues. Heterogeneity is already determined from development onwards and ranges from arterial/venous specification to microvascular fate determination in organ-specific differentiation. Acknowledging the different phenotypes of endothelial cells and the implications of this diversity is key for the development of more specialized tissue engineering and vascular repair approaches. However, although novel technologies in transcriptomics and proteomics are facilitating the unraveling of vascular bed-specific endothelial cell signatures, still much research is based on the use of insufficiently specialized endothelial cells. Endothelial cells are not only heterogeneous, but their specialized phenotypes are also dynamic and adapt to changes in their microenvironment. During the last decades, strong collaborations between molecular biology, mechanobiology, and computational disciplines have led to a better understanding of how endothelial cells are modulated by their mechanical and biochemical contexts. Yet, because of the use of insufficiently specialized endothelial cells, there is still a huge lack of knowledge in how tissue-specific biomechanical factors determine organ-specific phenotypes. With this review, we want to put the focus on how organ-specific endothelial cell signatures are determined from development onwards and conditioned by their microenvironments during adulthood. We discuss the latest research performed on endothelial cells, pointing out the important implications of mimicking tissue-specific biomechanical cues in culture.
MeSH term(s)	Animals ; Cell Differentiation ; Cellular Microenvironment ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Organ Specificity ; Tissue Engineering
Language	English
Publishing date	2022-01-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23031477
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Organ-Specific Endothelial Cell Differentiation and Impact of Microenvironmental Cues on Endothelial Heterogeneity

Laia Gifre-Renom / Margo Daems / Aernout Luttun / Elizabeth A. V. Jones

International Journal of Molecular Sciences, Vol 23, Iss 1477, p

2022 Volume 1477

Abstract	Endothelial cells throughout the body are heterogeneous, and this is tightly linked to the specific functions of organs and tissues. Heterogeneity is already determined from development onwards and ranges from arterial/venous specification to microvascular fate determination in organ-specific differentiation. Acknowledging the different phenotypes of endothelial cells and the implications of this diversity is key for the development of more specialized tissue engineering and vascular repair approaches. However, although novel technologies in transcriptomics and proteomics are facilitating the unraveling of vascular bed-specific endothelial cell signatures, still much research is based on the use of insufficiently specialized endothelial cells. Endothelial cells are not only heterogeneous, but their specialized phenotypes are also dynamic and adapt to changes in their microenvironment. During the last decades, strong collaborations between molecular biology, mechanobiology, and computational disciplines have led to a better understanding of how endothelial cells are modulated by their mechanical and biochemical contexts. Yet, because of the use of insufficiently specialized endothelial cells, there is still a huge lack of knowledge in how tissue-specific biomechanical factors determine organ-specific phenotypes. With this review, we want to put the focus on how organ-specific endothelial cell signatures are determined from development onwards and conditioned by their microenvironments during adulthood. We discuss the latest research performed on endothelial cells, pointing out the important implications of mimicking tissue-specific biomechanical cues in culture.
Keywords	endothelial cell ; vascular development ; heterogeneity ; organ-specific signature ; phenotypic drift ; microenvironment ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	571
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The BMP Pathway in Blood Vessel and Lymphatic Vessel Biology.

Ponomarev, Ljuba C / Ksiazkiewicz, Jakub / Staring, Michael W / Luttun, Aernout / Zwijsen, An

International journal of molecular sciences

2021 Volume 22, Issue 12

Abstract: Bone morphogenetic proteins (BMPs) were originally identified as the active components in bone extracts that can induce ectopic bone formation. In recent decades, their key role has broadly expanded beyond bone physiology and pathology. Nowadays, the BMP ...

Abstract	Bone morphogenetic proteins (BMPs) were originally identified as the active components in bone extracts that can induce ectopic bone formation. In recent decades, their key role has broadly expanded beyond bone physiology and pathology. Nowadays, the BMP pathway is considered an important player in vascular signaling. Indeed, mutations in genes encoding different components of the BMP pathway cause various severe vascular diseases. Their signaling contributes to the morphological, functional and molecular heterogeneity among endothelial cells in different vessel types such as arteries, veins, lymphatic vessels and capillaries within different organs. The BMP pathway is a remarkably fine-tuned pathway. As a result, its signaling output in the vessel wall critically depends on the cellular context, which includes flow hemodynamics, interplay with other vascular signaling cascades and the interaction of endothelial cells with peri-endothelial cells and the surrounding matrix. In this review, the emerging role of BMP signaling in lymphatic vessel biology will be highlighted within the framework of BMP signaling in the circulatory vasculature.
MeSH term(s)	Animals ; Blood Vessels/metabolism ; Bone Morphogenetic Proteins/metabolism ; Humans ; Lymphatic Vessels/metabolism ; Signal Transduction
Chemical Substances	Bone Morphogenetic Proteins
Language	English
Publishing date	2021-06-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22126364
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Article ; Online: Multipotent adult progenitor cells grown under xenobiotic-free conditions support vascularization during wound healing.

Vaes, Bart / Van Houtven, Ellen / Caluwé, Ellen / Luttun, Aernout

Stem cell research & therapy

2020 Volume 11, Issue 1, Page(s) 389

Abstract: Background: Cell therapy has been evaluated pre-clinically and clinically as a means to improve wound vascularization and healing. While translation of this approach to clinical practice ideally requires the availability of clinical grade xenobiotic- ... ...

Abstract	Background: Cell therapy has been evaluated pre-clinically and clinically as a means to improve wound vascularization and healing. While translation of this approach to clinical practice ideally requires the availability of clinical grade xenobiotic-free cell preparations, studies proving the pre-clinical efficacy of the latter are mostly lacking. Here, the potential of xenobiotic-free human multipotent adult progenitor cell (XF-hMAPC®) preparations to promote vascularization was evaluated. Methods: The potential of XF-hMAPC cells to support blood vessel formation was first scored in an in vivo Matrigel assay in mice. Next, a dose-response study was performed with XF-hMAPC cells in which they were tested for their ability to support vascularization and (epi) dermal healing in a physiologically relevant splinted wound mouse model. Results: XF-hMAPC cells supported blood vessel formation in Matrigel by promoting the formation of mature (smooth muscle cell-coated) vessels. Furthermore, XF-hMAPC cells dose-dependently improved wound vascularization associated with increasing wound closure and re-epithelialization, granulation tissue formation, and dermal collagen organization. Conclusions: Here, we demonstrated that the administration of clinical-grade XF-hMAPC cells in mice represents an effective approach for improving wound vascularization and healing that is readily applicable for translation in humans.
MeSH term(s)	Adult Stem Cells ; Animals ; Granulation Tissue ; Mice ; Neovascularization, Physiologic ; Re-Epithelialization ; Wound Healing
Language	English
Publishing date	2020-09-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2548671-8
ISSN	1757-6512 ; 1757-6512
ISSN (online)	1757-6512
ISSN	1757-6512
DOI	10.1186/s13287-020-01912-3
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Article ; Online: Multipotent adult progenitor cells grown under xenobiotic-free conditions support vascularization during wound healing

Bart Vaes / Ellen Van Houtven / Ellen Caluwé / Aernout Luttun

Stem Cell Research & Therapy, Vol 11, Iss 1, Pp 1-

2020 Volume 14

Abstract: Abstract Background Cell therapy has been evaluated pre-clinically and clinically as a means to improve wound vascularization and healing. While translation of this approach to clinical practice ideally requires the availability of clinical grade ... ...

Abstract	Abstract Background Cell therapy has been evaluated pre-clinically and clinically as a means to improve wound vascularization and healing. While translation of this approach to clinical practice ideally requires the availability of clinical grade xenobiotic-free cell preparations, studies proving the pre-clinical efficacy of the latter are mostly lacking. Here, the potential of xenobiotic-free human multipotent adult progenitor cell (XF-hMAPC®) preparations to promote vascularization was evaluated. Methods The potential of XF-hMAPC cells to support blood vessel formation was first scored in an in vivo Matrigel assay in mice. Next, a dose-response study was performed with XF-hMAPC cells in which they were tested for their ability to support vascularization and (epi) dermal healing in a physiologically relevant splinted wound mouse model. Results XF-hMAPC cells supported blood vessel formation in Matrigel by promoting the formation of mature (smooth muscle cell-coated) vessels. Furthermore, XF-hMAPC cells dose-dependently improved wound vascularization associated with increasing wound closure and re-epithelialization, granulation tissue formation, and dermal collagen organization. Conclusions Here, we demonstrated that the administration of clinical-grade XF-hMAPC cells in mice represents an effective approach for improving wound vascularization and healing that is readily applicable for translation in humans.
Keywords	Stem cells ; Xenobiotic-free culture media ; Wound healing ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The BMP Pathway in Blood Vessel and Lymphatic Vessel Biology

Ljuba C. Ponomarev / Jakub Ksiazkiewicz / Michael W. Staring / Aernout Luttun / An Zwijsen

International Journal of Molecular Sciences, Vol 22, Iss 6364, p

2021 Volume 6364

Abstract	Bone morphogenetic proteins (BMPs) were originally identified as the active components in bone extracts that can induce ectopic bone formation. In recent decades, their key role has broadly expanded beyond bone physiology and pathology. Nowadays, the BMP pathway is considered an important player in vascular signaling. Indeed, mutations in genes encoding different components of the BMP pathway cause various severe vascular diseases. Their signaling contributes to the morphological, functional and molecular heterogeneity among endothelial cells in different vessel types such as arteries, veins, lymphatic vessels and capillaries within different organs. The BMP pathway is a remarkably fine-tuned pathway. As a result, its signaling output in the vessel wall critically depends on the cellular context, which includes flow hemodynamics, interplay with other vascular signaling cascades and the interaction of endothelial cells with peri-endothelial cells and the surrounding matrix. In this review, the emerging role of BMP signaling in lymphatic vessel biology will be highlighted within the framework of BMP signaling in the circulatory vasculature.
Keywords	BMP ; BMP pathway fine-tuning ; lymphatic vessel biology ; mechano-transduction ; vascular malformations ; signaling cross-talk ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Pericyte loss initiates microvascular dysfunction in the development of diastolic dysfunction.

Simmonds, Steven J / Grootaert, Mandy O J / Cuijpers, Ilona / Carai, Paolo / Geuens, Nadeche / Herwig, Melissa / Baatsen, Pieter / Hamdani, Nazha / Luttun, Aernout / Heymans, Stephane / Jones, Elizabeth A V

European heart journal open

2023 Volume 4, Issue 1, Page(s) oead129

Abstract: Aims: Microvascular dysfunction has been proposed to drive heart failure with preserved ejection fraction (HFpEF), but the initiating molecular and cellular events are largely unknown. Our objective was to determine when microvascular alterations in ... ...

Abstract	Aims: Microvascular dysfunction has been proposed to drive heart failure with preserved ejection fraction (HFpEF), but the initiating molecular and cellular events are largely unknown. Our objective was to determine when microvascular alterations in HFpEF begin, how they contribute to disease progression, and how pericyte dysfunction plays a role herein. Methods and results: Microvascular dysfunction, characterized by inflammatory activation, loss of junctional barrier function, and altered pericyte-endothelial crosstalk, was assessed with respect to the development of cardiac dysfunction, in the Zucker fatty and spontaneously hypertensive (ZSF1) obese rat model of HFpEF at three time points: 6, 14, and 21 weeks of age. Pericyte loss was the earliest and strongest microvascular change, occurring before prominent echocardiographic signs of diastolic dysfunction were present. Pericytes were shown to be less proliferative and had a disrupted morphology at 14 weeks in the obese ZSF1 animals, who also exhibited an increased capillary luminal diameter and disrupted endothelial junctions. Microvascular dysfunction was also studied in a mouse model of chronic reduction in capillary pericyte coverage ( Conclusion: We propose pericytes are important for maintaining endothelial cell function, where loss of pericytes enhances the reactivity of endothelial cells to inflammatory signals and promotes microvascular dysfunction, thereby accelerating the development of HFpEF.
Language	English
Publishing date	2023-12-09
Publishing country	England
Document type	Journal Article
ISSN	2752-4191
ISSN (online)	2752-4191
DOI	10.1093/ehjopen/oead129
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Article ; Online: Stimulation of the atypical chemokine receptor 3 (ACKR3) by a small-molecule agonist attenuates fibrosis in a preclinical liver but not lung injury model.

Van Loy, Tom / De Jonghe, Steven / Castermans, Karolien / Dheedene, Wouter / Stoop, Reinout / Verschuren, Lars / Versele, Matthias / Chaltin, Patrick / Luttun, Aernout / Schols, Dominique

Cellular and molecular life sciences : CMLS

2022 Volume 79, Issue 6, Page(s) 293

Abstract: Atypical chemokine receptor 3 (ACKR3, formerly CXC chemokine receptor 7) is a G protein-coupled receptor that recruits β-arrestins, but is devoid of functional G protein signaling after receptor stimulation. In preclinical models of liver and lung ... ...

Abstract	Atypical chemokine receptor 3 (ACKR3, formerly CXC chemokine receptor 7) is a G protein-coupled receptor that recruits β-arrestins, but is devoid of functional G protein signaling after receptor stimulation. In preclinical models of liver and lung fibrosis, ACKR3 was previously shown to be upregulated after acute injury in liver sinusoidal and pulmonary capillary endothelial cells, respectively. This upregulation was linked with a pro-regenerative and anti-fibrotic role for ACKR3. A recently described ACKR3-targeting small molecule agonist protected mice from isoproterenol-induced cardiac fibrosis. Here, we aimed to evaluate its protective role in preclinical models of liver and lung fibrosis. After confirming its in vitro pharmacological activity (i.e., ACKR3-mediated β-arrestin recruitment and receptor binding), in vivo administration of this ACKR3 agonist led to increased mouse CXCL12 plasma levels, indicating in vivo interaction of the agonist with ACKR3. Whereas twice daily in vivo administration of the ACKR3 agonist lacked inhibitory effect on bleomycin-induced lung fibrosis, it had a modest, but significant anti-fibrotic effect in the carbon tetrachloride (CCl
MeSH term(s)	Animals ; Mice ; beta-Arrestins/metabolism ; Chemokine CXCL12/genetics ; Chemokine CXCL12/metabolism ; Chemokine CXCL12/pharmacology ; Endothelial Cells/metabolism ; Liver/metabolism ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/drug therapy ; Receptors, CXCR/chemistry ; Receptors, CXCR/genetics ; Receptors, CXCR/metabolism
Chemical Substances	beta-Arrestins ; Chemokine CXCL12 ; Receptors, CXCR ; Cmkor1 protein, mouse
Language	English
Publishing date	2022-05-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04317-y
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Article ; Online: Arteriovenous Fistulae in Chronic Kidney Disease and the Heart: Physiological, Histological, and Transcriptomic Characterization of a Novel Rat Model.

Van den Eynde, Jef / Jacquemyn, Xander / Cloet, Nicolas / Noé, Dries / Gillijns, Hilde / Lox, Marleen / Gsell, Willy / Himmelreich, Uwe / Luttun, Aernout / McCutcheon, Keir / Janssens, Stefan / Oosterlinck, Wouter

Journal of the American Heart Association

2022 Volume 11, Issue 20, Page(s) e027593

Abstract: Background Arteriovenous fistulae (AVFs) are the gold standard for vascular access in those requiring hemodialysis but may put an extra hemodynamic stress on the cardiovascular system. The complex interactions between the heart, kidney, and AVFs remain ... ...

Abstract	Background Arteriovenous fistulae (AVFs) are the gold standard for vascular access in those requiring hemodialysis but may put an extra hemodynamic stress on the cardiovascular system. The complex interactions between the heart, kidney, and AVFs remain incompletely understood. Methods and Results We characterized a novel rat model of five-sixths partial nephrectomy (NX) and AVFs. NX induced increases in urea, creatinine, and hippuric acid. The addition of an AVF (AVF+NX) further increased urea and a number of uremic toxins such as trimethylamine N-oxide and led to increases in cardiac index, left and right ventricular volumes, and right ventricular mass. Plasma levels of uremic toxins correlated well with ventricular morphology and function. Heart transcriptomes identified altered expression of 8 genes following NX and 894 genes following AVF+NX, whereas 290 and 1431 genes were altered in the kidney transcriptomes, respectively. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis revealed gene expression changes related to cell division and immune activation in both organs, suppression of ribosomes and transcriptional activity in the heart, and altered renin-angiotensin signaling as well as chronodisruption in the kidney. All except the latter were worsened in AVF+NX compared with NX. Conclusions Inflammation and organ dysfunction in chronic kidney disease are exacerbated following AVF creation. Furthermore, our study provides important information for the discovery of novel biomarkers and therapeutic targets in the management of cardiorenal syndrome.
MeSH term(s)	Rats ; Animals ; Arteriovenous Shunt, Surgical ; Transcriptome ; Creatinine ; Renin ; Renal Dialysis/methods ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/genetics ; Arteriovenous Fistula ; Biomarkers ; Angiotensins ; Urea ; Kidney Failure, Chronic/therapy
Chemical Substances	Creatinine (AYI8EX34EU) ; Renin (EC 3.4.23.15) ; Biomarkers ; Angiotensins ; Urea (8W8T17847W)
Language	English
Publishing date	2022-10-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.027593
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Article ; Online: Peer review: (r)evolution needed.

Sipido, Karin R / Gal, Diane / Luttun, Aernout / Janssens, Stefan / Sampaolesi, Maurilio / Holvoet, Paul

Cardiovascular research

2017 Volume 113, Issue 13, Page(s) e54–e56

MeSH term(s)	Editorial Policies ; Humans ; Information Dissemination ; Journal Impact Factor ; Peer Review, Research/standards ; Periodicals as Topic/standards ; Quality Control
Language	English
Publishing date	2017-12-04
Publishing country	England
Document type	Editorial
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvx191
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Zs.A 565: Show issues

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ab Jg. 2022: Lesesaal (EG)

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