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Molecular Research in Vascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 March 2024) | Viewed by 2321

Special Issue Editor


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Guest Editor
Department of Obstetrics and Gynecology, Institute of Women’s Medical Life Science, Placenta-Derived Stem Cell and Genomic Research Lab, Yonsei University Health System, Yonsei University College of Medicine, Seoul 03722, Republic of Korea
Interests: angiogenesis; lymphangiogenesis; endothelial progenitor cell; endothelial cells; stem cell differentiation; molecular cell biology; signal transduction; vascular disease; pregnancy complication; tumor metastasis

Special Issue Information

Dear Colleagues,

The lymphatic and blood circulatory systems are essential to maintaining human health. These vessels are made up of lymphatic and blood endothelial cells, respectively. Blood endothelial cells make up the inner lining of blood vessels and are in charge of a number of crucial tasks, such as controlling blood clotting, promoting inflammation or anti-inflammatory responses, and making it easier for nutrients and oxygen to reach the tissues around the bloodstream. The walls of lymphatic vessels, which create a parallel network to the blood vessels, are lined by a particular type of cell called lymphatic endothelial cells. They are essential for preserving fluid balance, immunological responses, and the transport of various substances within the lymphatic system. Endothelial cell dysfunction or developmental malformation can cause a number of illnesses, such as atherosclerosis, cardiovascular disease, pulmonary disease, diabetes mellitus, sepsis, hypertension, thrombosis, inflammation, aging, lymphedema, cancer metastasis, and immunological problems. Understanding the relationship between the causes of vascular diseases and the molecular mechanisms within endothelial cells is essential for maintaining vascular health and preventing related diseases. This Special Issue, “Molecular Research in Vascular Disease”, welcomes original research and review articles in the field, with a focus on the molecular and mechanistic basis for the vascular disease, and therapeutics.

Dr. Yong-sun Maeng
Guest Editor

Manuscript Submission Information

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Keywords

  • angiogenesis
  • lymphangiogenesis
  • blood endothelial cell
  • lymphatic endothelial cell
  • umbilical cord blood
  • progenitor cell
  • pregnancy complication
  • vascular disease
  • stem cell differentiation

Published Papers (2 papers)

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Research

23 pages, 4534 KiB  
Article
Renal Endothelial Single-Cell Transcriptomics Reveals Spatiotemporal Regulation and Divergent Roles of Differential Gene Transcription and Alternative Splicing in Murine Diabetic Nephropathy
by Alex-Xianghua Zhou, Marie Jeansson, Liqun He, Leif Wigge, Pernilla Tonelius, Ramesh Tati, Linda Cederblad, Lars Muhl, Martin Uhrbom, Jianping Liu, Anna Björnson Granqvist, Lilach O. Lerman, Christer Betsholtz and Pernille B. L. Hansen
Int. J. Mol. Sci. 2024, 25(8), 4320; https://doi.org/10.3390/ijms25084320 - 13 Apr 2024
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Abstract
Endothelial cell (EC) injury is a crucial contributor to the progression of diabetic kidney disease (DKD), but the specific EC populations and mechanisms involved remain elusive. Kidney ECs (n = 5464) were collected at three timepoints from diabetic BTBRob/ob mice and [...] Read more.
Endothelial cell (EC) injury is a crucial contributor to the progression of diabetic kidney disease (DKD), but the specific EC populations and mechanisms involved remain elusive. Kidney ECs (n = 5464) were collected at three timepoints from diabetic BTBRob/ob mice and non-diabetic littermates. Their heterogeneity, transcriptional changes, and alternative splicing during DKD progression were mapped using SmartSeq2 single-cell RNA sequencing (scRNAseq) and elucidated through pathway, network, and gene ontology enrichment analyses. We identified 13 distinct transcriptional EC phenotypes corresponding to different kidney vessel subtypes, confirmed through in situ hybridization and immunofluorescence. EC subtypes along nephrons displayed extensive zonation related to their functions. Differential gene expression analyses in peritubular and glomerular ECs in DKD underlined the regulation of DKD-relevant pathways including EIF2 signaling, oxidative phosphorylation, and IGF1 signaling. Importantly, this revealed the differential alteration of these pathways between the two EC subtypes and changes during disease progression. Furthermore, glomerular and peritubular ECs also displayed aberrant and dynamic alterations in alternative splicing (AS), which is strongly associated with DNA repair. Strikingly, genes displaying differential transcription or alternative splicing participate in divergent biological processes. Our study reveals the spatiotemporal regulation of gene transcription and AS linked to DKD progression, providing insight into pathomechanisms and clues to novel therapeutic targets for DKD treatment. Full article
(This article belongs to the Special Issue Molecular Research in Vascular Disease)
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18 pages, 6303 KiB  
Article
Impaired Angiogenic Function of Fetal Endothelial Progenitor Cells via PCDH10 in Gestational Diabetes Mellitus
by Hayan Kwon, Yun Ji Jung, Yeji Lee, Ga-Hyun Son, Hyun Ok Kim, Yong-Sun Maeng and Ja-Young Kwon
Int. J. Mol. Sci. 2023, 24(22), 16082; https://doi.org/10.3390/ijms242216082 - 8 Nov 2023
Cited by 1 | Viewed by 1010
Abstract
Maternal hyperglycemia, induced by gestational diabetes mellitus (GDM), has detrimental effects on fetal vascular development, ultimately increasing the risk of cardiovascular diseases in offspring. The potential underlying mechanisms through which these complications occur are due to functional impairment and epigenetic changes in fetal [...] Read more.
Maternal hyperglycemia, induced by gestational diabetes mellitus (GDM), has detrimental effects on fetal vascular development, ultimately increasing the risk of cardiovascular diseases in offspring. The potential underlying mechanisms through which these complications occur are due to functional impairment and epigenetic changes in fetal endothelial progenitor cells (EPCs), which remain less defined. We confirm that intrauterine hyperglycemia leads to the impaired angiogenic function of fetal EPCs, as observed through functional assays of outgrowth endothelial cells (OECs) derived from fetal EPCs of GDM pregnancies (GDM-EPCs). Notably, PCDH10 expression is increased in OECs derived from GDM-EPCs, which is associated with the inhibition of angiogenic function in fetal EPCs. Additionally, increased PCDH10 expression is correlated with the hypomethylation of the PCDH10 promoter. Our findings demonstrate that in utero exposure to GDM can induce angiogenic dysfunction in fetal EPCs through altered gene expression and epigenetic changes, consequently increasing the susceptibility to cardiovascular diseases in the offspring of GDM mothers. Full article
(This article belongs to the Special Issue Molecular Research in Vascular Disease)
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