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The article discusses how leukocytes, specifically neutrophils, use endothelial membrane tunnels to extravasate from blood vessels during inflammation. The study found that endothelial cells form membrane tunnels that allow neutrophils to cross through the vessel walls. This discovery provides insight into the 3D multicellular architecture involved in the process of leukocyte transmigration. The research has not yet undergone peer review and can be accessed on biorxiv.org for further information. [Extracted from the article]

The article explores the endothelial features in chronic thromboembolic pulmonary hypertension (CTEPH), a rare complication of pulmonary embolism. It discusses the potential role of defective angiogenesis and altered pulmonary arterial endothelial cell function in disease progression. The study focuses on histological characteristics of the pulmonary vascular tree, specifically looking at angiogenic capacities and endothelial barrier function in pulmonary arterial lesions obtained during pulmonary endarterectomy. Despite differences in angiogenic cues between large and (sub)-segmental pulmonary arterial lesions, in vitro angiogenic capacities and barrier function of pulmonary arterial endothelial cells remain unchanged. [Extracted from the article]

The article discusses how mutations in the MeCP2 gene in Rett syndrome patients can impact vascular integrity, leading to potential neurodegenerative effects. Researchers used patient-derived induced pluripotent stem cells to study the vascular network and found higher permeability in cells with the MeCP2 mutation, indicating altered barrier function. They identified miR126-3p as a key player in the vascular impairment seen in Rett syndrome, suggesting potential applications for translational medicine. The study has not yet undergone peer review and provides valuable insights into the non-neurogenic effects of Rett syndrome on vascular health. [Extracted from the article]

A study conducted at the Fifth Affiliated Hospital focused on the role of Spinster homolog 2 (SPNS2) in endothelial cell senescence and vascular aging. The research found that SPNS2 deficiency led to mitochondrial dysfunction and accelerated cellular senescence in endothelial cells. The study suggests that SPNS2 expression and its functions in mitochondria play a crucial role in regulating endothelial cell senescence and vascular aging. For more information, the full article can be accessed at https://doi.org/10.1186/s12964-024-01859-5. [Extracted from the article]

According to a preprint abstract, researchers have found that plasminogen activator inhibitor-1 (PAI1), a protein involved in blood clotting and a biomarker for cardiovascular disease, can be internalized by endothelial cells in an energy-dependent manner. This internalization allows PAI1 to persist in the cell for at least 6 hours and evade degradation, which in turn inhibits endothelial nitric oxide synthase (eNOS). The mechanism of internalization is not dependent on specific cell surface receptors or clathrin-mediated endocytosis, but rather occurs through macropinocytosis. This research provides insights into the intracellular biology of PAI1 and its potential role in cardiovascular disease. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of liver sinusoidal endothelial cells (LSEC) and laminin in determining the fate of reactive cholangiocytes in chronic liver disease (CLD). The study found that laminin, an extracellular matrix protein, plays a crucial role in maintaining cholangiocytes in a biliary phenotype, preventing their differentiation into hepatocytes. LSECs were identified as the cells that regulate laminin degradation around cholangiocytes. By preventing LSEC capillarization during CLD, the differentiation of cholangiocytes into hepatocytes was enhanced. The study also demonstrated this mechanism in human samples, providing new insights into the regeneration process in CLD. [Extracted from the article]

According to a preprint abstract from biorxiv.org, researchers have found that the RalB isoform controls the regulated exocytosis of Weibel-Palade bodies (WPBs), which are specialized endothelial secretory granules that store the hemostatic protein von Willebrand factor. Unlike typical small GTPase-effector interactions, RalB binds to the exocyst in its GDP-bound state in resting endothelium. However, upon endothelial cell stimulation, the exocyst is uncoupled from RalB-GTP, resulting in WPB tethering and exocytosis. The researchers also discovered that phosphorylation of the C-terminal hypervariable region (HVR) of RalB modulates its interaction with the exocyst in endothelium. This research suggests that the uncoupling of the exocyst from RalB mediates endothelial Weibel-Palade body exocytosis, and that Ral function may be dynamically regulated by phosphorylation. [Extracted from the article]

A systematic review was conducted to examine the mechanisms by which traditional Chinese medicine (TCM) modulates cardiac microvascular endothelial cells (CMECs) in various injury models. The review included 63 papers that investigated TCM's intervention capabilities in different damage conditions of CMECs. The findings suggest that TCM exhibits antioxidant, anti-apoptotic, anti-inflammatory effects, and regulates energy metabolism through signaling pathways such as HIF-1alpha/VEGF, PI3K/AKT, MAPK, and NF-kappaB. These mechanisms confer protection on the coronary microcirculation. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A recent preprint abstract discusses the discovery of bipotent endothelial-macrophage progenitor cells in the postnatal aorta. These cells are thought to be derived from yolk sac progenitors and contribute to the renewal of tissue-resident macrophages and endothelial cells after birth. The study found that these progenitor cells are present in the aorta from early embryonic stages and display high proliferative activity. They have the ability to differentiate into both macrophages and endothelial cells, and their expansion is regulated by angiotensin II. This research provides new insights into the maintenance of these cell populations in postnatal tissues. [Extracted from the article]

The article highlights the patent application no. for endothelial immunosuppression in atherosclerosis, filed by researchers on August 19, 2024. It also discusses the role of endothelial cells in suppressing CD8 T cell responses, the impact of the RNA-binding protein Elavl1 on immune regulation, and the translation shifts in chronic inflammation.

According to a preprint abstract from biorxiv.org, pericytes are important in vascularization as they protect endothelial cells and promote the formation of new blood vessels. The relationship between pericytes and other cell types, such as mesenchymal stromal/stem cells, is still debated. In a study using microfluidic chips to replicate vessel formation processes, it was found that pericytes promote more and longer sproutings in angiogenesis compared to stromal cells. In vasculogenesis, stromal cells promote the formation of structures resembling the embryonic capillary plexus, while pericytes wrap around endothelial cells, arresting their division and forcing them into tubulogenesis. This research provides new insights into the relationship between pericytes and endothelial cells, as well as the identity of mesenchymal stromal cells, which is relevant in vascular biology and tissue engineering. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the association between endothelial cell dysfunction and retinal arteriolar narrowing in young adults with elevated blood pressure. The study found that individuals with elevated blood pressure had impaired endothelial colony-forming cell (ECFC) growth, cell proliferation, and angiogenesis. There was also a correlation between reduced ECFC colony-forming capacity and retinal arteriolar diameter. Proteomic analysis revealed differences in extracellular matrix organization, blood coagulation, exocytosis, and vesicle transport proteins in individuals with elevated blood pressure. The study suggests that endothelial molecular mechanisms may contribute to early microvascular changes in individuals with elevated blood pressure. [Extracted from the article]

According to a preprint abstract, neutrophils and monocytes/macrophages are important cells in the immune system that migrate along the endothelial cell layer to reach sites of inflammation. Researchers conducted co-culture experiments with human umbilical vein endothelial cells (HUVECs) and found that these immune cells optimize their search efficiency by migrating along the boundaries of endothelial cells. This motion pattern increases the number of cells sampled and enhances sensitivity to chemokines. However, it should be noted that this research has not yet undergone peer review. [Extracted from the article]

A recent study conducted at the Second Affiliated Hospital of Nanjing Medical University has identified the central role of RNA polymerase mitochondrial (POLRMT) in angiogenesis, the formation of new blood vessels. The researchers found that silencing or knockout of POLRMT in endothelial cells resulted in anti-angiogenic effects, inhibiting cell proliferation, migration, and capillary tube formation. Depletion of POLRMT also led to impaired mitochondrial function and increased apoptosis. The study suggests that POLRMT plays an essential role in angiogenesis and may have implications for conditions such as diabetic retinopathy. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the mechanisms of cell fate specification in developmental biology and regenerative medicine. The study focuses on the pioneer factor ETV2, which is a master regulator for endothelial cell (EC) lineage specification. Through various analyses, including single-cell RNA sequencing and chromatin sequencing, the researchers characterized the transcriptomic profiles and molecular features of EC cell differentiation mediated by ETV2. The study also identified the important role of pioneer factors in recruiting repressors, such as the transcriptional repressor REST, to suppress commitment to alternative lineages. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

Liver sinusoidal endothelial cells (LSECs) have been identified as the primary cells responsible for the uptake of hemoglobin (Hb) in the liver. This process, which involves macropinocytosis, occurs independently of the Hb-haptoglobin receptor CD163. LSECs have high iron content and proteomic signatures that indicate their adaptation to Hb turnover. They play a crucial role in Hb clearance, contributing to heme detoxification during hemolysis and restoring iron homeostasis. This information is based on a preprint abstract and has not been peer-reviewed. [Extracted from the article]

A recent study conducted by researchers at the University of Bologna in Italy has found that naringenin (NRG), a compound found in citrus fruits, has the potential to counteract mitochondrial dysfunction associated with cardiovascular diseases. The study focused on the interaction between NRG and the F1FO-ATPase enzyme, which plays a role in energy transmission. The researchers discovered that NRG acts as a selective inhibitor of the enzyme, particularly when activated by calcium. Additionally, the study found that NRG had a protective effect on salt-induced injury in cerebral endothelial cells. This research provides valuable insights into the potential therapeutic applications of NRG in cardiovascular health. [Extracted from the article]

A recent preprint study published in Drug Week explores the effects of calcitonin gene-related peptide (CGRP) and intermedin (IMD) on primary human lymphatic endothelial cells (HDLEC). The study found that both CGRP and IMD induced phosphorylation of p44/42 MAPK in proliferating HDLEC in a time- and dose-dependent manner. These findings suggest that CGRP and IMD may play a role in regulating lymphatic endothelial cell biology and could be further investigated for their potential involvement in lymphatic function-related pathologies. However, it is important to note that this study has not yet undergone peer review. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of endothelial SHP-1 in diabetes-induced abnormal collateral vessel formation and endothelial cell senescence. The study found that diabetes-induced premature senescence of endothelial cells can lead to impaired angiogenesis. The researchers also discovered that hyperglycemia reduced vascular endothelial growth factor (VEGF) activity in diabetic mice, which was associated with increased expression of SHP-1. Deletion of SHP-1 in endothelial cells restored blood flow reperfusion and limb function in diabetic mice, suggesting that SHP-1 may be a promising therapeutic target. However, it is important to note that this preprint has not been peer-reviewed. [Extracted from the article]

A preprint abstract from biorxiv.org discusses the role of hepatic progenitor cells (HPCs) in angiogenesis, a process associated with chronic liver disease progression. The study used HPC-specific Rbpj conditional knockout mice to investigate the relationship between HPCs and angiogenesis in a mouse model of cholestatic liver disease. The results showed that Rbpj deletion in HPCs reduced HPC proliferation and ductular reactions, as well as attenuated vascular and fibrotic areas. The study suggests that HPCs regulate endothelial responses to cholestatic liver disease and that Rbpj deletion in HPCs could be a potential target for modulating angiogenesis during disease progression. [Extracted from the article]

A recent preprint abstract discusses the role of the RERE gene in lymphatic endothelial cell (LEC) proliferation and survival, as well as its connection to human cystic lymphatic malformations (CLMs). The study found that RERE, a transcriptional regulator, interacts with key lymphangiogenic factors and modulates retinoic acid signaling, which is important for lymphatic vascular development. Knockdown of RERE in human LECs resulted in reduced proliferation, increased apoptosis, altered gene expression, and disrupted Notch signaling. These findings suggest that the loss of RERE may contribute to the development of CLMs. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]

According to a preprint abstract, researchers have developed an in vitro model system to study the vascular barrier in white adipose tissue, which plays a crucial role in fatty acid handling. The study found that the vascular barrier in white adipose tissue is comparable in impermeability to that of the heart and muscle. The researchers also discovered that the endothelial cells in white adipose tissue selectively transport fatty acid tracers while excluding other tracers, which is not observed in other cultured human endothelial cells. These findings contribute to our understanding of how microvascular permeability and transport dynamics have adapted to the specific physiology of different organs. Please note that this research has not yet undergone peer review. [Extracted from the article]

A recent preprint abstract discusses the lack of standardized treatments for Idiopathic Pulmonary Fibrosis (IPF) and non-IPF progressive fibrotic interstitial lung diseases (non-IPF-PF) and the need for identifying common therapeutic targets. The study utilized single-cell RNA sequencing data from six disease groups, including IPF and non-IPF-PF, to identify cells exhibiting upregulated expression. Pulmonary venous endothelial cells (PVECs) were identified as a significant subpopulation, and the molecule PLVAP was consistently elevated in both conditions. In vivo experiments showed that knocking down PLVAP in endothelial cells mitigated pulmonary fibrosis and reduced mesenchymal macrophage interactions. These findings offer new directions for treatment strategies for IPF and non-IPF-PF. [Extracted from the article]

This article discusses the role of cytokines and chemokines in endothelial cell (EC) dysfunction and its contribution to cardiovascular disease in people living with HIV (PLWH). The study used single cell transcriptomic analysis to examine chemokine and cytokine receptor expression in adipose tissue vasculature of PLWH. The researchers found that arterial and capillary ECs expressed higher interferon and tumor necrosis factor (TNF) receptors, while venous ECs had more interleukin (IL)-1R1 and ACKR1 receptors, and vascular smooth muscle cells (VSMCs) had high IL-6R expression. Experiments with human arterial ECs cultured in plasma-conditioned media from PLWH showed increased expression of TNF-a and reactive oxidative phosphorylation pathways. Further research is needed to fully understand the role of cytokines and chemokines in EC dysfunction and develop effective therapeutic strategies. [Extracted from the article]

A recent preprint abstract discusses the discovery of a small molecule that can reduce the formation of hybrid receptors in human endothelial cells. These hybrid receptors consist of insulin receptor (IR) and insulin-like growth factor-1 receptor (IGF-1R) subunits. The small molecule was found to decrease hybrid formation by over 50% in endothelial cells, without affecting the overall expression of IR or IGF-1R. This reduction in hybrid receptors led to increased insulin-induced phosphorylation of Akt, a critical downstream signaling kinase. The study suggests that this small molecule could have potential therapeutic implications for diabetes mellitus. However, it is important to note that this research has not yet undergone peer review. [Extracted from the article]

A recent study conducted by researchers at Grenoble Alpes University explored the signaling pathways modulated by BMP9 and BMP10 stimulation in endothelial cells. The study utilized a phosphoproteomic-based strategy to identify and validate phosphosites and regulated targets. The findings revealed that BMP9 and BMP10 activated a non-canonical transcriptional SMAD-dependent MAPK pathway, which required the expression of the protein GADD45b. Additionally, the study highlighted the modulation of proteins involved in transcriptional regulation and cell cycle inhibition. These findings contribute to a better understanding of the molecular mechanisms regulated by BMP signaling in vascular diseases. [Extracted from the article]