Cell adhesion molecules and incident hypertension in black and white adults: the REGARDS studyHarkness, Wilkinson, Loo
et alJ Hypertens (2025)
Abstract: Higher C-reactive protein-quantified inflammation associates with greater incident hypertension risk. E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) are cell adhesion molecules that aid leukocyte adhesion during inflammation. Their association with incident hypertension is unclear.REGARDS enrolled 30 239 Black and White US adults aged ≥45 years from across the contiguous United States in 2003-2007, with a second exam in 2013-2016. The Biomarkers as Mediators of Racial Disparities in Risk Factors (BioMedioR) study included 4400 REGARDS participants who attended both exams. We excluded participants with hypertension or missing biomarkers at baseline. Hypertension used a 140/90 mmHg threshold or self-reported use of blood pressure (BP) lowering medications. Modified Poisson regression estimated relative risk (RR) of incident hypertension by tertile of baseline E-Selectin, ICAM-1, and VCAM-1.Among 1879 nonhypertensive participants (mean [SD] age 62 [8] years, 25% Black race, 55% women) with 9 years median follow up, 36% developed hypertension. E-selectin and ICAM-1 were higher among Black participants; VCAM-1 was higher among White participants. Higher E-selectin was associated with greater risk of incident hypertension among White but not Black adults in some models (e.g., minimally adjusted: RR 1.27; 95% confidence interval (CI) 1.04-1.44 comparing tertile 3 vs. 1) ICAM-1 was associated with greater hypertension risk in only an unadjusted model.In a prospective study of Black and White US adults, E-selectin was associated with incident hypertension among White adults and ICAM-1 in White and Black adults in partially or unadjusted models. Modification of E-selectin might be tested to lower risk of hypertension development.Copyright © 2025 Wolters Kluwer Health, Inc. All rights reserved.
Annexin A3 Represses Endothelial Permeability and Inflammation During Sepsis via Actin Cytoskeleton ModulationXing, Liang, Cao
et alAdv Sci (Weinh) (2025)
Abstract: Increased endothelial permeability and a dysregulated inflammatory response play key roles in organ damage in sepsis. The role of annexin A3 (ANXA3) in regulating endothelial permeability and inflammation during sepsis is explored using ANXA3 knockout mice and primary human umbilical vein endothelial cells (HUVECs). The absence of ANXA3 exacerbated sepsis outcomes, including increased mortality, lung injury, leukocyte infiltration, and vascular permeability. ANXA3 is highly expressed in endothelial cells and its loss results in the formation of cytoskeletal stress fibers and a decrease in the expression of the junction proteins zonula occludens (Zo)-1, vascular endothelial (VE)-cadherin, and claudin 5, leading to increase permeability. ANXA3 knockdown also upregulates E-selectin (CD62E) expression through the phosphorylation of activating transcription factor 2 (ATF2), which increases monocyte adhesion in HUVECs after LPS stimulation. Inhibiting actin polymerization reverse these effects. Thus, ANXA3 stabilizes the actin cytoskeleton, playing a protective role in endothelial dysfunction during sepsis.© 2025 The Author(s). Advanced Science published by Wiley‐VCH GmbH.
The combination of Korean Sajabal mugwort (Artemisia princeps Pampanini) and green tea (Camellia sinensis) extracts and that of their major constituents improved blood flow in vitro and in vivoSon, Lee, Kim
et alFood Sci Biotechnol (2025) 34 (8), 1725-1735
Abstract: This study aimed to evaluate the effects of Korean Sajabal mugwort extract (SME), green tea extract (GTE), and their optimized combination on improving blood flow. We first found that SME and GTE significantly suppressed TNF-α-induced ICAM-1 expression and enhanced endothelial nitric oxide synthase (eNOS) activation in EA.hy926 endothelial cells. Based on synergistic effects on regulation of IκBα, the mixture of SME and GTE at 9:1 ratio was determined as the optimal combination, and it also suppressed integrin LFA-1 expression, reducing leukocyte-endothelial cell interactions. The major components of SME (eupatilin and jaceosidin) and GTE (EGCG) were quantified, and their effects were consistent with the extracts. Furthermore, the mixture alleviated pulmonary vein occlusion, and decreased mRNA levels of ICAM-1, VCAM-1, P-selectin, and E-selectin in aortic tissue in collagen/epinephrine-induced thrombosis rat model. Taken together, the SME and GTE mixture effectively improved blow flow and may be a potent agent for preventing thrombosis and atherosclerosis.© The Korean Society of Food Science and Technology 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
Paeonol Inhibits the MAPK Signaling Pathway by Targeting SIRT1 in AGE-Induced HUVECs InjuryLiu, Gao, Wu
et alComb Chem High Throughput Screen (2025)
Abstract: Chronic hyperglycemia in diabetes is a significant contributor to endothelial injury through the induction of oxidative stress. Paeonol is anticipated to address oxidative stress with the aim of ameliorating endothelial injury. Our study delved into the effects of paeonol on endothelial damage induced by diabetes and elucidated the underlying mechanisms.This research presented a novel endothelial injury model employing advanced glycation end products (AGEs) in human umbilical vein endothelial cells (HUVECs). Additionally, a network analysis was carried out to pinpoint the targets influenced by paeonol, with pivotal targets substantiated via polymerase chain reaction (PCR), western blot analysis, and immunofluorescence staining. Ultimately, the introduction of small interfering RNA transfection validated the involvement of SIRT1 in AGEs-induced HUVECs injury.Twelve metabolites of paeonol were conclusively detected in vivo. Paeonol demonstrated substantial efficacy in ameliorating and diminishing levels of various cytokines and biochemical indicators, including AGEs, Col IV, ET-1, E-selectin, FN, hs-CRP, ICAM-1, MMP2, and sVCAM-1. Notably, network analysis accentuated the pivotal role of the MAPK signaling pathway. Furthermore, paeonol exhibited significantly elevated mRNA and protein levels of SIRT1 and ERK across varying dosage regimens compared to the model group while displaying relatively decreased mRNA expression levels of p38MAPK.This research revealed that paeonol inhibited the activation of p38 and ERK within the MAPK signaling pathway. Moreover, the regulatory influence of paeonol over p38 and ERK was compromised subsequent to the silencing of SIRT1, indicating a SIRT1-dependent suppressive action of paeonol on the MAPK pathway. The potential therapeutic utility of SIRT1 in mitigating diabetic endothelial impairment and its concomitant cardiovascular ramifications is underscored by these findings.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
膜杰作
Star Staining
