Characterization of synaptopodin in striated and smooth muscles: isoform spectrum, expression patterns, localization and protein interactions.

Piezo1 aggravates diabetic vascular calcification by enhancing OGT-mediated RUNX2 O-GlcNAcylation in vascular smooth muscle cells.

Ferroptosis-driven coronary plaque vulnerability: A tandem mechanism involving endothelial cells, macrophages, and smooth muscle cells.

PPP1R14A in male erectile dysfunction: key role in smooth muscle cells.

Calcitonin gene-related peptide/protein kinase A: A novel pathway to regulate patency of ductus arteriosus.

Biomimetic flowing vessel-on-a-chip recruiting glycocalyx features for investigating dexmedetomidine function.

Lycorine hydrochloride reveals a novel role in preventing neointimal hyperplasia through MAPK-mediated phenotypic switching of smooth muscle cells.

Unveiling Telocytes architecture and distribution in the embryonic duodenum of quail (Coturnix japonica): Morphological and ultrastructural insights.

Vascular relaxation induced by 5-HT2B receptor is thought to be mediated by stimulation of endothelial nitric oxide synthase (eNOS), but this assumption still requires investigation. To investigate potential mechanisms, BW723C86 (5-HT2B receptor agonist) was added to guinea pig aorta rings precontracted by KCl, phenylephrine (Phe) or 5-hydroxytryptamine (5-HT). The effect of Nω-nitro-L-arginine methyl ester (L-NAME) (NOS inhibitor), charybdotoxin (potassium channels blocker) or endothelium removal on the BW723C86 response was also explored. 5-HT2B receptor expression was evaluated through immunofluorescence and NOS expression by means of qPCR and ELISA. Stimulation of the 5-HT2B receptor relaxed all precontracted aorta rings, and L-NAME fully abolished such relaxations, while charybdotoxin prevented the relaxation only in aortas precontracted by Phe or 5-HT. Immunolabelling confirmed a strong expression of the 5-HT2B receptor in endothelium and much less in smooth muscle. Interestingly, BW723C86 was still able to produce relaxation on endothelium-denuded aortas precontracted by KCl or Phe but caused a potent contraction on 5-HT precontracted aortas. Because it is known that NOS activity is upregulated by KCl and Phe, but downregulated by 5-HT, we explored whether smooth muscle NOS could be responsible for these effects, but L-NAME did not prevent it. These results pointed out that mechanisms other than NOS activation are also involved in the relaxing effect of 5-HT2B receptor stimulation.

Acute pulmonary embolism (PE) remains a leading cause of cardiovascular mortality, driven primarily by a sudden increase in pulmonary artery (PA) resistance. Brain Natriuretic Peptide (BNP) may hold promise for reducing PA resistance. However, its role and mechanism in acute PE are not yet fully understood. This study aims to determine whether BNP alleviates PE-induced pulmonary vasoconstriction by targeting Natriuretic Peptide Receptor C (NPRC) and evaluate its therapeutic potential. Here, we established an acute PE rat model using autologous thrombi, and right ventricle (RV) pressure was monitored to approximate PA resistance. A small group of intermediate-high-risk acute PE patients were observed, who received BNP in addition to anticoagulation, and their clinical outcomes were compared to matched patients receiving anticoagulation alone. BNP at varying doses was administered to optimize therapeutic efficacy in the acute PE rat model. Mechanistic studies assessed BNP's impact on oxidative stress in PA endothelium. In the rats, BNP infusion significantly reduced RV pressure overload and improved survival. Clinically, patients receiving adjunctive BNP experienced more rapid improvement in heart rate, oxygen saturation, and blood pressure stability than anticoagulation alone. BNP decreased NADPH oxidase 2-dependent ROS levels in rats' PA endothelium, thereby reducing myosin light chain phosphorylation in smooth muscle. NPRC, as the central receptor, antagonizes the protective effect of BNP. Collectively, BNP offers a novel choice to mitigate PE-induced pulmonary vasoconstriction via NPRC-mediated mechanisms, which support BNP's therapeutic potential for intermediate-high-risk PE.

Selected calix[4]arene as an effective modulator of mitochondrial function and smooth muscle contractility.

Histological study of the canine ovarian suspensory ligament and its implications for neutering procedures.

The formation, dynamics, and disassembly of caveolae.

Keloids are benign fibrous lesions characterized by tumor-like behavior, including continuous expansion beyond the original wound boundaries, absence of natural regression, and a strong tendency to recur after treatment. While cellular heterogeneity and intercellular signaling are recognized contributors to keloid progression, the specific phenotypic transitions and regulatory interactions among involved cell types remain poorly defined. We analyzed transcriptomic profiles from six samples in the GSE163973 dataset, including three keloid and three normal scar tissues. Single-cell RNA sequencing datasets were analyzed to classify cellular populations and to investigate gene expression patterns and ligand-receptor interactions within distinct subgroups. Nine primary cell types were identified: endothelial cells, fibroblasts, smooth muscle cells/pericytes, keratinocytes, macrophage/dendritic cells, lymphatic endothelial cells, T cells, Schwann cells, and melanocytes. Among these, endothelial cells and Schwann cells showed the greatest transcriptional variability. Subcluster analysis and ligand-receptor mapping revealed pronounced heterogeneity and complex intercellular communication within keloid tissues. Notably, one subcluster of keloid endothelial cells shared transcriptional features with endothelial cells in cutaneous malignant tumors and demonstrated strong migratory potential. PLPP3 was identified as a key regulator of endothelial tubulogenesis within this subpopulation. This study highlights the distinct heterogeneity and dynamic intercellular interaction between endothelial cells (ECs) and Schwann cells (SCs) in the pathogenesis of keloids. The identification of tumor-like endothelial subclusters and their regulatory networks provides novel insights into keloid biology and suggests PLPP3 as a potential target for therapeutic intervention.

Multifaceted cell death in atherosclerosis: Mechanisms, pathological impact, and therapeutic targeting.

Tanfloc and carboxymethyl-kappa-carrageenan polyelectrolyte multilayers impart antithrombotic activity, enhanced re-endothelialization and antimicrobial activity on blood-contacting materials.

Asthma is a chronic respiratory condition characterized by airway inflammation, remodeling, and hyperresponsiveness to triggers that lead to airway constriction and impaired airflow. Bronchial smooth muscle (BSM) plays a central role in these processes by constricting the airways and producing proinflammatory cytokines in response to environmental triggers, allergens, and cytokines. Although current therapies, including bronchodilators, corticosteroids, and biologics, effectively treat many patients, additional strategies are needed for difficult-to-treat asthma. Emerging evidence suggests that therapeutic ketosis, achieved through dietary interventions or exogenous ketone supplementation, may reduce airway hyperresponsiveness and inflammation. Classically known as metabolic fuels, ketone bodies also signal through cell-surface receptors and transporters to elicit their activities. Increased ketone body levels in vivo, such as during weight loss or caloric restriction, correlate with improved asthma symptoms, reduced oxidative stress, and decreased inflammation. Here, we investigated the predominant ketone body, β-hydroxybutyrate (BHB), as a potential modulator of BSM function. Using human bronchial smooth muscle cells in vitro, we found that BHB suppresses IL-1β-induced proinflammatory cytokine production and attenuates histamine-induced contraction through a mechanism involving activation of the free fatty acid receptor 3 (FFAR3). In mouse precision-cut lung slices (PCLS) ex vivo, we demonstrated that both BHB and an FFAR3 agonist reduce histamine-induced airway narrowing and epithelial cellular extrusion. Collectively, these findings identify BSM and FFAR3 as cellular targets of therapeutic ketosis and support BHB as a potential beneficial agent for mitigating inflammation and bronchoconstriction in asthma.NEW & NOTEWORTHY Asthma is characterized by airway inflammation and bronchoconstriction, with aberrant bronchial smooth muscle function contributing to disease severity. Therapeutic ketosis, achieved through a ketogenic diet or exogenous ketone supplementation, attenuates airway inflammation and bronchial hyperresponsiveness. Using bronchial smooth muscle cells and precision-cut lung slices, we demonstrate that the ketone body β-hydroxybutyrate (BHB) suppresses IL-1β-induced proinflammatory cytokine production and histamine-evoked bronchoconstriction via activation of the free fatty acid receptor FFAR3.

Vascular calcification (VC) is a major complication of type 2 diabetes mellitus (T2DM) and is associated with increased cardiovascular risk. Myricetin, a natural flavonoid with reported cardiovascular protective properties, has not been fully evaluated in the context of diabetic VC. In this study, the effects of myricetin were examined in vascular smooth muscle cells (VSMCs) exposed to hyperglycemic and phosphate (Pi) conditions in vitro. Myricetin attenuated calcification in VSMCs under hyperglycemic/Pi conditions. It decreased the expression of osteogenic markers RUNX2 and BMP-2, while restoring the expression of contractile markers α-SMA and SM22-α. Myricetin also reduced inflammatory responses, as indicated by decreased interleukin-6 mRNA and NLRP3 protein expression. In addition, myricetin reduced oxidative stress by lowering intracellular reactive oxygen species and malondialdehyde levels, decreasing the Fe2+/Fe3+ ratio, and increasing the GSH/GSSG ratio. Furthermore, myricetin restored the expression of ferroptosis-related regulators, including SLC7A11, GPX4, and FTH1, which were reduced under hyperglycemic/Pi conditions. The protective effects of myricetin were partially reversed by ferroptosis inducers, suggesting the involvement of ferroptosis-related mechanisms. Collectively, these findings suggest that myricetin may inhibit vascular calcification in vitro and has therapeutic potential for diabetic vascular complications.

Lack of evidence for the involvement of non-canonical pyroptosis in a mouse model of thoracic aortic dissection.

Kisspeptin-10 attenuates pulmonary arterial hypertension via restoration of mitochondrial function in pulmonary artery smooth muscle cells.