Specialized Retinal Endothelial Cells Modulate Blood-Retina Barrier in Diabetic Retinopathy.

Endothelial cells (EC) play essential roles in retinal vascular homeostasis. This study aimed to characterize retinal EC heterogeneity and functional diversity using single-cell RNA sequencing. Systematic analysis of cellular compositions and cell-cell interaction networks identified a unique EC cluster with high inflammatory gene expression in diabetic retina; sphingolipid metabolism is a prominent aspect correlated with changes in retinal function.

MST1 Suppresses Disturbed Flow Induced Atherosclerosis.

Background: Atherosclerosis occurs mainly at arterial branching points exposed to disturbed blood flow. How MST1 (mammalian sterile 20-like kinase 1), the primary kinase in the mechanosensitive Hippo pathway modulates disturbed flow induced endothelial cells (ECs) activation and atherosclerosis remains unclear.

Methods: To assess the role of MST1 in vivo, mice with EC-specific deficiency on background () were used in an atherosclerosis model generated by carotid artery ligation.

COMP (Cartilage Oligomeric Matrix Protein), a Novel PIEZO1 Regulator That Controls Blood Pressure.

Background: Vascular endothelial cells are critical for maintaining blood pressure (BP) by releasing biologically active molecules, such as nitric oxide. A non-endothelial cell resident matricellular protein, COMP (cartilage oligomeric matrix protein), plays a pivotal role in maintaining cardiovascular homeostasis, but little is known about its regulatory effect on BP.

Methods: Mice were infused with AngII (angiotensin II; 450 ng/kg per minute) for 3 days via an osmotic minipump, and BP was monitored by a tail-cuff system.

Hippo/yes-associated protein signaling functions as a mechanotransducer in regulating vascular homeostasis.

Cells are constantly exposed to various mechanical forces, including hydrostatic pressure, cyclic stretch, fluid shear stress, and extracellular matrix stiffness. Mechanical cues can be translated into the cell-specific transcriptional process by a cellular mechanic-transducer. Evidence suggests that mechanical signals assist activated intracellular signal transduction pathways and the relative phenotypic adaptation to coordinate cell behavior and disease appropriately.

Macrophage MST1/2 Disruption Impairs Post-Infarction Cardiac Repair via LTB4.

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A Review on Nano-/Microstructured Materials Constructed by Electrochemical Technologies for Supercapacitors.

The article reviews the recent progress of electrochemical techniques on synthesizing nano-/microstructures as supercapacitor electrodes. With a history of more than a century, electrochemical techniques have evolved from metal plating since their inception to versatile synthesis tools for electrochemically active materials of diverse morphologies, compositions, and functions. The review begins with tutorials on the operating mechanisms of five commonly used electrochemical techniques, including cyclic voltammetry, potentiostatic deposition, galvanostatic deposition, pulse deposition, and electrophoretic deposition, followed by thorough surveys of the nano-/microstructured materials synthesized electrochemically.

Ammonium-Ion Storage Using Electrodeposited Manganese Oxides.

NH ions as charge carriers show potential for aqueous rechargeable batteries. Studied here for the first time is the NH -storage chemistry using electrodeposited manganese oxide (MnO ). MnO experiences morphology and phase transformations during charge/discharge in dilute ammonium acetate (NH Ac) electrolyte.

The nuclear and cytoplasmic roles of miR-320 in non-alcoholic fatty liver disease.

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder worldwide. Multiple metabolic disorders, such as hyperlipidemia, hyperglycemia, insulin resistance and obesity, have been reportedly associated with NAFLD, but little is known about the detailed mechanisms.

Methods And Results: Here, we explored the effects of multiple metabolic disorders, especially hyperglycemia on lipid accumulation in liver using several well-established animal models.

Cartilage oligomeric matrix protein fine-tunes disturbed flow-induced endothelial activation and atherogenesis.

Disturbed flow leads to increased inflammatory responses of endothelial cells (ECs) prone to atherogenic state. Currently, little is known about the physiological mechanisms protecting vasculature against disturbed flow-activated ECs leading to atherosclerosis. Understanding the protective mediators involved in EC activation could provide novel therapeutic strategies for atherosclerosis.

Macrophage K63-Linked Ubiquitination of YAP Promotes Its Nuclear Localization and Exacerbates Atherosclerosis.

The Hippo/Yes-associated protein (YAP) pathway has pivotal roles in innate immune responses against pathogens in macrophages. However, the role of YAP in macrophages during atherosclerosis and its mechanism of YAP activation remain unknown. Here, we find that YAP overexpression in myeloid cells aggravates atherosclerotic lesion size and infiltration of macrophages, whereas YAP deficiency reduces atherosclerotic plaque.

Coupling of Integrin α5 to Annexin A2 by Flow Drives Endothelial Activation.

Rationale: Atherosclerosis preferentially occurs at specific sites of the vasculature where endothelial cells (ECs) are exposed to disturbed blood flow. Translocation of integrin α5 to lipid rafts promotes integrin activation and ligation, which is critical for oscillatory shear stress (OSS)-induced EC activation. However, the underlying mechanism of OSS promoted integrin α5 lipid raft translocation has remained largely unknown.

Regulation of YAP by Mammalian Target of Rapamycin Complex 1 in Endothelial Cells Controls Blood Pressure Through COX-2/mPGES-1/PGE Cascade.

Endothelial cells regulate vascular tone by producing both relaxing and contracting factors to control the local blood flow. Hypertension is a common side effect of mTORC1 (mammalian target of rapamycin complex 1) inhibitors. However, the role of endothelial mTORC1 in hypertension remains elusive.

c-Abl regulates YAPY357 phosphorylation to activate endothelial atherogenic responses to disturbed flow.

Local flow patterns determine the uneven distribution of atherosclerotic lesions. This research aims to elucidate the mechanism of regulation of nuclear translocation of Yes-associated protein (YAP) under oscillatory shear stress (OSS) in the atheroprone phenotype of endothelial cells (ECs). We report here that OSS led to tyrosine phosphorylation and strong, continuous nuclear translocation of YAP in ECs that is dependent on integrin α5β1 activation.

Commutative regulation between endothelial NO synthase and insulin receptor substrate 2 by microRNAs.

Endothelial NO synthase (eNOS) expression is regulated by a number of transcriptional and post-transcriptional mechanisms, but the effects of competing endogenous RNAs (ceRNAs) on eNOS mRNA and the underlying mechanisms are still unknown. Our bioinformatic analysis revealed three highly expressed eNOS-targeting miRNAs (miR-15b, miR-16, and miR-30b) in human endothelial cells (ECs). Among the 1103 mRNA targets of these three miRNAs, 15 mRNAs share a common disease association with eNOS.

Yes-Associated Protein Promotes Angiogenesis via Signal Transducer and Activator of Transcription 3 in Endothelial Cells.

Rationale: Angiogenesis is a complex process regulating endothelial cell (EC) functions. Emerging lines of evidence support that YAP (Yes-associated protein) plays an important role in regulating the angiogenic activity of ECs.

Objective: The objective of this study was to specify the effect of EC YAP on angiogenesis and its underlying mechanisms.

Inhibition of soluble epoxide hydrolase alleviated atherosclerosis by reducing monocyte infiltration in Ldlr(-/-) mice.

Rationale: Circulating monocytes play pivotal roles in chronic inflammatory diseases. Epoxyeicosatrienoic acids (EETs), metabolites of arachidonic acid, are known to have anti-inflammatory effects and are hydrolyzed by soluble epoxide hydrolase (sEH).

Objective: We aimed to investigate the effect of sEH inhibition in atherogenesis.

[Strontium ranelate promotes osteogenic differentiation of rat bone mesenchymal stem cells through bone morphogenetic protein-2/Smad signaling pathway].

Objective: To explore whether strontium ranelate (Sr) promotes osteoblast lineage differentiation of rat bone mesenchymal stem cells (BMSCs) through the bone morphogenetic protein-2 (BMP-2)/Smad signaling pathway.

Methods: Cultured rat BMSCs were exposed to different concentrations of Sr, noggin (an inhibitor of BMP-2) or Smad1 siRNA. The activity of alkaline phosphatase (ALP) in the exposed cells was detected by colorimetry, and the formation of mineralized nodules was observed with alizarin red staining.