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• W4289792341 abstract "HomeCirculation ResearchVol. 131, No. 4In This Issue Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIn This Issue Ruth Williams Ruth WilliamsRuth Williams Search for more papers by this author Originally published4 Aug 2022https://doi.org/10.1161/RES.0000000000000565Circulation Research. 2022;131:287is related toDC ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive HypertensionMural Cell SRF Controls Pericyte Migration, Vessel Patterning and Blood FlowUnfolded Protein Response Differentially Modulates the Platelet PhenotypeUnfolded Protein Response Differentially Modulates the Platelet Phenotype (p 290)Jain et al investigate the unfolded protein response in platelets.Download figureDownload PowerPointWhen a cell is stressed, it often accumulates clumps of misfolded proteins, which in turn trigger reduced protein translation and reprogramming of gene transcription—collectively known as the unfolded protein response (UPR). Because platelets have no nuclei, and thus no transcription, it was possible they lacked a UPR, but Jain and colleagues now show this is not the case. They found that treating human and mouse platelets with various stressors caused aggregations of misfolded proteins and induction of particular UPR factors. Oxidative stress, for example, induced the UPR kinase PERK, while an endoplasmic reticulum stressor induced a branch of the UPR involving transcription factor XBP1. The team went on to study the UPR in platelets from people with type II diabetes (DM)— in which platelet mediated thrombosis is a major complication. They showed that protein aggregation and upregulation of the XBP1 pathway in DM platelets correlated with disease severity. Furthermore, treating the DM platelets with a chemical chaperone—to aid correct protein folding—reduced protein aggregations and prevented the cells’ pro-thrombotic activation. The work thus confirms that, even without transcription, platelets display stress-induced UPR and that targeting this response may be a way to reduce thrombosis risk in DM.Mural Cell SRF Controls Pericyte Migration, Vessel Patterning and Blood Flow (p 308)Orlich et al study the function of transcription factor SRF in mural cells.Download figureDownload PowerPointBlood vessels are lined with endothelial cells and surrounded by mural cells—vascular smooth muscle cells (VSMCs) in the case of veins and arteries, and pericytes (PCs) in the case of capillaries. PCs are essential for, among other things, blood-brain and blood-retina barrier function, while VSMCs, through their contractile activity, are required for vascular tone. Thus, while these cells are related, they have distinct roles and characteristics. To learn more about the similarities and differences of PCs and VSMCs, Orlich and colleagues examined how each would be affected by the absence of SRF—a transcription factor essential for non-vascular, or visceral, smooth muscle cell function. In visceral smooth muscle, SRF drives expression of smooth muscle actin and other smooth muscle genes (SMGs). Now, using mice engineered to lack SRF in mural cells, the team show SRF drives SMG expression in these cells too, its loss from VSMCs causing atriovenous malformations and diminished vascular tone. In PCs, loss of SRF impaired cell migration and angiogenic sprouting, while in a mouse model of retinopathy, activation of SRF drove pathological growth of PCs. The work thus not only highlights the various functions of SRF in mural cell biology, but also suggests it has a role in pathological capillary patterning.DC ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive Hypertension (p 328)Inflammasome activity contributes to salt-induced hypertension, say Pitzer et al.Download figureDownload PowerPointIt’s well known that ingesting salt can increase a person’s blood pressure and with it their risk of cardiovascular complications. While fluid retention is a major driver of sodium-induced hypertension, evidence suggests inflammation also contributes. Indeed, exposure of mouse and human immune cells to high sodium increases their production of pro-inflammatory cytokines, such as IL-1β. Additionally, humans with hypertension have high levels of circulating IL-1β. In immune cells, a major source of IL-1β is the multi-protein inflammasome complex, and Pitzer and colleagues now show inflammasome activity is ramped up in response to high sodium. In a cohort of patients with salt sensitivity of blood pressure (SSBP), they found expression of inflammasome components mirrored sodium-induced changes in blood pressure. Moreover, incubating mouse immune cells in high-salt media increased their expression of IL-1β in an inflammasome-dependent manner. And mice on a high salt diet had a less dramatic increase in blood pressure if they received regular injections of either an inflammasome inhibitor or antibodies against IL-1β. Together the results confirm the inflammasome’s role in hypertension and suggest targeting it, or IL-1β, could be an additional therapy for lowering blood pressure. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesDC ENaC-Dependent Inflammasome Activation Contributes to Salt-Sensitive HypertensionAshley Pitzer, et al. Circulation Research. 2022;131:328-344Mural Cell SRF Controls Pericyte Migration, Vessel Patterning and Blood FlowMichael M. Orlich, et al. Circulation Research. 2022;131:308-327Unfolded Protein Response Differentially Modulates the Platelet PhenotypeKanika Jain, et al. Circulation Research. 2022;131:290-307 August 5, 2022Vol 131, Issue 4 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/RES.0000000000000565 Originally publishedAugust 4, 2022 PDF download Advertisement" @default.
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