FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4246070880> ?p ?o ?g. }

• W4246070880 abstract "Investigation of immune mechanisms involved in hypertension (HTN) is one of the most emerging research area in the field. On this note, we found that hypertensive hits activate nervous system in splenic marginal zone (MZ) that represents the boundary between lymphoid white pulp and innate red pulp. The fact that both innate and adaptive immunity contribute to HTN strongly suggests that neuroimmune mechanisms couple myeloid and lymphoid cells in transducing hypertensive hits into increased blood pressure (BP). We previously showed that Placental Growth Factor (PlGF), a VEGF homolog, released in the splenic MZ upon Angiotensin II (AngII), mediates this interaction. Here we dissect the downstream pathway conveying nervous outflow into immune activation. PlGF is expected to act through its major receptor VEGFR1, its only known tyrosine kinase receptor. First we found that it is mainly expressed in splenic innate immune cells and vasculature, both in basal conditions and upon AngII. To test VEGFR1 in HTN, we challenged transgenic mice with defective VEGFR1 signaling (Flt1-TK) with AngII. To our surprise, they raised BP upon 28-days AngII as WT mice did (SBP: Flt1-TK 139±2; WT 138±2; ***p< 0.001), thus suggesting the existence of alternative pathways. PlGF may also act on a co-receptor, Neuropilin1 (Nrp1), known to enhance responses to ligands. In addition, Nrp1 has unique functions in neurons’ guidance during development and in the maturation of dendritic cells from monocytes. We found Nrp1 basally expressed and strongly increased upon AngII, especially in MZ macrophages. To test the hypothesis that PlGF/Nrp1 pathway could mediate a neuroimmune activation of dendritic cells relevant for HTN, we selectively deleted the receptor in myeloid lineage, generating Nrp1 fl;fl ;LysM-Cre transgenic mice. After assessing Nrp1deletion in splenic monocyte/macrophages by FACS, we infused AngII and found a protection from T cells costimulation and egression from the spleen. More important, they were protected from HTN (SBP: Nrp1 fl;fl ;LysM-Cre +/- 140±3; Nrp1 fl;fl ;LysM-Cre -/- 105±2; ***p< 0.001). Our data indicate a crucial role of Nrp1 in HTN, mediating non-canonical PlGF signaling in innate immunity that serves as a guidance of nerves priming adaptive immune responses." @default.
• W4246070880 created "2022-05-12" @default.
• W4246070880 creator A5014139677 @default.
• W4246070880 creator A5015962914 @default.
• W4246070880 creator A5027985482 @default.
• W4246070880 creator A5056657340 @default.
• W4246070880 creator A5068645306 @default.
• W4246070880 creator A5090777618 @default.
• W4246070880 date "2017-09-01" @default.
• W4246070880 modified "2023-09-26" @default.
• W4246070880 title "Abstract 002: Neuropilin1: New Splenic Mechanisms Mediating the Guidance of Neural Cues in Immune Cells Relevant for Hypertension" @default.
• W4246070880 doi "https://doi.org/10.1161/hyp.70.suppl_1.002" @default.
• W4246070880 hasPublicationYear "2017" @default.
• W4246070880 type Work @default.
• W4246070880 citedByCount "0" @default.
• W4246070880 crossrefType "journal-article" @default.
• W4246070880 hasAuthorship W4246070880A5014139677 @default.
• W4246070880 hasAuthorship W4246070880A5015962914 @default.
• W4246070880 hasAuthorship W4246070880A5027985482 @default.
• W4246070880 hasAuthorship W4246070880A5056657340 @default.
• W4246070880 hasAuthorship W4246070880A5068645306 @default.
• W4246070880 hasAuthorship W4246070880A5090777618 @default.
• W4246070880 hasConcept C126322002 @default.
• W4246070880 hasConcept C134018914 @default.
• W4246070880 hasConcept C136449434 @default.
• W4246070880 hasConcept C170493617 @default.
• W4246070880 hasConcept C193419808 @default.
• W4246070880 hasConcept C203014093 @default.
• W4246070880 hasConcept C2908929049 @default.
• W4246070880 hasConcept C71924100 @default.
• W4246070880 hasConcept C86803240 @default.
• W4246070880 hasConcept C8891405 @default.
• W4246070880 hasConceptScore W4246070880C126322002 @default.
• W4246070880 hasConceptScore W4246070880C134018914 @default.
• W4246070880 hasConceptScore W4246070880C136449434 @default.
• W4246070880 hasConceptScore W4246070880C170493617 @default.
• W4246070880 hasConceptScore W4246070880C193419808 @default.
• W4246070880 hasConceptScore W4246070880C203014093 @default.
• W4246070880 hasConceptScore W4246070880C2908929049 @default.
• W4246070880 hasConceptScore W4246070880C71924100 @default.
• W4246070880 hasConceptScore W4246070880C86803240 @default.
• W4246070880 hasConceptScore W4246070880C8891405 @default.
• W4246070880 hasIssue "suppl_1" @default.
• W4246070880 hasLocation W42460708801 @default.
• W4246070880 hasOpenAccess W4246070880 @default.
• W4246070880 hasPrimaryLocation W42460708801 @default.
• W4246070880 hasRelatedWork W1524155111 @default.
• W4246070880 hasRelatedWork W1556307916 @default.
• W4246070880 hasRelatedWork W1971613811 @default.
• W4246070880 hasRelatedWork W2103515427 @default.
• W4246070880 hasRelatedWork W2137237120 @default.
• W4246070880 hasRelatedWork W2141330728 @default.
• W4246070880 hasRelatedWork W2162471541 @default.
• W4246070880 hasRelatedWork W2582591980 @default.
• W4246070880 hasRelatedWork W2946615038 @default.
• W4246070880 hasRelatedWork W4206425682 @default.
• W4246070880 hasVolume "70" @default.
• W4246070880 isParatext "false" @default.
• W4246070880 isRetracted "false" @default.
• W4246070880 workType "article" @default.