The emergence of the vasopressin and oxytocin hormone receptor gene family lineage: Clues from the characterization of vasotocin receptors in the sea lamprey (Petromyzon marinus)

Mayasich, Sally A.; Clarke, Benjamin L.

doi:10.1016/j.ygcen.2016.01.001

Cited by 23 publications

(17 citation statements)

References 38 publications

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“…It regulates water permeability of the collecting ducts and induces the release of vascular von Willebrand factor VIII. Vasopressin receptor and oxytocin receptor belong to the same subfamily of the GPCR superfamily and AVP is a partial agonist of the oxytocin receptor . The present study is the first to show that NRCFs express V 1A R but not the other vasopressin receptor subtypes.…”

Section: Discussionsupporting

confidence: 46%

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

Chen

Zhang

et al. 2017

Clin Exp Pharma Physio

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Cardiac fibrosis is a pathological feature commonly found in hearts exposed to haemodynamic orneurohormonal stress. Elevated levels of arginine vasopressin (AVP) are closely associated with the progression of heart failure and could be an underlying cause of cardiac fibrosis. The aim of this study is to characterize the effect of AVP on neonatal rat cardiac fibroblasts (NRCFs) and to illustrate its signalling mechanism. The proliferative effect of AVP was assessed by methylthiazolyldiphenyl-tetrazolium assay and 5-bromo-2'-deoxyuridine (BrdU) incorporation assay, and the amounts of cellular signalling proteins α-smooth muscle actin (α-SMA), matrix metalloproteinase (MMP) 2, MMP9, and phosphorylated ERK were determined by western blotting. AVP, in a time- and concentration-dependent manner, promoted NRCF proliferation and the expression of MMP2 and MMP9. Inhibition of G protein-coupled receptor kinase2 (GRK2) by the inhibitory peptide GRK2-Ct or knock-down of GRK2 suppressed AVP-induced BrdU incorporation and the expression of MMP2 and α-SMA in NRCFs. Moreover, shRNA-mediated silencing of β-arrestin1 or β-arrestin 2 abolished AVP-induced BrdU incorporation and MMP2 expression. AVP-induced NRCF proliferation depended on the phosphorylation of ERK , and inhibition of GRK2 or silencing of β-arrestins blocked AVP-induced ERK phosphorylation. The effects of AVP on NRCF proliferation and α-SMA expression were blocked by SR45059, a vasopressin receptor type1A (V R) selective antagonist. In conclusion, AVP promotes NRCF proliferation through V R-mediated GRK2/β-arrestin/ERK signalling.

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Section: Discussionsupporting

confidence: 46%

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

Chen

Zhang

et al. 2017

Clin Exp Pharma Physio

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“…mRNA expression was normalized to beta actin, while small RNA expression was normalized to RNU6B (RNU6B_13, Qiagen). The polyA site was identified in BCAR3 from PEO4 and 2008 cells using Thermoscript RT (Invitrogen) and oligo dT as previously described [ 58 ]. PCR products were amplified using the 5’ forward BCAR3 primer with the Universal reverse primer from Qiagen and amplified using GoTaq Green (Promega, Madison, WI).…”

Section: Methodsmentioning

confidence: 99%

A tRNA fragment, tRF5-Glu, regulates BCAR3 expression and proliferation in ovarian cancer cells

et al. 2017

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Ovarian cancer is a complex disease marked by tumor heterogeneity, which contributes to difficulties in diagnosis and treatment. New molecular targets and better molecular profiles defining subsets of patients are needed. tRNA fragments (tRFs) offer a recently identified group of noncoding RNAs that are often as abundant as microRNAs in cancer cells. Initially their presence in deep sequencing data sets was attributed to the breakdown of mature tRNAs, however, it is now clear that they are actively generated and function in multiple regulatory events. One such tRF, a 5’ fragment of tRNA-Glu-CTC (tRF5-Glu), is processed from the mature tRNA-Glu and is shown in this study to be expressed in ovarian cancer cells. We confirmed that tRF5-Glu binds directly to a site in the 3’UTR of the Breast Cancer Anti-Estrogen Resistance 3 (BCAR3) mRNA thereby down regulating its expression. BCAR3 has not previously been studied in ovarian cancer cells and our studies demonstrate that inhibiting BCAR3 expression suppresses ovarian cancer cell proliferation. Furthermore, mimics of tRF5-Glu were found to inhibit proliferation of ovarian cancer cells. In summary, BCAR3 and tRF5-Glu contribute to the complex tumor heterogeneity of ovarian cancer cells and may provide new targets for therapeutic intervention.

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“…Our previous study in H9c2 cells has shown that AVP enhances cell survival via a GRK2/b-arrest-in1/ERK 1/2 -dependent pathway (Zhu et al, 2013) and that V 1A R blocker SR45049 abolished AVP-induced NRCF proliferation (Chen et al, 2017) and smooth muscle cell proliferation, although the V 2 R also exists in A7R5 rat aorta smooth muscle (Zhang et al, 2016). Vasopressin receptor and oxytocin receptor belong to the same subfamily of the GPCR superfamily (Mayasich and Clarke, 2016), and AVP is a partial agonist of the oxytocin receptor (Ramos et al, 2016). Thus, AVP-regulated inflammation should distinguish V 1A R from oxytocin receptor.…”

Section: Grk2 Mediates Il-6 Productionmentioning

confidence: 99%

GRK2 Mediates Arginine Vasopressin-Induced Interleukin-6 Production via Nuclear Factor-κB Signaling Neonatal Rat Cardiac Fibroblast

Sun

Wang

et al. 2017

Mol Pharmacol

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Interleukin 6 (IL-6), which is elevated in patients with congestive heart failure and acts as both a chronic marker of inflammation and an acute-phase reactant, is associated with myocardial damage. Circulating levels of arginine vasopressin (AVP) are elevated during cardiac stress and could be a factor for cardiac inflammation and fibrosis. Our previous study has shown that AVP promotes the proliferation of neonatal rat cardiac fibroblasts (NRCFs) throughV vasopressin receptor-mediated G protein-coupled receptor kinase 2 (GRK2) signaling. In the present study, we investigated the impact of the GRK2-dependent signaling. Using quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, we measured the levels of interleukin-6 (IL-6) mRNA and protein in NRCFs, respectively. Manipulation of GRK2 activation either pharmacologically or through overexpression of GRK2-ct was used to determine the role of GRK2 in regulating the effects of AVP on IL-6 production. Phosphorylation and activation of nuclear factor κ-B (NF-B) evoked by AVP stimulation were measured by immunoblot and NF-kB luciferase reporter gene transfected in NRCFs, respectively. Present studies have found that: 1) AVP increased the level of IL-6 protein and mRNA in a dose- and time-dependent manner in NRCFs; 2) inhibition of GRK2 abolished the AVP-induced IL-6 production and NF-B activation; and 3) blocking NF-B signaling using the pharmacologic approach diminished AVP-induced IL-6 production. In summary, AVP induces IL-6 production of NRCFs by activating V receptor signaling via a GRK2/NF-B pathway. These findings provide a possible molecular mechanism for inflammation that occurs in heart failure and other types of cardiac stress.

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The emergence of the vasopressin and oxytocin hormone receptor gene family lineage: Clues from the characterization of vasotocin receptors in the sea lamprey (Petromyzon marinus)

Cited by 23 publications

References 38 publications

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

GRK2/β‐arrestin mediates arginine vasopressin‐induced cardiac fibroblast proliferation

A tRNA fragment, tRF5-Glu, regulates BCAR3 expression and proliferation in ovarian cancer cells

GRK2 Mediates Arginine Vasopressin-Induced Interleukin-6 Production via Nuclear Factor-κB Signaling Neonatal Rat Cardiac Fibroblast

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