scholarly journals Transcriptome Profiling Reveals a Divergent Adaptive Response to Hyper- and Hypo-Salinity in the Yellow Drum, Nibea albiflora

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2201
Author(s):  
Xiang Zhao ◽  
Zhicheng Sun ◽  
Tianxiang Gao ◽  
Na Song
Keyword(s):  
Signaling Pathway ◽  
Salinity Stress ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Glutathione Metabolism ◽  
Pathway Enrichment Analysis ◽  
Northwest Pacific ◽  
Regulation Mechanism ◽  
Salinity Fluctuation ◽  
Nibea Albiflora

The yellow drum (Nibea albiflora) is an important marine economic fish that is widely distributed in the coastal waters of the Northwest Pacific. In order to understand the molecular regulatory mechanism of the yellow drum under salinity stress, in the present study, transcriptome analysis was performed under gradients with six salinities (10, 15, 20, 25, 30, and 35 psu). Compared to 25 psu, 907, 1109, 1309, 18, and 243 differentially expressed genes (DEGs) were obtained under 10, 15, 20, 30, and 35 psu salinities, respectively. The differential gene expression was further validated by quantitative real-time PCR (qPCR). The results of the tendency analysis showed that all DEGs of the yellow drum under salinity fluctuation were mainly divided into three expression trends. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that the PI3K-Akt signaling pathway, Jak-STAT signaling pathway as well as the glutathione metabolism and steroid biosynthesis pathways may be the key pathways for the salinity adaptive regulation mechanism of the yellow drum. G protein-coupled receptors (GPCRs), the solute carrier family (SLC), the transient receptor potential cation channel subfamily V member 6 (TRPV6), isocitrate dehydrogenase (IDH1), and fructose-bisphosphate aldolase C-B (ALDOCB) may be the key genes in the response of the yellow drum to salinity stress. This study explored the transcriptional patterns of the yellow drum under salinity stress and provided fundamental information for the study of salinity adaptability in this species.

Regulation of Transient Receptor Potential Canonical 4 Activity by Phospholipase C-δ1

2020 ◽  
Author(s):  
Juyeon Ko ◽  
Jongyun Myeong ◽  
Misun Kwak ◽  
Insuk So
Keyword(s):  
Phospholipase C ◽  
Transient Receptor Potential ◽  
Resonance Energy Transfer ◽  
Resonance Energy ◽  
Receptor Potential ◽  
Regulation Mechanism ◽  
Trpc Channels ◽  
Transient Receptor Potential Canonical ◽  
Cell Current ◽  
Transient Receptor

Abstract Transient receptor potential canonical (TRPC) channels are non-selective calcium-permeable cation channels. It is suggested that TRPC4β and TRPC5 channels are regulated by phospholipase C (PLC) signaling, and are especially maintained by phosphatidylinositol 4,5-bisphosphate (PIP2). The PLCδ subtype is the most Ca2+-sensitive form among the isozymes which cleaves phospholipids to respond to the calcium rise. In this study, we investigated the regulation mechanism of TRPC channel by Ca2+, PLCδ1 and PIP2 signaling cascades. The interaction between TRPC4β and PLCδ1 was identified through the Fӧster resonance energy transfer (FRET) and co-immunoprecipitation (Co-IP). With the electrophysiological experiments, we found that TRPC4β-bound PLCδ1 reduces the overall whole-cell current of channel. The Ca2+-via opened channel promotes the activation of PLCδ1, which subsequently decreases PIP2 level. By comparison TRPC4β activity with or without PLCδ1 using differently [Ca2+]i buffered solution, we demonstrated that PLCδ1 functions in normal condition with physiological calcium range. The negative regulation effect of PLCδ1 on TRPC4β helps to elucidate the roles of each PIP2 binding residues whether they are concerned in channel maintenance or inhibition of channel activity.

scholarly journals Heat Avoidance Is Regulated by Transient Receptor Potential (TRP) Channels and a Neuropeptide Signaling Pathway inCaenorhabditis elegans

Genetics ◽  
2011 ◽  
Vol 188 (1) ◽  
pp. 91-103 ◽  
Author(s):  
Dominique A. Glauser ◽  
Will C. Chen ◽  
Rebecca Agin ◽  
Bronwyn L. MacInnis ◽  
Andrew B. Hellman ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Transient Receptor

TRPV1 activation mitigates hypoxic injury in mouse cardiomyocytes by inducing autophagy through the AMPK signaling pathway

2020 ◽  
Vol 318 (5) ◽  
pp. C1018-C1029
Author(s):  
Jinyu Wei ◽  
Jiezhi Lin ◽  
Junhui Zhang ◽  
Di Tang ◽  
Fei Xiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Receptor Potential ◽  
Cell Counting ◽  
Transient Receptor Potential Vanilloid ◽  
Hypoxic Stress ◽  
Autophagy Flux ◽  
Ampk Signaling ◽  
Hypoxic Injury

Autophagy is a highly conserved self-protection mechanism that plays a crucial role in cardiovascular diseases. Cardiomyocyte hypoxic injury promotes oxidative stress and pathological alterations in the heart, although the interplay between these effects remains elusive. The transient receptor potential vanilloid 1 (TRPV1) ion channel is a nonselective cation channel that is activated in response to a variety of exogenous and endogenous physical and chemical stimuli. Here, we investigated the effects and mechanisms of action of TRPV1 on autophagy in hypoxic cardiomyocytes. In this study, primary cardiomyocytes isolated from C57 mice were subjected to hypoxic stress, and their expression of TRPV1 and adenosine 5′-monophosphate-activated protein kinase (AMPK) was regulated. The autophagy flux was assessed by Western blotting and immunofluorescence staining, and the cell viability was determined through Cell counting kit-8 assay and Lactate dehydrogenase assays. In addition, the calcium influx after the upregulation of TRPV1 expression in cardiomyocytes was examined. The results showed that the number of autophagosomes in cardiomyocytes was higher under hypoxic stress and that the blockade of autophagy flux aggravated hypoxic damage to cardiomyocytes. Moreover, the expression of TRPV1 was induced under hypoxic stress, and its upregulation by capsaicin improved the autophagy flux and protected cardiomyocytes from hypoxic damage, whereas the silencing of TRPV1 significantly attenuated autophagy. Our observations also revealed that AMPK signaling was activated and involved in TRPV1-induced autophagy in cardiomyocytes under hypoxic stress. Overall, this study demonstrates that TRPV1 activation mitigates hypoxic injury in cardiomyocytes by improving autophagy flux through the AMPK signaling pathway and highlights TRPV1 as a novel therapeutic target for the treatment of hypoxic cardiac disease.

scholarly journals How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension

2012 ◽  
Vol 302 (5) ◽  
pp. H1031-H1049 ◽  
Author(s):  
Mordecai P. Blaustein ◽  
Frans H. H. Leenen ◽  
Ling Chen ◽  
Vera A. Golovina ◽  
John M. Hamlyn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Signaling Pathway ◽  
Vascular Resistance ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Dietary Salt ◽  
New Paradigm

Excess dietary salt is a major cause of hypertension. Nevertheless, the specific mechanisms by which salt increases arterial constriction and peripheral vascular resistance, and thereby raises blood pressure (BP), are poorly understood. Here we summarize recent evidence that defines specific molecular links between Na+ and the elevated vascular resistance that directly produces high BP. In this new paradigm, high dietary salt raises cerebrospinal fluid [Na+]. This leads, via the Na+-sensing circumventricular organs of the brain, to increased sympathetic nerve activity (SNA), a major trigger of vasoconstriction. Plasma levels of endogenous ouabain (EO), the Na+ pump ligand, also become elevated. Remarkably, high cerebrospinal fluid [Na+]-evoked, locally secreted (hypothalamic) EO participates in a pathway that mediates the sustained increase in SNA. This hypothalamic signaling chain includes aldosterone, epithelial Na+ channels, EO, ouabain-sensitive α2 Na+ pumps, and angiotensin II (ANG II). The EO increases (e.g.) hypothalamic ANG-II type-1 receptor and NADPH oxidase and decreases neuronal nitric oxide synthase protein expression. The aldosterone-epithelial Na+ channel-EO-α2 Na+ pump-ANG-II pathway modulates the activity of brain cardiovascular control centers that regulate the BP set point and induce sustained changes in SNA. In the periphery, the EO secreted by the adrenal cortex directly enhances vasoconstriction via an EO-α2 Na+ pump-Na+/Ca2+ exchanger-Ca2+ signaling pathway. Circulating EO also activates an EO-α2 Na+ pump-Src kinase signaling cascade. This increases the expression of the Na+/Ca2+ exchanger-transient receptor potential cation channel Ca2+ signaling pathway in arterial smooth muscle but decreases the expression of endothelial vasodilator mechanisms. Additionally, EO is a growth factor and may directly participate in the arterial structural remodeling and lumen narrowing that is frequently observed in established hypertension. These several central and peripheral mechanisms are coordinated, in part by EO, to effect and maintain the salt-induced elevation of BP.

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