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A molecular complex of Cav1.2/CaMKK2/CaMK1a in caveolae is responsible for vascular remodeling through excitation-transcription coupling in vascular smooth muscle.

ABSTRACT: A molecular complex of Cav1.2/CaMKK2/CaMK1a in caveolae is responsible for vascular remodeling through excitation-transcription coupling in vascular smooth muscle.

PROVIDER: PRJNA761369 | ENA |

REPOSITORIES: ENA

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A molecular complex of Cav1.2/CaMKK2/CaMK1a in caveolae is responsible for vascular remodeling through excitation-transcription coupling in vascular smooth muscle.

Project description:Elevation of intracellular Ca2+ ([Ca2+]i) activates Ca2+/calmodulin-dependent kinases (CaMK) and promotes gene transcription. This essential signaling pathway is referred to as excitation-transcription (E-T) coupling. Although vascular myocytes can exhibit E-T coupling, the molecular mechanisms and physiological/pathological roles are unknown. Multiscale analysis spanning from single molecules to whole organisms has revealed essential steps in mouse vascular smooth muscle E-T coupling: (1) Upon depolarizing stimulus Ca2+ influx through voltage-dependent Ca2+ channel Cav1.2 activates CaMKK2, which results in phosphorylation of CaMK1a and CREB in the nucleus. (2) Within caveolae the formation of molecular complex of Cav1.2/CaMKK2/CaMK1a is promoted in the vascular myocytes. (3) Ca2+ influx through Cav1.2 localized to caveolae directly activates CaMKK2. (4) CaMK1a is phosphorylated by CaMKK2 at caveolae and translocated to the nucleus upon membrane depolarization. In addition, RNAseq analysis revealed that sustained depolarization of mesenteric artery preparation selectively induced genes related to chemotaxis, leukocyte adhesion and inflammation, and these changes were reversed by inhibitors of Cav1.2, CaMKK2 and CaMK or disruption of caveolae. In the context of pathophysiology, when mesenteric artery was loaded by high pressure in vivo, we noted CREB phosphorylation in myocytes, macrophage accumulation at adventitia, and increased thickness and cross-sectional area of tunica media. These changes were reduced in caveolin1-KO mice or in mice treated with a CaMKK2 inhibitor STO609. In summary, E-T coupling depend on Cav1.2/CaMKK2/CaMK1a localized to caveolae, and this molecular complex converts [Ca2+]i changes to gene transcription, leading to macrophage accumulation and media remodeling for adaptation to increased circumferential stretch.

2022-03-16 | GSE183588 | GEO

Adenine-induced chronic renal failure causes decreased aortic relaxation rate and altered expression of genes involved in excitation-contraction coupling in vascular smooth muscle cells

Project description:Rats with adenine-induced chronic renal failure (A-CRF) develop a reduction in the rate of relaxation of the thoracic aorta. The primary aim of this study was to elucidate the mechanisms underlying this abnormality. Male Sprague-Dawley rats received either chow containing adenine or were pair-fed with normal chow (controls). After 8-14 weeks arterial functions were analyzed ex vivo using wire myography and the thoracic aorta was analyzed by DNA microarray. Plasma creatinine levels were elevated ~8-fold in A-CRF rats. The rate of vascular relaxation following wash-out of KCl was reduced in A-CRF rats vs. controls in the thoracic aorta (P<0.01), abdominal aorta (P<0.05), and common carotid artery (P<0.05), but not in the common femoral artery. Endothelial denudation exaggerated the impairment in relaxation of thoracic aortas. Relaxation rates of thoracic aortas increased (P<0.01), but were not normalized, in response to wash-out of KCl with Ca2+-free buffer. Microarray and qRT-PCR analyses revealed altered gene expression levels for a number of genes involved in vascular smooth muscle cell excitation-contraction coupling in aortas of A-CRF rats. In conclusion, rats with A-CRF show a marked reduction in the rate of relaxation of larger conduit arteries localized proximal to the common femoral artery. This abnormality may be caused by reduced cytosolic Ca2+ clearance in vascular smooth muscle cells secondary to dysregulation of genes involved in excitation-contraction coupling.

2016-07-21 | GSE52897 | GEO

Small RNA profiling of differentiated and de-differentiated vascular smooth muscle cell

Project description:We report the application of small RNA sequencing for high-throughput profiling of small RNA under 75 bp in vascular smooth muscle cell. By a reading depth of 30M and single stranded sequencing, we generated the small RNA signature on differentiated and de-differentiated vascular smooth muscle cell induced by PDGF-BB and H3K4me2 editing. We found that PDGF-BB and H3K4me2 editing induced de-differentiation modulated miRNA profile significantly, which was demonstrated at least in part responsible for modulated vascular smooth muscle cell phenotype.

2022-04-01 | GSE186972 | GEO

LncVSM (AK098656) down-regulation in Vascular Smooth Muscle cells

Project description:The full length of LncVSM transfected into Vascular Smooth Muscle cells to down-regulation for screening differential expression prolifes of LncVSM effecting.The empty vector transfected Vascular Smooth Muscle cells as controls. Eight Samples analyzed.

2016-01-12 | E-GEOD-76720 | biostudies-arrayexpress

YAP/TAZ in vascular smooth muscle

Project description:YAP/TAZ in vascular smooth muscle

| PRJNA610067 | ENA

YAP/TAZ in vascular smooth muscle

Project description:Investigation of the physiogical functions of YAP/TAZ in vascular smooth muscle cells

2020-11-16 | GSE146317 | GEO

Rat vascular smooth muscle cells LC-MS/MS

Project description:Crotonylation of histones is discovered of late as one of post-translational modification that can regulate gene expression. However, the function of crotonylation on non-histone proteins in vascular smooth muscle cells (VSMC) is unclear. Here, we aim to use modification and proteomic analysis to find the cellular characteristic of crotonylated non-histone proteins and the crosstalk with ubiquitinated proteins in vascular smooth muscle cell (VSMC) phenotypic remodeling. We performed modification and proteomic analysis of VSMCs before and after stimulated with platelet-derived growth factor-BB (PDGF-BB). The crotonylated and ubiquitinated pan-antibody was used to enrich the protein and then subjected to high-throughput mass spectrometry analysis. The enrichment analysis was performed within differentially modified proteins in regards to GO terms, KEGG and protein domain.

2022-05-19 | PXD029070 | Pride

LncVSM (AK098656) down-regulation in Vascular Smooth Muscle cells

2016-01-12 | GSE76720 | GEO

Expression data of vascular smooth muscle cell in patients with suspected giant cell arteritis (GCA)

Project description:There is a remodelling process which occurs in affected vessels during GCA and vascular smooth muscle cells are key cells in this process. Thickening of vessel might be responsible for vessel occlusion. We isolated vascular smooth muscle cells from temporal artery biopsies of patients with suspected GCA and used expression chips in order to identify genes up- and down-regulated in VSMC from patients with proven GCA compared to VSMC from patients with possible GCA and to VSMC from patients with another diagnosis.

2015-11-18 | GSE63425 | GEO

mineralising murine vascular smooth muscle cell cultures

Project description:Vascular mineralization is a carefully orchestrated process, regulated by a number of promoters and inhibitors that function to ensure effective hydroxyapatite formation. Here we sought to identify new regulators of this process through a time series microarray analysis of mineralising primary vascular smooth muscle cell cultures over a 9 day culture period.

2013-06-24 | E-MTAB-1680 | biostudies-arrayexpress

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