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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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			Action	DRS
	SRR15738897_1.fastq.gz	Fastqsanger.gz
	SRR15738897_2.fastq.gz	Fastqsanger.gz
	SRR15738898_1.fastq.gz	Fastqsanger.gz
	SRR15738898_2.fastq.gz	Fastqsanger.gz

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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.

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Excitation transcription coupling during acute stretch and tachycardia in non-failing human myocardium

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Project description:Electrochemical gradients of monovalent cations across the plasma membrane (high intracellular potassium, [K+]i vs low intracellular sodium, [Na+]i) are created by the Na+,K+-pump and determine a large variety of physiologically important processes. We hypothesized that transcriptomics changes triggered by hypoxia are at least partially caused by Na+i/K+i-mediated excitation-transcription coupling . We used microarrays for identification and functional characterization of [Na+]i/]K+]i-sensitive transcriptome in RASMC

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A molecular complex of Ca<sub>v</sub>1.2/CaMKK2/CaMK1a in caveolae is responsible for vascular remodeling via excitation-transcription coupling.

Project description:Elevation of intracellular Ca2+ concentration ([Ca2+]i) activates Ca2+/calmodulin-dependent kinases (CaMK) and promotes gene transcription. This 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 myocyte E-T coupling. Upon a depolarizing stimulus, Ca2+ influx through Cav1.2 voltage-dependent Ca2+ channels activates CaMKK2 and CaMK1a, resulting in intranuclear CREB phosphorylation. Within caveolae, the formation of a molecular complex of Cav1.2/CaMKK2/CaMK1a is promoted in vascular myocytes. Live imaging using a genetically encoded Ca2+ indicator revealed direct activation of CaMKK2 by Ca2+ influx through Cav1.2 localized to caveolae. CaMK1a is phosphorylated by CaMKK2 at caveolae and translocated to the nucleus upon membrane depolarization. In addition, sustained depolarization of a mesenteric artery preparation 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 the mesenteric artery was loaded by high pressure in vivo, we observed CREB phosphorylation in myocytes, macrophage accumulation at adventitia, and an increase in thickness and cross-sectional area of the tunica media. These changes were reduced in caveolin1-knockout mice or in mice treated with the CaMKK2 inhibitor STO609. In summary, E-T coupling depends on Cav1.2/CaMKK2/CaMK1a localized to caveolae, and this complex converts [Ca2+]i changes into gene transcription. This ultimately leads to macrophage accumulation and media remodeling for adaptation to increased circumferential stretch.

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