Dataset Information

Phospho-proteome of vascular smooth muscle cells derived from abdominal aortic aneurysm patients

ABSTRACT: For this experiment, primary smooth muscle cells (SMC) were isolated from abdominal aortic aneurysm (AAA) patients. Control SMC (c-SMC) were isolated from non-dilated human aortas. SMC contraction from AAA-patients and controls was measured. SMC contraction from AAA patients shows a broad range, with higher, lower and normal contracting SMC, compared to c-smc in which a stable normal contraction is seen. We aim to understand the underlying mechanism explaining these differences in SMC contraction.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Heart

SUBMITTER: Thang Pham

LAB HEAD: Connie Jimenez

PROVIDER: PXD054353 | Pride | 2025-07-14

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	QE3_220126_OPL3023_KBR_aneurysm_IMAC_A.raw	Raw
	QE3_220126_OPL3023_KBR_aneurysm_IMAC_AA.raw	Raw
	QE3_220126_OPL3023_KBR_aneurysm_IMAC_AB.raw	Raw
	QE3_220126_OPL3023_KBR_aneurysm_IMAC_AC.raw	Raw
	QE3_220126_OPL3023_KBR_aneurysm_IMAC_AD.raw	Raw

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Insight in the (Phospho)proteome of Vascular Smooth Muscle Cells Derived From Patients With Abdominal Aortic Aneurysm Reveals Novel Disease Mechanisms.

Rombouts Karlijn B KB van Merrienboer Tara A R TAR Henneman Alex A AA Knol Jaco C JC Pham Thang V TV Piersma Sander R SR Jimenez Connie R CR Bogunovic Natalija N van der Velden Jolanda J Yeung Kak Khee KK

Arteriosclerosis, thrombosis, and vascular biology 20240829 10

<h4>Background</h4>Abdominal aortic aneurysm (AAA) is characterized by weakening and dilatation of the aortic wall in the abdomen. The aim of this study was to gain insight into cell-specific mechanisms involved in AAA pathophysiology by analyzing the (phospho)proteome of vascular smooth muscle cells derived from patients with AAA compared with those of healthy donors.<h4>Methods</h4>A (phospho)proteomics analysis based on tandem mass spectrometry was performed on vascular smooth muscle cells de ...[more]

PMID: 39206541

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Project description:Objective: Angiotensin-II (Ang-II) drives pathological vascular wall remodeling in hypertension and abdominal aortic aneurysm (AAA). Previous studies showed that the phosphatase activity of calcineurin (Cn) mediates Ang-II-induced AAA, but the cell type involved in the action of Cn in AAA formation remained unknown. Methods: Smooth muscle cell (SMC)-specific and endothelial cell (EC)-specific Cn-deficient mice (SM-Cn-/- and EC-Cn-/- mice, respectively) were created and assessed for Ang-II-induced AAA formation and hypertension vs controls. Osmotic minipumps were used to administer Ang-II and cyclosporine A (CsA), a pharmaceutical Cn inhibitor. AAA formation and hypertension were monitored by ultrasonography, arterial blood pressure monitoring, and histological analysis. Deep RNA sequencing was used to identify the Ang-II-regulated transcriptome sensitive to Cn deletion or pharmacological inhibition. Arterial and SMC contractility were also assessed. Results: Cn expressed in SMCs, but not ECs, was required for Ang-II-induced AAA. SMC Cn also played an unexpected structural role in the early onset and maintenance of Ang-II-induced hypertension independently of Cn phosphatase activity. Nearly 90% of the genes regulated by Ang-II in the aorta required Cn expression in SMCs. Cn orchestrated, independently of its enzymatic activity, the induction by Ang-II of a gene expression program closely related to SMC contractility and hypertension. Cn deletion in SMCs, but not its pharmacological inhibition, impaired the regulation of arterial contractility. Among the genes whose regulation by Ang-II required Cn expression but not its phosphatase activity, Serpine1 was critical for Ang-II-induced hypertension. Indeed, pharmacological inhibition of PAI-1, the protein encoded by Serpine1, impaired SMCs contractility and regressed hypertension. Conclusions: Whereas the phosphatase activity of Cn mediates Ang-II-induced AAA, a phosphatase-independent action of SMC Cn underlies blood pressure regulation by orchestrating a gene expression program closely related to contractility regulation and hypertension.