Keyword search (4,163 papers available)

"Scheede-Bergdahl C" Authored Publications:

Title Authors PubMed ID
1 Four-week prehabilitation program is sufficient to modify exercise behaviors and improve preoperative functional walking capacity in patients with colorectal cancer. Chen BP, Awasthi R, Sweet SN, Minnella EM, Bergdahl A, Santa Mina D, Carli F, Scheede-Bergdahl C 27539131
HKAP
2 Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells. Scheede-Bergdahl C, Bergdahl A 28846852
HKAP
3 Evaluation of supervised multimodal prehabilitation programme in cancer patients undergoing colorectal resection: a randomized control trial. Bousquet-Dion G, Awasthi R, Loiselle SÈ, Minnella EM, Agnihotram RV, Bergdahl A, Carli F, Scheede-Bergdahl C 29327644
HKAP
4 Maximizing patient adherence to prehabilitation: what do the patients say? Ferreira V, Agnihotram RV, Bergdahl A, van Rooijen SJ, Awasthi R, Carli F, Scheede-Bergdahl C 29478189
HKAP
5 Cardiac mitochondrial respiration following a low-carbohydrate, high-fat diet in apolipoprotein E-deficient mice. Rocha C, Koury OH, Scheede-Bergdahl C, Bergdahl A 30362048
HKAP

 

Title:Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells.
Authors:Scheede-Bergdahl C,  Bergdahl A
Link:https://www.ncbi.nlm.nih.gov/pubmed/28846852?dopt=Abstract
Publication:
Keywords:
PMID:28846852 Category:Can J Physiol Pharmacol Date Added:2019-05-31
Dept Affiliation: HKAP
1 a Department of Kinesiology & Physical Education, McGill University, Montreal, QC H2W 1S4, Canada.
2 b McGill Research Centre for Physical Activity & Health, McGill University, Montreal, QC H2W 1S4, Canada.
3 c Department of Exercise Science, Concordia University, Montreal, QC H4B 1R6, Canada.

Description:

Adaptation of mitochondrial expression and ATP production in dedifferentiating vascular smooth muscle cells.

Can J Physiol Pharmacol. 2017 Dec;95(12):1473-1479

Authors: Scheede-Bergdahl C, Bergdahl A

Abstract

Atherosclerosis is one of the leading causes of morbidity and mortality in the Western world. Although the clinical manifestations of this disease are well documented, the etiology and progression remain to be fully understood. Recently, the mitochondria have been implicated in important cellular processes involved in development of atherosclerosis. Despite the link between mitochondria and atherosclerosis, early-phase mechanisms of the disease have yet to be elucidated. The aim of this project was to explore the role of mitochondria in vascular smooth muscle (VSMC) dedifferentiation. A murine in vitro model, involving organ culture of aortic tissue in serum-free media, was used. Mitochondrial function was measured by high-resolution respirometry. Proteins associated with the VSMC phenotype switch, as well as mitochondrial density, were assessed by immunoblotting. The findings show that intrinsic mitochondrial Complex I activity is significantly upregulated during VSMC dedifferentiation. Diminished coupling between phosphorylation and oxidation was also found, indicating a greater ADP:ATP ratio. This data suggests increased leak in the electron transport chain and altered mitochondrial function specifically at Complex I. This project provides important information regarding the role of mitochondria in the early atherosclerotic process and that detectable changes in mitochondrial function and expression are related to VSMC dedifferentiation.

PMID: 28846852 [PubMed - indexed for MEDLINE]




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