Peroxisome Proliferator-activated Receptor γ Coactivator 1β (PGC-1β) Protein Attenuates Vascular Lesion Formation by Inhibition of Chromatin Loading of Minichromosome Maintenance Complex in Smooth Muscle Cells

Guo, Yanhong; Fan, Yanbo; Zhang, Jifeng; Chang, Lin; Lin, Jiandie D.; Chen, Y. Eugene

doi:10.1074/jbc.m112.407452

Cited by 8 publications

(10 citation statements)

References 57 publications

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“…Proteins of the Mcm family configure the prereplication complex necessary for eukaryotic DNA replication (22). Contrarily, PGC-1␣1 or PGC-1␣4 expression reduced Mcm3-6 levels (statistically significant only in the case of PGC-1␣1 but with a clear trend for PGC-1␣4), an effect that has also been observed upon expression of PGC-1␤ (23). As shown in Fig.…”

Section: Analysis Of Gene Network Under the Control Of Pgc-1␣supporting

confidence: 48%

“…Although our results were obtained in fully differentiated myotubes, this could indicate a potential positive role on muscle regeneration and growth. Interestingly, PGC-1␣ homolog PGC-1␤ represses Mcm expression and prevents proliferation of vascular smooth cells (23). Of note and contrary to PGC-1␣2 and -␣3, PGC-1␣1 and -␣4 repress the expression of several members of the Mcm family (Fig.…”

Section: Discussionmentioning

confidence: 99%

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Peroxisome Proliferator-activated Receptor γ Coactivator-1 α Isoforms Selectively Regulate Multiple Splicing Events on Target Genes

Martínez-Redondo

Jannig

Correia

et al. 2016

Journal of Biological Chemistry

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Endurance and resistance exercise training induces specific and profound changes in the skeletal muscle transcriptome. Peroxisome proliferator-activated receptor ␥ coactivator-1 ␣ (PGC-1␣) coactivators are not only among the genes differentially induced by distinct training methods, but they also participate in the ensuing signaling cascades that allow skeletal muscle to adapt to each type of exercise. Although endurance training preferentially induces PGC-1␣1 expression, resistance exercise activates the expression of PGC-1␣2, -␣3, and -␣4. These three alternative PGC-1␣ isoforms lack the arginine/serine-rich (RS) and RNA recognition motifs characteristic of PGC-1␣1. Discrete functions for PGC-1␣1 and -␣4 have been described, but the biological role of PGC-1␣2 and -␣3 remains elusive. Here we show that different PGC-1␣ variants can affect target gene splicing through diverse mechanisms, including alternative promoter usage. By analyzing the exon structure of the target transcripts for each PGC-1␣ isoform, we were able to identify a large number of previously unknown PGC-1␣2 and -␣3 target genes and pathways in skeletal muscle. In particular, PGC-1␣2 seems to mediate a decrease in the levels of cholesterol synthesis genes. Our results suggest that the conservation of the N-terminal activation and repression domains (and not the RS/RNA recognition motif) is what determines the gene programs and splicing options modulated by each PGC-1␣ isoform. By using skeletal muscle-specific transgenic mice for PGC-1␣1 and -␣4, we could validate, in vivo, splicing events observed in in vitro studies. These results show that alternative PGC-1␣ variants can affect target gene expression both quantitatively and qualitatively and identify novel biological pathways under the control of this system of coactivators.

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Section: Analysis Of Gene Network Under the Control Of Pgc-1␣supporting

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor γ Coactivator-1 α Isoforms Selectively Regulate Multiple Splicing Events on Target Genes

Martínez-Redondo

Jannig

Correia

et al. 2016

Journal of Biological Chemistry

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“…PGC-1b expression was decreased in the carotid artery of rats with balloon injury (Guo et al, 2013). Overexpression of PGC-1b in vivo significantly inhibits neointimal formation and significantly reduces proliferation of VSMCs (Guo et al, 2013). Furthermore, metformin can inhibit the proliferation of VSMCs by upregulating the expression of PGC-1b (Guo et al, 2013).…”

Section: Intimal Thickeningmentioning

confidence: 99%

“…Peroxisome proliferatoractivated receptor g coactivator-1 (PGC-1) is a very important regulator of many biological processes such as energy metabolism (Islam et al, 2018;Lee et al, 2019). PGC-1b expression was decreased in the carotid artery of rats with balloon injury (Guo et al, 2013). Overexpression of PGC-1b in vivo significantly inhibits neointimal formation and significantly reduces proliferation of VSMCs (Guo et al, 2013).…”

Section: Intimal Thickeningmentioning

confidence: 99%

“…Overexpression of PGC-1b in vivo significantly inhibits neointimal formation and significantly reduces proliferation of VSMCs (Guo et al, 2013). Furthermore, metformin can inhibit the proliferation of VSMCs by upregulating the expression of PGC-1b (Guo et al, 2013). In a rat model of insulin resistance formed by high fructose diet for 4 weeks, the rat carotid artery was damaged by balloon catheter.…”

Section: Intimal Thickeningmentioning

confidence: 99%

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Metformin and Vascular Diseases: A Focused Review on Smooth Muscle Cell Function

Mingying

et al. 2020

Front. Pharmacol.

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Metformin has been used in diabetes for more than 60 years and has excellent safety in the therapy of human type 2 diabetes (T2D). There is growing evidence that the beneficial health effects of metformin are beyond its ability to improve glucose metabolism. Metformin not only reduces the incidence of cardiovascular diseases (CVD) in T2D patients, but also reduces the burden of atherosclerosis (AS) in pre-diabetes patients. Vascular smooth muscle cells (VSMCs) function is an important factor in determining the characteristics of the entire arterial vessel. Its excessive proliferation contributes to the etiology of several types of CVD, including AS, restenosis, and pulmonary hypertension. Current studies show that metformin has a beneficial effect on VSMCs function. Therefore, this review provides a timely overview of the role and molecular mechanisms by which metformin acts through VSMCs to protect CVD.

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Metabolic adaptations of cells at the vascular-immune interface during atherosclerosis

Bonacina

Dalt

Catapano

et al. 2021

Molecular Aspects of Medicine

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Metabolic reprogramming is a physiological cellular adaptation to intracellular and extracellular stimuli that couples to cell polarization and function in multiple cellular subsets. Pathological conditions associated to nutrients overload, such as dyslipidaemia, may disturb cellular metabolic homeostasis and, in turn, affect cellular response and activation, thus contributing to disease progression. At the vascular/immune interface, the site of atherosclerotic plaque development, many of these changes occur. Here, an intimate interaction between endothelial cells (ECs), vascular smooth muscle cells (VSMCs) and immune cells, mainly monocytes/macrophages and lymphocytes, dictates physiological versus pathological response. Furthermore, atherogenic stimuli trigger metabolic adaptations both at systemic and cellular level that affect the EC layer barrier integrity, VSMC proliferation and migration, monocyte infiltration, macrophage polarization, lymphocyte T and B activation. Rewiring cellular metabolism by repurposing “metabolic drugs” might represent a pharmacological approach to modulate cell activation at the vascular immune interface thus contributing to control the immunometabolic response in the context of cardiovascular diseases.

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Peroxisome Proliferator-activated Receptor γ Coactivator 1β (PGC-1β) Protein Attenuates Vascular Lesion Formation by Inhibition of Chromatin Loading of Minichromosome Maintenance Complex in Smooth Muscle Cells

Cited by 8 publications

References 57 publications

Peroxisome Proliferator-activated Receptor γ Coactivator-1 α Isoforms Selectively Regulate Multiple Splicing Events on Target Genes

Peroxisome Proliferator-activated Receptor γ Coactivator-1 α Isoforms Selectively Regulate Multiple Splicing Events on Target Genes

Metformin and Vascular Diseases: A Focused Review on Smooth Muscle Cell Function

Metabolic adaptations of cells at the vascular-immune interface during atherosclerosis

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