STAT4 and the proliferation of artery smooth muscle cells in atherosclerosis

Guo, Feng; Zarella, Christopher

doi:10.1016/j.yexmp.2006.04.009

Cited by 10 publications

(10 citation statements)

References 37 publications

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“…STAT4 has previously been shown to function in mediating proliferative and anti-proliferative signals, for example, STAT4 with STAT1 mediates IL-35-induced suppression of conventional T cells, 19 and STAT4 suppresses the proliferation of connective tissue-type mast cells. 41 However, our data suggest that the role of STAT4 is greater than one which simply mediates signals from extracellular stimuli to promote initiation of cell division. 41 However, our data suggest that the role of STAT4 is greater than one which simply mediates signals from extracellular stimuli to promote initiation of cell division.…”

Section: Discussionmentioning

confidence: 68%

STAT4 expression and activation is increased during mitosis in vitro and in vivo in skin‐ and mucosa‐derived cell types: implications in neoplastic and inflammatory skin diseases

Ferreli

Lai

August

et al. 2017

Acad Dermatol Venereol

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Section: Discussionmentioning

confidence: 68%

STAT4 expression and activation is increased during mitosis in vitro and in vivo in skin‐ and mucosa‐derived cell types: implications in neoplastic and inflammatory skin diseases

Ferreli

Lai

August

et al. 2017

Acad Dermatol Venereol

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“…Of special interest in the WC-As are genes encoding the signal transducers and activators of transcription (STAT). One member of the STAT family, STAT4, may play a role in VSMC proliferation and has recently been demonstrated to be upregulated in cholesterol-fed WC-As pigeons in vivo (Guo et al, 2006). In the current study, cyclin D2 (CCND2) in WC-As aortic cells was placed in the STAT signaling by pathway analysis.…”

Section: Theme 3: Cell Signaling Pathwaysmentioning

confidence: 97%

Differentially expressed genes in aortic smooth muscle cells from atherosclerosis-susceptible and atherosclerosis-resistant pigeons

et al. 2012

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Susceptibility to spontaneous atherosclerosis in the White Carneau (WC-As) pigeon shows autosomal recessive inheritance. Aortic smooth muscle cells (SMC) cultured from susceptible WC-As and resistant Show Racer (SR-Ar) pigeons exhibit developmental and degenerative features corresponding to the respective SMC at atherosclerosis-prone sites in vivo. We used representational difference analysis to identify differentially expressed genes between WC-As and SR-Ar aortic SMC. Total RNA was extracted from cultured primary SMC of each breed, converted to double-stranded cDNA, followed by direct comparison in reciprocal representational difference analysis experiments. Difference products were cloned, sequenced, and identified by BLAST against the chicken genome. Six putative biochemical pathways were distinctly different between breeds with genes involved in energy metabolism and contractility exhibiting the most striking disparity. Genes associated with glycolysis and a synthetic SMC phenotype were expressed in WC-As cells. In contrast, SR-Ar cells expressed genes indicative of oxidative phosphorylation and a contractile SMC phenotype. In WC-As cells, the alternatives of insufficient ATP production limiting contractile function or the lack of functional contractile elements downregulating ATP synthesis cannot be distinguished due to the compressed in vitro versus in vivo developmental time frame. However, the genetic potential for effectively coupling energy production to muscle contraction present in the resistant SR-Ar was lacking in the susceptible WC-As.

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“…Consistent with this observation, several genes associated with increased vascular inflammation are Ͼ2-fold down-regulated by E 2 in aorta, including AGER, the advanced glycation end-product receptor, which induces inflammation in vascular cells and is strongly associated with atherosclerosis (36), CRP, Creactive protein, a well-established serum marker for atherosclerotic CVD risk (37), SELPLG, the selectin P ligand expressed on vascular endothelial cells and critical for capture of leukocytes in early inflammatory reactions (38), STAT4, a TF controlling inflammatory gene expression in response to several inflammatory signals, which is expressed at high levels in atherosclerosis-prone aortas and promotes smooth muscle cell proliferation in response to IL-12 (39), and IL1RL1/ST2L, interleukin 1 receptor-like 1, an interleukin receptor that mediates the inflammatory response of endothelial cells to IL-33 (40), as well as 6 other chemokine and interleukin receptors (Cxcr4, Ccr7, Il1r2, IL2rb, IL2rg, and Il27ra) and the chemokine Xcl1.…”

Section: Estrogen Regulates Distinct Biological Functions In Aorta Vsmentioning

confidence: 99%

Research Resource: Aorta- and Liver-Specific ERα-Binding Patterns and Gene Regulation by Estrogen

Gordon

Vallaster

Westerling

et al. 2014

Molecular Endocrinology

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Estrogen has vascular protective effects in premenopausal women and in women younger than 60 years who are receiving hormone replacement therapy. However, estrogen also increases the risks of breast and uterine cancers and of venous thromboses linked to up-regulation of coagulation factors in the liver. In mouse models, the vasculoprotective effects of estrogen are mediated by the estrogen receptor α (ERα) transcription factor. Here, through next-generation sequencing approaches, we show that almost all of the genes regulated by 17β-estradiol (E2) differ between mouse aorta and mouse liver, ex vivo, and that this difference is associated with a distinct genomewide distribution of ERα on chromatin. Bioinformatic analysis of E2-regulated promoters and ERα binding site sequences identify several transcription factors that may determine the tissue specificity of ERα binding and E2-regulated genes, including the enrichment of NF-κB, AML1, and AP1 sites in the promoters of E2 down-regulated inflammatory genes in aorta but not liver. The possible vascular-specific functions of these factors suggest ways in which the protective effects of estrogen could be promoted in the vasculature without incurring negative effects in other tissues.

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STAT4 and the proliferation of artery smooth muscle cells in atherosclerosis

Cited by 10 publications

References 37 publications

STAT4 expression and activation is increased during mitosis in vitro and in vivo in skin‐ and mucosa‐derived cell types: implications in neoplastic and inflammatory skin diseases

STAT4 expression and activation is increased during mitosis in vitro and in vivo in skin‐ and mucosa‐derived cell types: implications in neoplastic and inflammatory skin diseases

Differentially expressed genes in aortic smooth muscle cells from atherosclerosis-susceptible and atherosclerosis-resistant pigeons

Research Resource: Aorta- and Liver-Specific ERα-Binding Patterns and Gene Regulation by Estrogen

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