Macrophage Products Inhibit Human Aortic Smooth Muscle Cell Proliferation and Alter 1α(I) Procollagen Expression

Halloran, Brian G.; Grange, Janet J.; So, Byung Jun; Baxter, B. Timothy

doi:10.1007/s100169900014

Cited by 12 publications

(8 citation statements)

References 11 publications

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“…Mechanical forces may also act to alter ECM synthesis in an indirect manner by stimulating cellular release of cytokines such as tumor necrosis factor-␣, 72 which inhibits procollagen expression in human aortic SMCs. 73 In sum, these studies support the idea that stress concentrations in the AAA wall may lead to altered ECM synthesis.…”

Section: Stress-mediated or Strain-mediated Wall Weakeningsupporting

confidence: 62%

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Vorp

Geest

2005

ATVB

228

172

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Abstract-Rupture of abdominal aortic aneurysm (AAA) represents a significant clinical event, having a mortality rate of 90% and being currently ranked as the 13th leading cause of death in the US. The ability to reliably evaluate the susceptibility of a particular AAA to rupture on a case-specific basis could vastly improve the clinical management of these patients. Because AAA rupture represents a mechanical failure of the degenerated aortic wall, biomechanical considerations are important to understand this process and to improve our predictions of its occurrence. Presented here is an overview of research to date related to the biomechanics of AAA rupture. This includes a summary of results related to ex vivo and in vivo mechanical testing, noninvasive AAA wall stress estimations, and potential mechanisms of AAA wall weakening. We conclude with a demonstration of a biomechanics-based approach to predicting AAA rupture on a patient-specific basis, which may ultimately prove to be superior to the widely and currently used maximum diameter criterion. Key Words: abdominal aortic aneurysm Ⅲ biomechanics Ⅲ rupture Ⅲ strength Ⅲ stress A bdominal aortic aneurysm (AAA) is a focal enlargement of the infrarenal aorta, which occurs over a time course of several years. This condition is present in Ϸ2% of the elderly population, with Ϸ150 000 new cases diagnosed each year, and the incidence is increasing. 1,2 If left untreated, AAA will gradually expand until rupture; it is an event that carries a mortality rate of 90% and that is ranked as the 13th most common cause of death in the US. 3 Current AAA repair procedures are expensive and carry significant morbidity and mortality risks.Open repair of AAA is a major surgical procedure that requires patients to be hospitalized typically for 1 week and to recuperate at home for several more weeks. The mean postoperative mortality for elective repair is Ϸ5% and for emergency operations 47% (range 27% to 69%). 4 The major drawback of open repair is the compromised quality of life after surgery because of postoperative pain, the prolonged recovery period, and the high costs associated with both the surgery and the recovery.An alternative approach that avoids the extensive tissue dissection associated with open repair is the minimally invasive endovascular repair procedure. The potential advantages of endovascular AAA repair include reductions in mortality, morbidity, blood loss, hospital stay, intensive careOriginal

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Section: Stress-mediated or Strain-mediated Wall Weakeningsupporting

confidence: 62%

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Vorp

Geest

2005

ATVB

228

172

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“…RAW264.7 cells were co-cultured with smooth muscle cell line, MOVAS, in an indirect co-culture system as described [27, 28]. Totally 2×10 5 RAW264.7 cells after 50 mg/L ox-LDL challenging for 24 hours were seeded in the up layer in the Transwell units, and 2×10 5 MOVAS cells were seeded in the down layer in the well of six-well plates (In Vitro Scientific, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

PTPRO Promotes Oxidized Low-Density Lipoprotein Induced Oxidative Stress and Cell Apoptosis through Toll-Like Receptor 4/Nuclear Factor κB Pathway

Liang

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Critical roles of phosphatase receptor type O (PTPRO) and toll-like receptor 4 (TLR4) have been implicated in inflammation. However, little is known about their functional effects on atherosclerosis (AS). We aim to study their potential function in AS. Methods: An oxidized low-density lipoprotein (ox-LDL) induced AS model constructed with PTPRO over-expressing RAW264.7 cells and PTPRO knockout macrophages. Cell apoptosis was assayed by flow cytometry and fatty accumulation was evaluated by oil red staining. The production of ROS (reactive oxygen species), SOD (superoxide dismutase), MDA (malondialdehyde), TC (Triglyceride), and TG (total cholesterol) was evaluated. Western blot was performed to detect the expression of CD36, TLR4 and nuclear factor kB (NF-κB). Results: PTPRO expression was promoted in a dose-dependent and time-dependent manner following ox-LDL challenging. In PTPRO-over-expressing cells, CD36 expression and the level of oil-red staining, TC and TG were increased; ROS production, MDA and level of cell apoptosis were improved, but SOD was reduced. However, in PTPRO knockout cells opposite results were found. TLR4 and NF-κB/p65 phosphorylation was significantly enhanced in PTPRO over-expressing cells, while significantly down-regulated in PTPRO knockout cells. Conclusion: PTPRO plays ital roles in AS via promoting ox-LDL induced oxidative stress and cell apoptosis through TLR4/NF-κB pathway.

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“…The extracellular matrix content, particularly the collagen type I content, usually determines the stability and durability of tissues, including arteries (Lee and Libby, 1997). Previous studies have reported that an activated macrophage supernatant can inhibit 1a(I) procollagen mRNA expression in arterial VSMC (Halloran et al, 1997). To further confirm whether IFN could affect collagen synthesis in VSMC in vitro, we incubated VSMC with the supernatant from LPS-or IFN-a-stimulated macrophages.…”

Section: Ifn-α Inhibited Col1a1 Gene Expression In Vsmcmentioning

confidence: 99%

Vulnerability of atherosclerotic plaques is associated with type I interferon in a murine model of lupus and atherosclerosis

Zhang¹,

Qu²,

Ye³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. This study aimed to investigate the relationship between type I interferon (IFN-I) and plaque stability in pristane-treated apolipoprotein E-knockout (ApoE -/-) mice. Antinuclear antibody (ANA) and extractable nuclear antigen antibody (ENA) levels were measured by immunofluorescence and enzyme-linked immunospot assay. Atherosclerotic plaques were detected by Sirius red/fast green staining. Cell apoptosis was detected by terminal deoxynucleotidyltransferasemediated dUTP-biotin nick-end labeling. Gene expression was determined by real-time PCR analyses. We found that pristane-treated ApoE -/-mice developed a lupus-like syndrome characterized by an increased production of serum ANA and ENA. Pristane treatment decreased the collagen content and increased the number of apoptotic cells in plaques. Moreover, IFN-induced ISG15, IFIT1-1, and IFIT1-2 gene expression was increased in peripheral blood cells and aortic plaques. An IFN-a-stimulated macrophage supernatant inhibited collagen type I, alpha 1 gene expression in vascular smooth muscle cells. We concluded that the vulnerability of plaques was associated C.Y. Zhang et al. 14872©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 14871-14881 (2015) with the activation of IFN-I in pristane-treated ApoE -/-mice. Thus, we speculated that the higher prevalence of cardiovascular events in patients with systemic lupus erythematosus could be due to plaque instability.

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Macrophage Products Inhibit Human Aortic Smooth Muscle Cell Proliferation and Alter 1α(I) Procollagen Expression

Cited by 12 publications

References 11 publications

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

PTPRO Promotes Oxidized Low-Density Lipoprotein Induced Oxidative Stress and Cell Apoptosis through Toll-Like Receptor 4/Nuclear Factor κB Pathway

Vulnerability of atherosclerotic plaques is associated with type I interferon in a murine model of lupus and atherosclerosis

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Macrophage Products Inhibit Human Aortic Smooth Muscle Cell Proliferation and Alter 1α(I) Procollagen Expression

Cited by 12 publications

References 11 publications

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

PTPRO Promotes Oxidized Low-Density Lipoprotein Induced Oxidative Stress and Cell Apoptosis through Toll-Like Receptor 4/Nuclear Factor κB Pathway

Vulnerability of atherosclerotic plaques is as­sociated with type I interferon in a murine model of lupus and atherosclerosis

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Vulnerability of atherosclerotic plaques is associated with type I interferon in a murine model of lupus and atherosclerosis