TRAIL-Expressing Monocyte/Macrophages Are Critical for Reducing Inflammation and Atherosclerosis

Cartland, Siân P.; Genner, Scott; Martínez, Gonzalo; Robertson, S. E. J.; Kockx, Maaike; Lin, Ruby C.Y.; O’Sullivan, John; Koay, Yen Chin; Cholan, Pradeep Manuneedhi; Kebede, Melkam A.; Murphy, Andrew; Masters, Seth L.; Bennett, Martin R.; Jessup, Wendy; Kritharides, Leonard; Geczy, Carolyn L.; Patel, Sanjay; Kavurma, Mary M.

doi:10.1016/j.isci.2018.12.037

Cited by 41 publications

(50 citation statements)

References 47 publications

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“…Interestingly, genetic deletion of the receptor for TNF‐related apoptosis‐inducing ligand (TRAIL) exacerbates the ductular reaction and causes parenchymal, bridging fibrosis in the Mdr2 −/− mouse ( Mdr2 −/− Tr −/− ), suggesting that TRAIL proapoptotic signaling may restrain the expansion of DRCs, which, in turn, can influence HSC activation. Indeed, these mice exhibit expansion of a subpopulation of restorative macrophages (Mer protooncogene tyrosine kinase + /cluster of differentiation 206 + /galectin 2 + ) expressing TRAIL, pointing to an ongoing compensatory process to restrain the number of DRCs …”

Section: The Proliferative Cholangiocyte Compartment In Psc: Drcsmentioning

confidence: 99%

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The Spectrum of Reactive Cholangiocytes in Primary Sclerosing Cholangitis

et al. 2020

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Cholangiocytes are the target of a group of chronic liver diseases termed the “cholangiopathies,” in which cholangiocytes react to exogenous and endogenous insults, leading to disease initiation and progression. In primary sclerosing cholangitis (PSC), the focus of this review, the cholangiocyte response to genetic or environmental insults can lead to a heterogeneous response; that is, a subpopulation acquires a ductular reactive and proliferative phenotype, while another subpopulation undergoes senescence and growth arrest. Both ductular reactive cholangiocytes and senescent cholangiocytes can modify the periductal microenvironment through their ability to secrete various cytokines, chemokines, and growth factors, initiating and perpetuating inflammatory and profibrotic responses. This review discusses the similarities and differences, the interrelationships, and the potential pathogenic roles of these reactive proliferative and senescent cholangiocyte subpopulations in PSC.

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Section: The Proliferative Cholangiocyte Compartment In Psc: Drcsmentioning

confidence: 99%

“…Indeed, these mice exhibit expansion of a subpopulation of restorative macrophages (Mer protooncogene tyrosine kinase + /cluster of differentiation 206 + /galectin 2 + ) expressing TRAIL, pointing to an ongoing compensatory process to restrain the number of DRCs. (30)(31)(32)…”

Section: The Proliferative Cholangiocyte Compartment In Psc: Drcsmentioning

confidence: 99%

The Spectrum of Reactive Cholangiocytes in Primary Sclerosing Cholangitis

et al. 2020

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“…Indeed, recombinant TRAIL administration to diabetic Apoe −/− mice increased VSMC-positive cell numbers within the plaque cap with a tendency for increased collagen ( 76 ). These are significant since plasma TRAIL levels are suppressed in patients with atherosclerosis ( 77 , 78 , 79 , 80 ).…”

Section: Trail Signals and Vascular Remodellingmentioning

confidence: 99%

TRAIL signals, extracellular matrix and vessel remodelling

2020

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The extracellular matrix (ECM) is an essential part of the vasculature, not only providing structural support to the blood vessel wall, but also in its ability to interact with cells to regulate cell phenotype and function including proliferation, migration, differentiation and death; processes important in vascular remodelling. Increasing evidence implicates TNF-related apoptosis-inducing ligand (TRAIL) signalling in the modulation of vascular cell function and remodelling under normal and pathological conditions such as in atherosclerosis. TRAIL can also stimulate synthesis of multiple ECM components within blood vessels. This review explores the relationship between TRAIL signals, the ECM, and its implications in vessel remodelling in cardiovascular disease.

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“…11 cDNA was synthesized as described. 11,12 Real-time qPCR was performed, and relative expression was determined using the 2 −∆∆Ct method using rat primers described in Table 1, normalized to GAPDH or β-actin house-keeping genes.…”

Section: Quantitative Pcr (Qpcr)mentioning

confidence: 99%

“…15 2-8 wk, n = 4-6). Body weights (C) at the beginning of the study (n = [11][12] and (D) after 8-wk feeding (n = 5-6), and (E) weight gain over the course of the study (n = 5-6). Results are mean ± SEM two-way ANOVA, t test or one-way ANOVA; *P < .05, **P < .01, ***P < .001, ****P < .0001…”

Section: Shr Rats Have Altered Plasma Chemistriesmentioning

confidence: 99%

A “Western Diet” promotes symptoms of hepatic steatosis in spontaneously hypertensive rats

Cartland

Tamer

Patil

et al. 2020

Int J Experimental Path

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Summary Systemic hypertension, characterized by elevated blood pressure ≥140/90 mm Hg, is a major modifiable risk factor for cardiovascular disease. Hypertension also associates with non‐alcoholic fatty liver disease (NAFLD), which is becoming common due to a modern diet and lifestyle. The aim of the present study was to examine whether a high‐fat "Western" diet had effects on hypertension and associated NAFLD. Normotensive Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were placed on a normal chow or high‐fat diet for 8 weeks; blood pressure was measured fortnightly and body weight recorded weekly. As expected, SHR had elevated blood pressure compared to WKY. Diet did not influence blood pressure. Compared to SHR, WKY rats gained more weight, associating with increased white adipose tissue weight. Normotensive rats also had higher plasma cholesterol and triglycerides in response to a “Western” diet, with no changes in plasma glucose levels. Neither strain developed atherosclerosis. Interestingly, high‐fat diet‐fed SHR had increased liver weight, associating with a significant level of hepatic lipid accumulation not observed in WKY. Further, they exhibited hepatocellular ballooning and increased hepatic inflammation, indicative of steatohepatitis. These findings suggest that a high‐fat “Western” diet promotes features of NAFLD in SHR, but not WKY rats. Importantly, the high‐fat diet had no effect on blood pressure.

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TRAIL-Expressing Monocyte/Macrophages Are Critical for Reducing Inflammation and Atherosclerosis

Cited by 41 publications

References 47 publications

The Spectrum of Reactive Cholangiocytes in Primary Sclerosing Cholangitis

The Spectrum of Reactive Cholangiocytes in Primary Sclerosing Cholangitis

TRAIL signals, extracellular matrix and vessel remodelling

A “Western Diet” promotes symptoms of hepatic steatosis in spontaneously hypertensive rats

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