CD36, but not G2A, modulates efferocytosis, inflammation, and fibrosis following bleomycin-induced lung injury

Parks, Brian W.; Black, Leland L.; Zimmerman, Kurt A.; Metz, Allison E.; Steele, Chad; Murphy-Ullrich, Joanne E.; Kabarowski, Janusz H.

doi:10.1194/jlr.m035352

Cited by 44 publications

(39 citation statements)

References 60 publications

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“…Results of our IR model studies further suggest that CD36-mediated removal of apoptotic cells during acute kidney injury may be an important link in the pathway toward chronic kidney disease, because clinical studies have identified acute kidney injury as a major factor in chronic kidney disease progression. 49 A recent study by Parks et al 50 showed that during acute lung injury CD36 was required for the timely removal of apoptotic cells, and pulmonary fibrosis was reduced in the absence of CD36. Alternatively, CD36 macrophages could have provided an important mitogenic stimulus to fibrogenic cells such as myofibroblasts, whereby loss of this CD36 subpopulation led to subsequent apoptosis.…”

Section: Cd36-dependent Phagocytosis Alters Fibrogenesismentioning

confidence: 98%

The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

Pennathur

Pasichnyk

Bahrami

et al. 2015

The American Journal of Pathology

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The removal of apoptotic cells is an innate function of tissue macrophages; however, its role in disease progression is unclear. The present study was designed to investigate the role of macrophage CD36, a recognized receptor of apoptotic cells and oxidized lipids, in two models of kidney injury: unilateral ureteral obstruction (UUO) and ischemia reperfusion. To differentiate the macrophage CD36-specific effects in vivo, we generated CD36 chimeric mice by bone marrow transplantation and evaluated the two models. Fibrosis severity was substantially decreased after UUO with a corresponding decrease in matrix synthesis in macrophage CD36-deficient mice. Despite a reduction in fibrosis severity, a 56% increase in apoptotic cells was found without an increase in apoptotic effectors. In addition, a substantial reduction was observed in tumor necrosis factor-α and transforming growth factor-β1 mRNA levels and intracellular bioactive oxidized lipid levels in CD36-deficient macrophages. To validate the functional role of macrophage CD36, we performed unilateral ischemia reperfusion, followed by contralateral nephrectomy. Similarly, we found that the severity of fibrosis was reduced by 55% with a corresponding improvement in kidney function by 88% in macrophage CD36-deficient mice. Taken together, these data suggest that macrophage CD36 is a critical regulator of oxidative fibrogenic signaling and that CD36-mediated phagocytosis of apoptotic cells may serve as an important pathway in the progression of fibrosis.

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Section: Cd36-dependent Phagocytosis Alters Fibrogenesismentioning

confidence: 98%

The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

Pennathur

Pasichnyk

Bahrami

et al. 2015

The American Journal of Pathology

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“…Professional phagocytes recognize externalized negatively charged glycerophospholipid phosphatidylserine (PS) in dying cells through their receptors (e.g., the TIM (T cell/transmembrane, immunoglobulin, and mucin) and TAM (Tyro3-, Axl-, and Mer-tyrosine kinase) families of PS receptors, macrophage scavenger receptor CD36, and integrins), which triggers the engulfment of dying cells [150,153]. In CD36 knockout mice, reduced efferocytosis is observed in lungs following bleomycin treatment [154,155]. miR-34a, a tumor suppressor transcriptionally induced by p53, is shown to negatively regulate efferocytosis by tissue macrophages, through reduction in the expression of an apoptotic cell-recognizing receptor tyrosine kinase Axl and NAD-dependent deacetylase sirtuin-1 [155,156].…”

Section: Efferocytosismentioning

confidence: 99%

Non-Canonical Cell Death Induced by p53

Ranjan

Iwakuma

2016

IJMS

106

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Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms. p53 impacts these non-canonical forms of cell death through transcriptional regulation of its downstream targets, as well as direct interactions with key players involved in these mechanisms, in a cell type- or tissue context-dependent manner. In this review article, we summarize and discuss the involvement of p53 in several non-canonical modes of cell death, including caspase-independent apoptosis (CIA), ferroptosis, necroptosis, autophagic cell death, mitotic catastrophe, paraptosis, and pyroptosis, as well as its role in efferocytosis which is the process of clearing dead or dying cells.

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“…FULLERTON et al, 2013;ORTEGA-GOMEZ et al, 2013;GABELLONI et al, 2013) e a maioria dos efeitos anti-apoptótica do ACG parece ser devido à sua ação antioxidante (LI et al, 2008;JI et al, 2013;JANG et al, 2013;PARKS et al, 2013).…”

Section: Efeitos Do Acg Sobre a Expressão De Cd36 E Mhciiunclassified

“…Ainda, o CD36 parece ser o mecanismo importante na fagocitose mediada pelo PPAR (BERRY et al, 2007). O papel fundamental do CD36 tem sido observado na fagocitose de neutrófilos apoptóticos em condições de hipóxia e na reação inflamatória pulmonar (ORTIZ-MASIA et al, 2012;PARKS et al, 2013). Da mesma forma, não há relatos da ação do ACG sobre a expressão de CD36.…”

Section: Efeitos Do Acg Sobre a Expressão De Cd36 E Mhciiunclassified

“…Da mesma forma, não há relatos da ação do ACG sobre a expressão de CD36. Nossas hipóteses, que conduzirão as etapas seguintes de investigação do laboratório, visarão investigar se o ACG estimula a expressão de TIM-4, que reconhecidamente é ligante para fosfatidilserina, fazendo ponte importante entre neutrófilos apoptóticos e macrófagos (NURTANIO & YANG, 2011;NISHI et al, 2014); se o ACG induz a expressão dos receptores de PPAR, um receptor nuclear que atua como fator de transcrição e possui inúmeros efeitos anti-inflamatórios, entre os quais a fagocitose de neutrófilos apoptóticos (PARKS et al, 2013); se o ACG induz a expressão de anexina A1, uma proteína induzida por glicocorticoides endógenos e que inibe o recrutamento de neutrófilos para o foco de lesão e estimula a apoptose de neutrófilos e sua subsequente fagocitose por macrófagos (ORTEGA-GOMEZ et al, 2013). As duas últimas hipóteses são reforçadas pelas habilidades dos agonistas PPAR e da anexina favorecerem a apoptose de neutrófilos (STANDIFORD et al, 2005;ORTEGA-GOMEZ et al, 2013), o que também foi observado pelo ACG.…”

Section: Efeitos Do Acg Sobre a Expressão De Cd36 E Mhciiunclassified

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Efeitos do ácido clorogênico sobre fenômenos celulares da resolução da inflamação

Moreira¹

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Peritoneal neutrophils were recruited 4 hours after local injection of 1% oyster glycogen and used for assessment of cell death mechanism, besides being used as apoptotic cells to be phagocyted. Peritoneal macrophages recruited 96 hours after the injection of 3% thioglycollate medium were used to 1) phagocytosis assay 2)Quantification of inflammatory mediators in the supernatant 3) quantification of MHC-II and CD36. The results showed that treatment with ACG, during 24 hours, at concentrations of 1, 10, 50 or 100 mM increased the percentage of apoptotic neutrophils and did not induced necrosis; incubation of macrophages during 1 hour with 1, 10, 50 or 100 mM increased the capacity of these cells to phagocyte apoptotic neutrophils; reduced tumor secretion of tumor necrosis factor (TNF-alpha) and did not alter the secretion of interleukin-10, and did not interfere with the expression of MHC-II and CD36. Together, these data suggest that the ACG can control the resolution of inflammation, by interfering with events in neutrophils and macrophages.

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CD36, but not G2A, modulates efferocytosis, inflammation, and fibrosis following bleomycin-induced lung injury

Cited by 44 publications

References 60 publications

The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

The Macrophage Phagocytic Receptor CD36 Promotes Fibrogenic Pathways on Removal of Apoptotic Cells during Chronic Kidney Injury

Non-Canonical Cell Death Induced by p53

Efeitos do ácido clorogênico sobre fenômenos celulares da resolução da inflamação

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