Neutrophil and Macrophage Cell Surface Colony-Stimulating Factor 1 Shed by ADAM17 Drives Mouse Macrophage Proliferation in Acute and Chronic Inflammation

Tang, Jingjing; Frey, Jeremy M.; Wilson, Carole L.; Moncada-Pazos, Ángela; Levet, Clémence; Freeman, Matthew; Rosenfeld, Michael E.; Stanley, E. Richard; Raines, Elaine W.; Bornfeldt, Karin E.

doi:10.1128/mcb.00103-18

Cited by 25 publications

(18 citation statements)

References 66 publications

(100 reference statements)

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“…Renal ADAM17 is elevated in acute and chronic kidney injury and can activate TNF-␣ and EGFR ligands, leading to the synthesis and release of inflammatory and profibrotic factors (20,31,32,56,74). Experimental studies have demonstrated that EGFR inhibition attenuates renal fibrosis and renal disease progression (10,41,75).…”

Section: Adam17 and Acute Kidney Injurymentioning

confidence: 99%

“…Clinical and experimental studies have shown that ADAM17 is involved in chronic kidney disease (CKD) with a proinflammatory and profibrotic role, suggesting that it could be an important mediator on CKD progression (20,32,56,74). For this reason, in this review, we aimed to summarize the importance of ADAM17 under physiological and pathological conditions related to renal function.…”

Section: Introductionmentioning

confidence: 99%

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Role of ADAM17 in kidney disease

Palau

Pascual

Soler

et al. 2019

American Journal of Physiology-Renal Physiology

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It is known that the renin-angiotensin system plays a major role in the pathophysiology of cardiovascular disease and renal injury. Within the renin-angiotensin system, angiotensin-converting enzyme 2 (ACE2) cleaves ANG II to generate ANG(1–7) peptide, which counteracts the adverse effects of ANG II accumulation. ACE2 can undergo cleavage or shedding to release the catalytically active ectodomain into the circulation by a disintegrin and metalloprotease (ADAM)17, also known as TNF-α-converting enzyme. ADAM17 is involved in many pathological processes such as cancer, inflammatory diseases, neurological diseases, cardiovascular diseases, atherosclerosis, diabetes, and hypertension. Clinical and experimental studies have shown that ADAM17 is involved in chronic kidney disease (CKD) with a proinflammatory and profibrotic role, suggesting that it could be an important mediator of CKD progression. ADAM17 inhibition attenuates fibrosis and inflammation, suggesting that its inhibition may be a possible new valuable therapeutic tool in fibrotic kidney disease treatment. In addition, in renal disease, some experimental studies have demonstrated that ADAM17 is differently expressed in the kidney. Thus, ADAM17 is highly expressed in distal renal tubules and increased in the whole kidney in diabetic models. In this article, we will review the role of ADAM17 under physiological and pathological conditions. We will mainly focus on the importance of ADAM17 in the context of CKD.

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Section: Adam17 and Acute Kidney Injurymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of ADAM17 in kidney disease

Palau

Pascual

Soler

et al. 2019

American Journal of Physiology-Renal Physiology

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“…In particular, macrophage proliferation that is dependent on ADAM17-mediated shedding of macrophage colony-stimulating factor-1 (CSF-1) from both neutrophils and macrophages is a key contributory process in these inflammation states [72]. Consistent with what we know about iRhom2 function, it was shown, using both acute thioglycollate-induced peritonitis and high-fat induced chronic atherosclerosis models, that iRhom2 is critical for driving macrophage proliferation [73].…”

Section: Irhoms and Disease Relevancementioning

confidence: 98%

The molecular, cellular and pathophysiological roles of iRhom pseudoproteases

2019

Self Cite

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iRhom proteins are catalytically inactive relatives of rhomboid intramembrane proteases. There is a rapidly growing body of evidence that these pseudoenzymes have a central function in regulating inflammatory and growth factor signalling and consequent roles in many diseases. iRhom pseudoproteases have evolved new domains from their proteolytic ancestors, which are integral to their modular regulation and functions. Although we cannot yet conclude the full extent of their molecular and cellular mechanisms, there is a clearly emerging theme that they regulate the stability and trafficking of other membrane proteins. In the best understood case, iRhoms act as regulatory cofactors of the ADAM17 protease, controlling its function of shedding cytokines and growth factors. It seems likely that as the involvement of iRhoms in human diseases is increasingly recognized, they will become the focus of pharmaceutical interest, and here we discuss what is known about their molecular mechanisms and relevance in known pathologies.

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“…A connection to most of the known hallmarks of cancer can be established for rhomboid pseudoproteases, most notably iRhom2 [69,89–96] and iRhom1 [47,71,97–99] but also RHBDD2 [100–102] and Derlin 1 [103–106] (Fig. 6).…”

Section: Physiological Roles Of Rhomboid Pseudoproteasesmentioning

confidence: 98%

The complex life of rhomboid pseudoproteases

Adrain

Cavadas

2020

The FEBS Journal

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Rhomboid pseudoproteases are catalytically inactive members of the rhomboid superfamily. The founding members, rhomboids, were first identified in Drosophila as serine intramembrane proteases that cleave transmembrane proteins, enabling signaling. This led to the discovery of the wider rhomboid superfamily, a clan that in metazoans is dominated by pseudoproteases. These so-called rhomboid pseudoproteases inherited from their catalytically active ancestors a conserved rhomboid-like domain and a propensity to regulate signaling. Lacking catalytic activity, they developed new 'pseudoenzyme' functions that include regulating the trafficking, turnover, and activity of their client proteins. Rhomboid pseudoproteases have preeminent roles in orchestrating immune cell activation, antiviral responses, and cytokine release in response to microbial infection, or in chronic diseases, and have also been implicated in growth factor signaling, cancer, and, more recently, metabolism. Here, we discuss the mechanism(s) of action of rhomboid pseudoproteases, contrasted with rhomboid proteases. We also highlight the roles of rhomboid pseudoproteases in mammalian physiology, which, quite paradoxically among pseudoenzymes, is understood much better than active rhomboids.

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Neutrophil and Macrophage Cell Surface Colony-Stimulating Factor 1 Shed by ADAM17 Drives Mouse Macrophage Proliferation in Acute and Chronic Inflammation

Cited by 25 publications

References 66 publications

Role of ADAM17 in kidney disease

Role of ADAM17 in kidney disease

The molecular, cellular and pathophysiological roles of iRhom pseudoproteases

The complex life of rhomboid pseudoproteases

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