Macrophage polarization in kidney diseases

doi:10.14800/macrophage.679

Cited by 27 publications

(20 citation statements)

References 62 publications

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“…Likewise, only Tlr5 of the four genes related to the M2 subset of macrophages ( Ccl3 , Il10 , Tlr1 , Tlr5 ) 33–35 was upregulated at this time. Sixty and 120 days after renal ablation 3 of the 4 M1-related genes, and none of the M2-related genes, were significantly overexpressed (Fig.…”

Section: Resultsmentioning

confidence: 86%

Innate And Adaptive Immunity are Progressively Activated in Parallel with Renal Injury in the 5/6 Renal Ablation Model

Fanelli

Arias

Machado

et al. 2017

Sci Rep

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The mechanisms triggering renal inflammation in chronic kidney disease (CKD) are unclear. We performed a detailed analysis of the time course of innate and adaptive immunity activation in the 5/6 renal ablation (Nx) model. Munich-Wistar rats undergoing Nx were studied 15, 60 and 120 days after ablation. Hypertension, albuminuria, creatinine retention, interstitial expansion and infiltration by macrophages and T-lymphocytes were already evident 15 days after Nx. PCR-array was used to screen for altered gene expression, whereas gene and protein expressions of TLR4, CASP1, IL-1β and NLRP3 were individually assessed. Tlr4, Tlr5, Lbp, Nlrp3, Casp1, Irf7 and Il1b were already upregulated 15 days after Nx, while activation of Tlr2, Tlr7, Tlr9, Nod2, Tnf and Il6 was seen after 60 days post-ablation. The number of genes related to innate or adaptive immunity grew steadily with time. These observations indicate that parallel activation of innate and adaptive immunity antecedes glomerular injury and involves a growing number of intricate signaling pathways, helping to explain the difficulty in detaining renal injury in Nx as CKD advances, and, stressing the need for early treatment. Additionally, these findings may contribute to the search of therapeutic targets specific for advanced phases of CKD.

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Section: Resultsmentioning

confidence: 86%

Innate And Adaptive Immunity are Progressively Activated in Parallel with Renal Injury in the 5/6 Renal Ablation Model

Fanelli

Arias

Machado

et al. 2017

Sci Rep

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“…In response to various physiological or pathological cues, macrophages display an extended life span and acquire different functional phenotypes through a process called macrophage polarization that are generally categorized into two broad but distinct subsets as either classically activated (M1) or alternatively activated (M2). In general, M1 macrophages have high motility and promote inflammation and damage through a combination of transcription factors such as NF-κB, whereas M2 macrophages help to resolve inflammation and promote tissue remodeling [ 78 , 79 ]. M1 macrophage accumulation has been documented during early stages of kidney injury, while M2 macrophages are more prevalent during later stages of injury as there is effort to resolve inflammation and promote repair [ 80 , 81 ].…”

Section: Tpa and Nf-κb In Kidney Diseasementioning

confidence: 99%

NF-κB and tPA Signaling in Kidney and Other Diseases

White

Lin

2020

Cells

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The activation of the nuclear factor-κB (NF-κB) pathway plays a central role in the initiation and progression of inflammation, which contributes to the pathogenesis and progression of various human diseases including kidney, brain, and other diseases. Tissue plasminogen activator (tPA), a serine protease regulating homeostasis of blood coagulation, fibrinolysis, and matrix degradation, has been shown to act as a cytokine to trigger profound receptor-mediated intracellular events, modulate the NF-κB pathway, and mediate organ dysfunction and injury. In this review, we focus on the current understanding of NF-κB and tPA signaling in the development and progression of kidney disease. Their roles in the nervous and cardiovascular system are also briefly discussed.

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“…Under pathological conditions microglia can be “activated”, e.g., by infectious agents, tissue damage or functional modifications of neighboring neurons. This is accompanied by a drastic morphological change towards an ameboid phenotype and an altered expression of surface molecules and releasable factors (Kettenmann et al, 2011; Hu et al, 2015) that is strongly dependent on the brain region and the nature of the activating agent. It was shown that microglia isolated from different brain regions and the spinal cord differ in the severity of a pro-inflammatory response (Baskar Jesudasan et al, 2014).…”

Section: Microglial Polarization and Phenotypesmentioning

confidence: 99%

“…The “M2” phenotype provides a rather neuroprotective environment by the release of anti-inflammatory cytokines (e.g., IL-4, IL-10, IL-13) or growth factors such as TGF-β and promotes tissue repair and regeneration. A growing body of evidence suggests different “M2” subpopulations with distinct biological functions (Hu et al, 2015; Tang and Le, 2016). …”

Section: Microglial Polarization and Phenotypesmentioning

confidence: 99%

Modulation of Microglial Activity by Rho-Kinase (ROCK) Inhibition as Therapeutic Strategy in Parkinson’s Disease and Amyotrophic Lateral Sclerosis

Roser

Tönges

Lingor

2017

Front. Aging Neurosci.

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Neurodegenerative diseases are characterized by the progressive degeneration of neurons in the central and peripheral nervous system (CNS, PNS), resulting in a reduced innervation of target structures and a loss of function. A shared characteristic of many neurodegenerative diseases is the infiltration of microglial cells into affected brain regions. During early disease stages microglial cells often display a rather neuroprotective phenotype, but switch to a more pro-inflammatory neurotoxic phenotype in later stages of the disease, contributing to the neurodegeneration. Activation of the Rho kinase (ROCK) pathway appears to be instrumental for the modulation of the microglial phenotype: increased ROCK activity in microglia mediates mechanisms of the inflammatory response and is associated with improved motility, increased production of reactive oxygen species (ROS) and release of inflammatory cytokines. Recently, several studies suggested inhibition of ROCK signaling as a promising treatment option for neurodegenerative diseases. In this review article, we discuss the contribution of microglial activity and phenotype switch to the pathophysiology of Parkinson’s disease (PD) and Amyotrophic lateral sclerosis (ALS), two devastating neurodegenerative diseases without disease-modifying treatment options. Furthermore, we describe how ROCK inhibition can influence the microglial phenotype in disease models and explore ROCK inhibition as a future treatment option for PD and ALS.

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Macrophage polarization in kidney diseases

Cited by 27 publications

References 62 publications

Innate And Adaptive Immunity are Progressively Activated in Parallel with Renal Injury in the 5/6 Renal Ablation Model

Innate And Adaptive Immunity are Progressively Activated in Parallel with Renal Injury in the 5/6 Renal Ablation Model

NF-κB and tPA Signaling in Kidney and Other Diseases

Modulation of Microglial Activity by Rho-Kinase (ROCK) Inhibition as Therapeutic Strategy in Parkinson’s Disease and Amyotrophic Lateral Sclerosis

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