The Role of Chemokine Receptors in Renal Fibrosis

2020 ◽  
pp. 1-24
Author(s):  
Fenglei Wu ◽  
Chi Sun ◽  
Jianquan Lu
Keyword(s):  
Chemokine Receptors ◽  
Renal Fibrosis

scholarly journals Emerging role of miRNAs in renal fibrosis

RNA Biology ◽  
2019 ◽  
Vol 17 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Youling Fan ◽  
Hongtao Chen ◽  
Zhenxing Huang ◽  
Hong Zheng ◽  
Jun Zhou
Keyword(s):  
Renal Fibrosis

scholarly journals Role of IL-17 and Th17 Cells in Liver Diseases

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Linda Hammerich ◽  
Felix Heymann ◽  
Frank Tacke
Keyword(s):  
Chemokine Receptors ◽  
Liver Diseases ◽  
Th17 Cells ◽  
Hepatic Inflammation ◽  
T Helper ◽  
Disease Etiology ◽  
Cell Recruitment ◽  
Cell Responses ◽  
Injured Liver

Unbalanced Th1/Th2 T-cell responses in the liver are a characteristic of hepatic inflammation and subsequent liver fibrosis. The recently discovered Th17 cells, a subtype of CD4+T-helper cells mainly producing IL-17 and IL-22, have initially been linked to host defense against infections and to autoimmunity. Their preferred differentiation upon TGFβand IL-6, two cytokines abundantly present in injured liver, makes a contribution of Th17 cells to hepatic inflammation very likely. Indeed, initial studies in humans revealed activated Th17 cells and Th17-related cytokines in various liver diseases. However, functional experiments in mouse models are not fully conclusive at present, and the pathogenic contribution of Th17 cells to liver inflammation might vary upon the disease etiology, for example, between infectious and autoimmune disorders. Understanding the chemokines and chemokine receptors promoting hepatic Th17 cell recruitment (possibly CCR6 or CCR4) might reveal new therapeutic targets interfering with Th17 migration or differentiation in liver disease.

scholarly journals Identification of a microRNA signature in renal fibrosis: role of miR-21

2011 ◽  
Vol 301 (4) ◽  
pp. F793-F801 ◽  
Author(s):  
Abolfazl Zarjou ◽  
Shanzhong Yang ◽  
Edward Abraham ◽  
Anupam Agarwal ◽  
Gang Liu
Keyword(s):  
Epithelial Cells ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Response To Treatment ◽  
Tubular Epithelial Cells ◽  
Altered Expression ◽  
Tnf Α ◽  
Tgf Β1

Renal fibrosis is a final stage of many forms of kidney disease and leads to impairment of kidney function. The molecular pathogenesis of renal fibrosis is currently not well-understood. microRNAs (miRNAs) are important players in initiation and progression of many pathologic processes including diabetes, cancer, and cardiovascular disease. However, the role of miRNAs in kidney injury and repair is not well-characterized. In the present study, we found a unique miRNA signature associated with unilateral ureteral obstruction (UUO)-induced renal fibrosis. We found altered expression in UUO kidneys of miRNAs that have been shown to be responsive to stimulation by transforming growth factor (TGF)-β1 or TNF-α. Among these miRNAs, miR-21 demonstrated the greatest increase in UUO kidneys. The enhanced expression of miR-21 was located mainly in distal tubular epithelial cells. miR-21 expression was upregulated in response to treatment with TGF-β1 or TNF-α in human renal tubular epithelial cells in vitro. Furthermore, we found that blocking miR-21 in vivo attenuated UUO-induced renal fibrosis, presumably through diminishing the expression of profibrotic proteins and reducing infiltration of inflammatory macrophages in UUO kidneys. Our data suggest that targeting specific miRNAs could be a novel therapeutic approach to treat renal fibrosis.

scholarly journals The Role of Apelin on the Alleviative Effect of Angiotensin Receptor Blocker in Unilateral Ureteral Obstruction-Induced Renal Fibrosis

Nephron Extra ◽  
2012 ◽  
Vol 2 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Masashi Nishida ◽  
Yasuko Okumura ◽  
Tatsujiro Oka ◽  
Kentaro Toiyama ◽  
Seiichiro Ozawa ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Angiotensin Receptor Blocker ◽  
Unilateral Ureteral Obstruction ◽  
Receptor Blocker ◽  
Angiotensin Receptor

scholarly journals Molecular Basis for CCRL2 Regulation of Leukocyte Migration

2020 ◽  
Vol 8 ◽  
Author(s):  
Tiziana Schioppa ◽  
Francesca Sozio ◽  
Ilaria Barbazza ◽  
Sara Scutera ◽  
Daniela Bosisio ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Chemokine Receptors ◽  
Transmembrane Domain ◽  
Nk Cell ◽  
Structural Features ◽  
Negative Regulator ◽  
Leukocyte Migration ◽  
Genetic Ablation

CCRL2 is a seven-transmembrane domain receptor that belongs to the chemokine receptor family. At difference from other members of this family, CCRL2 does not promote chemotaxis and shares structural features with atypical chemokine receptors (ACKRs). However, CCRL2 also differs from ACKRs since it does not bind chemokines and is devoid of scavenging functions. The only commonly recognized CCRL2 ligand is chemerin, a non-chemokine chemotactic protein. CCRL2 is expressed both by leukocytes and non-hematopoietic cells. The genetic ablation of CCRL2 has been instrumental to elucidate the role of this receptor as positive or negative regulator of inflammation. CCRL2 modulates leukocyte migration by two main mechanisms. First, when CCRL2 is expressed by barrier cells, such endothelial, and epithelial cells, it acts as a presenting molecule, contributing to the formation of a non-soluble chemotactic gradient for leukocytes expressing CMKLR1, the functional chemerin receptor. This mechanism was shown to be crucial in the induction of NK cell-dependent immune surveillance in lung cancer progression and metastasis. Second, by forming heterocomplexes with other chemokine receptors. For instance, CCRL2/CXCR2 heterodimers were shown to regulate the activation of β2-integrins in mouse neutrophils. This mini-review summarizes the current understanding of CCRL2 biology, based on experimental evidence obtained by the genetic deletion of this receptor in in vivo experimental models. Further studies are required to highlight the complex functional role of CCRL2 in different organs and pathological conditions.

scholarly journals PET Imaging Radiotracers of Chemokine Receptors

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5174
Author(s):  
Santosh R. Alluri ◽  
Yusuke Higashi ◽  
Kun-Eek Kil
Keyword(s):  
Small Molecules ◽  
Chemokine Receptors ◽  
Brain Disorders ◽  
Infectious Agents ◽  
Cardiovascular Research ◽  
Critical Signal ◽  
Inflammatory Reactions ◽  
Positron Emission

Chemokines and chemokine receptors have been recognized as critical signal components that maintain the physiological functions of various cells, particularly the immune cells. The signals of chemokines/chemokine receptors guide various leukocytes to respond to inflammatory reactions and infectious agents. Many chemokine receptors play supportive roles in the differentiation, proliferation, angiogenesis, and metastasis of diverse tumor cells. In addition, the signaling functions of a few chemokine receptors are associated with cardiac, pulmonary, and brain disorders. Over the years, numerous promising molecules ranging from small molecules to short peptides and antibodies have been developed to study the role of chemokine receptors in healthy states and diseased states. These drug-like candidates are in turn exploited as radiolabeled probes for the imaging of chemokine receptors using noninvasive in vivo imaging, such as positron emission tomography (PET). Recent advances in the development of radiotracers for various chemokine receptors, particularly of CXCR4, CCR2, and CCR5, shed new light on chemokine-related cancer and cardiovascular research and the subsequent drug development. Here, we present the recent progress in PET radiotracer development for imaging of various chemokine receptors.

scholarly journals Personalized Health and the Coronavirus Vaccines --Do Individual Genetics Matter?

2021 ◽  
Author(s):  
Bianca N Valdés-Fernández ◽  
Jorge Duconge ◽  
Ana M Espino ◽  
Gualberto Ruaño
Keyword(s):  
Chemokine Receptors ◽  
Viral Vectors ◽  
Time Course ◽  
New Era ◽  
Vaccine Responses ◽  
Histocompatibility Complex ◽  
Technology Platforms ◽  
Preventative Interventions ◽  
Personalized Health

This article assesses the role of recipient genetics to COVID-19 vaccine responses. Vaccines represent preventative interventions suitable to an immunogenetic perspective to predict how human variability will influence their safety and efficacy. The genetic polymorphism among individuals within any population can make possible that the immunity elicited by a vaccine is variable in length and strength. The same immune challenge (either virus or vaccine) could provoke partial, complete or even failed protection for some individuals treated under the same conditions. We review genetic variants and mechanistic relationships among chemokines, chemokine receptors, interleukins, interferons, interferon receptors, toll-like receptors, histocompatibility antigens, various immunoglobulins and major histocompatibility complex antigens. These are the targets for variation among macrophages, dendritic cells, Natural Killer cells, T- and B- lymphocytes, and complement. The acute nature of vaccine reactogenicity is reminiscent of the time course of adverse drug reaction mediated by the immune system. The variety of technology platforms (mRNA, viral vectors) utilized currently to produce vaccines against SARS-CoV-2 infections may each also trigger genetically distinct immune reactogenic profiles. With biobanking of recipient genomic DNA and serum immunoprofiling, global COVID-19 vaccinations could launch a new era of research and clinical translation in personalized health.

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