Exosomes derived from calcium oxalate-exposed macrophages enhance IL-8 production from renal cells, neutrophil migration and crystal invasion through extracellular matrix

Singhto, Nilubon; Thongboonkerd, Visith

doi:10.1016/j.jprot.2018.06.015

Cited by 57 publications

(55 citation statements)

References 41 publications

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“…IL‐8 is well believed to be a key chemotactic cytokine, which is involved in the recruitment of monocyte (Meniailo et al, ). Profibrotic mediators such as TGF‐β induced proximal tubular cells to secrete IL‐8, and its production was markedly enhanced in urine proteins obtained from patients with tubular injury (Huang, Wen, Zhou, & Yu, ; Qi et al, ; Singhto & Thongboonkerd, ). In our results, FSH‐treated HK‐2 cells resulted in the production of chemokine IL‐8, which, in turn, induced FSHR‐mediated macrophage migration.…”

Section: Discussionmentioning

confidence: 99%

Follicle‐stimulating hormone promotes renal tubulointerstitial fibrosis in aging women via the AKT/GSK‐3β/β‐catenin pathway

et al. 2019

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Estrogen withdrawal in aging women contributes to the progression of chronic kidney disease (CKD). However, the effect of high circulating follicle‐stimulating hormone (FSH) levels on renal dysfunction remains unknown. In this study, blood samples from 3,055 postmenopausal women were collected and tested, which showed that there was a strong negative correlation between eGFR and FSH levels (p < 0.001), independent of LH, testosterone, and estradiol. Functional FSHR was detected in renal tubular epithelial cells. In vivo, high circulating FSH levels promoted a phenotype of tubulointerstitial fibrosis, characterized by increases in 24‐hr urine protein/creatinine ratio, serum Cr, serum BUN, and ECM deposition. Similar results obtained from cultured HK‐2 cells showed that FSH increased the transcriptional and protein expression of profibrotic mediators (collagen IV, fibronectin, and PAI‐1). This promotion of fibrosis by FSH occurred through the activation of AKT/GSK‐3β/β‐catenin pathway, which could be attenuated by silencing FSHR by siRNA or by LY294002 or MK2206. In addition, FSH‐stimulated HK‐2 cells secreted IL‐8, which promoted macrophage migration to exacerbate tubulointerstitial fibrosis. These results revealed a previously unknown effect of FSH on kidney injury, which may offer a critical insight into the development of CKD in aging postmenopausal women.

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Section: Discussionmentioning

confidence: 99%

Follicle‐stimulating hormone promotes renal tubulointerstitial fibrosis in aging women via the AKT/GSK‐3β/β‐catenin pathway

et al. 2019

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“…CID–MS/MS acquisition was performed on the same mass range, resolution, and acquisition set for MS scanning, whereas singly charged ions were excluded. Smart exclusion parameters were set to minimize repeated acquisitions of the same intense precursor ions (repeated count was 2, dynamic exclusion was set at 0.50 min) …”

Section: Methodsmentioning

confidence: 99%

“…Smart exclusion parameters were set to minimize repeated acquisitions of the same intense precursor ions (repeated count was 2, dynamic exclusion was set at 0.50 min). [16,17] The MS/MS raw spectra were converted into mzData.xml using MassHunter Qualitative Analysis software (Agilent Technologies). Mascot search engine (http://www.matrixscience.com) was used to query MS/MS spectra against UniProtKB/Swiss-Prot mammalian database with the following standard Mascot parameters for CID: enzyme = trypsin, maximal number of missed cleavages = 1, peptide tolerance = ±0.1 Da, MS/MS tolerance = ±0.5 Da, fixed modification = carbamidomethyl (C), variable modification = oxidation (M), charge states = 2+ and 3+, and instrument type = ESI-QUAD-TOF.…”

Section: Spot Matching and Comparative Analysismentioning

confidence: 99%

Protective Cellular Mechanism of Estrogen Against Kidney Stone Formation: A Proteomics Approach and Functional Validation

Peerapen

Thongboonkerd

2019

Proteomics

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Females have less incidence/prevalence of kidney stone disease than males. Estrogen thus may serve as the protective factor but with unclear mechanism. This study explores cellular mechanism underlying such stone preventive mechanism of estrogen. Madin darby canine kidney (MDCK) renal tubular cells are incubated with or without 20 nm 17β‐estradiol for 7 days. Comparative proteomics reveals 58 differentially expressed proteins in estrogen‐treated versus control cells that are successfully identified by nanoLC–ESI–Q‐TOF‐MS/MS. Interestingly, these altered proteins are involved mainly in “binding and receptor,” “metabolic process,” and “migration and healing” networks. Functional investigations demonstrate reduction of calcium oxalate (CaOx) crystal‐binding capability of the estrogen‐treated cells consistent with the decreased levels of annexin A1 and α‐enolase (the known CaOx crystal‐binding receptors) on the cell surface. High‐calcium and high‐oxalate challenge initially enhances surface expression of annexin A1 and α‐enolase, respectively, both of which return to their basal levels by estrogen. Additionally, estrogen reduces intracellular ATP level and promotes cell migration and tissue healing. Taken together, estrogen causes changes in cellular proteome of renal tubular cells that lead to decreased surface expression of CaOx crystal receptors, reduced intracellular metabolism, and enhanced cell proliferation and tissue healing, all of which may contribute, at least in part, to stone prevention.

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“…In addition to secretion of EVs to spread signals, TECs also accept information from other cells via EVs. When macrophages were incubated with calcium oxalate (CaOx) crystals, exosomes were secreted to enhance IL‐8 production in renal tubular cells . Microparticles (MPs) released by activated endothelial cells up‐regulate HIF‐1/HIF‐2 and increase the production of HIF‐/VEGF‐A in human proximal tubular cells.…”

Section: Evs‐mediated Intranephron Communicationmentioning

confidence: 99%

“…52 As EV-associated MMPs can contribute to degradation of extracellular matrix surrounding cells, and sometimes stimulate critical signalling pathways, 47,48,53 whether EV-associated MMPs participated in the development of renal fibrosis is an interesting question that deserves further investigation.In addition to secretion of EVs to spread signals, TECs also accept information from other cells via EVs. When macrophages were incubated with calcium oxalate (CaOx) crystals, exosomes were secreted to enhance IL-8 production in renal tubular cells 54. Microparticles (MPs) released by activated endothelial cells up-regulate HIF-1/HIF-2 and increase the production of HIF-/VEGF-A in human proximal tubular cells.…”

mentioning

confidence: 99%

New insight into the role of extracellular vesicles in kidney disease

Feng

Tang

et al. 2018

J Cellular Molecular Medi

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Extracellular vesicles (EVs) are released to maintain cellular homeostasis as well as to mediate cell communication by spreading protective or injury signals to neighbour or remote cells. In kidney, increasing evidence support that EVs are signalling vesicles for different segments of tubules, intra‐glomerular, glomerular‐tubule and tubule‐interstitial communication. EVs released by kidney resident and infiltrating cells can be isolated from urine and were found to be promising biomarkers for kidney disease, reflecting deterioration of renal function and histological change. We have here summarized the recent progress about the functional role of EVs in kidney disease as well as challenges and future directions involved.

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Exosomes derived from calcium oxalate-exposed macrophages enhance IL-8 production from renal cells, neutrophil migration and crystal invasion through extracellular matrix

Cited by 57 publications

References 41 publications

Follicle‐stimulating hormone promotes renal tubulointerstitial fibrosis in aging women via the AKT/GSK‐3β/β‐catenin pathway

Follicle‐stimulating hormone promotes renal tubulointerstitial fibrosis in aging women via the AKT/GSK‐3β/β‐catenin pathway

Protective Cellular Mechanism of Estrogen Against Kidney Stone Formation: A Proteomics Approach and Functional Validation

New insight into the role of extracellular vesicles in kidney disease

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