Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis

He, Liyu; Peng, Xiaofei; Wang, Jiayi; Tang, Chengyuan; Zhou, Xun; Liu, Hong; Liu, Fuyou; Sun, Lin; Peng, Youming

doi:10.1159/000440819

Cited by 15 publications

(11 citation statements)

References 51 publications

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“…The method inducted a successful rat model of IgAN based on our previous studies [24]. In brief, rats were induced with continuous oral immunization containing 0.1% bovine gamma globulin (BGG) (Sigma) with 6 m M HCl in tap water for 18 weeks, followed by tail intravenous injection of 1 mg BGG daily for 3 consecutive days.…”

Section: Methodsmentioning

confidence: 99%

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Rapamycin Enhances Repressed Autophagy and Attenuates Aggressive Progression in a Rat Model of IgA Nephropathy

Liu

Chen

et al. 2017

Am J Nephrol

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Background: IgA nephropathy (IgAN) has been considered to be the most frequent form of primary glomerulonephritis that occurs worldwide with a variety of factors involved in its occurrence and development. The impact of autophagy in IgAN, however, remains partially unclear. This study was designed to investigate the effects of rapamycin in an IgAN model. Method: After establishing an IgAN rat model, SD rats were divided into 4 groups: control, control + rapamycin, IgAN, IgAN + rapamycin. Proteinuria and the pathological changes and the level of autophagy of kidney were texted. Identify the expression of phosphorylation and total mammalian target of rapamycin (mTOR) and s6k1 as well as cyclin D1 in the kidney of rats through Western blot and immunohistochemistry. Results: With rapamycin treatment, we observed a significant reduction in the progression of proteinuria as well as alleviation of pathological lesions in IgAN rats. Besides, autophagy was inhibited, while the mTOR/S6k1 pathway was activated and expression of cyclin D1 was increased in IgAN. Rapamycin treatment increased autophagy and decreased the expression of cyclin D1. Conclusion: These results may suggest that mTOR-mediated autophagy inhibition may result in mesangial cell proliferation in IgAN.

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Section: Methodsmentioning

confidence: 99%

“…All the renal staining was performed on 4-μm paraffin sections as we previously described [24]. In brief, immunohistochemical stains were performed on formalin-fixed, paraffin-embedded 4-μm sections.…”

Section: Methodsmentioning

confidence: 99%

Rapamycin Enhances Repressed Autophagy and Attenuates Aggressive Progression in a Rat Model of IgA Nephropathy

Liu

Chen

et al. 2017

Am J Nephrol

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“…Furthermore, TLR1 (CT and CC genotype in rs4833095, TT genotype in rs5743557) (23) and TLR10 genes (TA and AA genotype in rs1004195) (24) may be associated with susceptibility to IgAN in Korean children. Recently, He et al (25) reported that the TLR3-B-cell activating factor axis was involved in IgA class switch recombination in IgAN.…”

Section: Discussionmentioning

confidence: 99%

Differentially expressed long non-coding RNAs and mRNAs in patients with IgA nephropathy

Zuo

Liu

et al. 2017

Molecular Medicine Reports

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Long non‑coding RNAs (lncRNAs) have been reported to serve a crucial role in renal diseases; however, their role in immunoglobulin A nephropathy (IgAN) remains unclear. In the present study, peripheral blood mononuclear cells (PBMCs) were collected from both patients with IgAN and healthy controls. A microarray analysis was then performed to identify differentially expressed lncRNAs and mRNAs in PBMCs, which were confirmed by quantitative polymerase chain reaction. In addition, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and lncRNA‑mRNA co‑expression network analyses were conducted. The present study identified 167 differentially expressed lncRNAs and 94 differentially expressed mRNAs. Numerous GO terms, including innate immune response, inflammatory response, IPAF inflammasome complex and UDP‑galactose:β‑N‑acetylglucosamine β‑1, and 3‑galactosyltransferase activity, were significantly enriched in the differentially expressed mRNAs. The top five KEGG signaling pathways included nucleotide‑binding oligomerization domain‑like receptor signaling pathway, hematopoietic cell lineage, inflammatory bowel disease, tumor necrosis factor signaling pathway and other types of O‑glycan biosynthesis. In addition, a total of 149 lncRNAs were shown to interact with 7 mRNAs that were associated with the 'innate immune response' GO term. The results of the present study demonstrated that differentially expressed lncRNAs and mRNAs may have a role in the development of IgAN. These results may aid in the elucidation of a basic pathogenic mechanism, the identification of possible biomarkers and the generation of potential novel treatment strategies for IgAN.

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“…The group of He L. et al [103] offered more direct evidence of the involvement of dsRNA in IgAN. In this paper, human leukocytes, isolated from tonsil tissue and whole blood, were cultured with or without poly(I:C) for 1-7 days.…”

Section: The Interplay Between the Microbiome And Virome: A New Visiomentioning

confidence: 99%

“…The TLR3 crosstalk with BAFF plays a vital role in the over-production of IgA and in the Recombinant Class Switch to IgA in IgAN. Thus, the inhibition of TLR3/BAFF axis activation could be an interesting option for preventing IgAN progression [103].…”

Section: The Interplay Between the Microbiome And Virome: A New Visiomentioning

confidence: 99%

A New Vision of IgA Nephropathy: The Missing Link

Sallustio,

Curci,

Di Leo

et al. 2019

IJMS

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IgA Nephropathy (IgAN) is a primary glomerulonephritis problem worldwide that develops mainly in the 2nd and 3rd decade of life and reaches end-stage kidney disease after 20 years from the biopsy-proven diagnosis, implying a great socio-economic burden. IgAN may occur in a sporadic or familial form. Studies on familial IgAN have shown that 66% of asymptomatic relatives carry immunological defects such as high IgA serum levels, abnormal spontaneous in vitro production of IgA from peripheral blood mononuclear cells (PBMCs), high serum levels of aberrantly glycosylated IgA1, and an altered PBMC cytokine production profile. Recent findings led us to focus our attention on a new perspective to study the pathogenesis of this disease, and new studies showed the involvement of factors driven by environment, lifestyle or diet that could affect the disease. In this review, we describe the results of studies carried out in IgAN patients derived from genomic and epigenomic studies. Moreover, we discuss the role of the microbiome in the disease. Finally, we suggest a new vision to consider IgA Nephropathy as a disease that is not disconnected from the environment in which we live but influenced, in addition to the genetic background, also by other environmental and behavioral factors that could be useful for developing precision nephrology and personalized therapy.

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Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis

Cited by 15 publications

References 51 publications

Rapamycin Enhances Repressed Autophagy and Attenuates Aggressive Progression in a Rat Model of IgA Nephropathy

Rapamycin Enhances Repressed Autophagy and Attenuates Aggressive Progression in a Rat Model of IgA Nephropathy

Differentially expressed long non-coding RNAs and mRNAs in patients with IgA nephropathy

A New Vision of IgA Nephropathy: The Missing Link

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