Increased miR‐374b promotes cell proliferation and the production of aberrant glycosylated IgA1 in B cells of IgA nephropathy

Zhou, Tianjun; Bao, Hanying; Xu, Xiaodong; Zhou, Xianghui; Qin, Weisong; Zeng, Caihong; Liu, Fei

doi:10.1016/j.febslet.2015.10.033

Cited by 51 publications

(43 citation statements)

References 26 publications

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“…Of note, in IgAN, decreased C1GALT1C1 expression (independent from mutations) and increased O‐glycan defective IgA have been found. Molecular and cellular mechanisms reported to lessen C1GALT1C1 expression include T lymphocyte subgroup drifting and IL‐17, TGF‐β1 and IL‐4/STAT6/HIPK2‐mediated gene downregulation, among others . This is evidence that an anomalous B/T cell response is the underlying mechanism interfering with C1GALT1C1 expression and mediated O‐glycosylation.…”

Section: The Immunological Impact Of Glycosylation Defects—an Update mentioning

confidence: 98%

CDG and immune response: From bedside to bench and back

Pascoal

Francisco

Ferro

et al. 2019

J of Inher Metab Disea

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Glycosylation is an essential biological process that adds structural and functional diversity to cells and molecules, participating in physiological processes such as immunity. The immune response is driven and modulated by protein‐attached glycans that mediate cell‐cell interactions, pathogen recognition and cell activation. Therefore, abnormal glycosylation can be associated with deranged immune responses. Within human diseases presenting immunological defects are congenital disorders of glycosylation (CDG), a family of around 130 rare and complex genetic diseases. In this review, we have identified 23 CDG with immunological involvement, characterized by an increased propensity to—often life‐threatening—infection. Inflammatory and autoimmune complications were found in 7 CDG types. CDG natural history(ies) and the mechanisms behind the immunological anomalies are still poorly understood. However, in some cases, alterations in pathogen recognition and intracellular signaling (eg, TGF‐β1, NFAT, and NF‐κB) have been suggested. Targeted therapies to restore immune defects are only available for PGM3‐CDG and SLC35C1‐CDG. Fostering research on glycoimmunology may elucidate the involved pathophysiological mechanisms and open new therapeutic avenues, thus improving CDG patients' quality of life.

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Section: The Immunological Impact Of Glycosylation Defects—an Update mentioning

confidence: 98%

CDG and immune response: From bedside to bench and back

Pascoal

Francisco

Ferro

et al. 2019

J of Inher Metab Disea

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“…The firefly and Renilla luciferase activity were determined using the Dual-Luciferase Reporter Assay System (E1910, Promega, Madison, WI). Values were normalized with Renilla luciferase (38,45).…”

Section: Luciferase Assaysmentioning

confidence: 99%

The long noncoding RNA LOC105374325 causes podocyte injury in individuals with focal segmental glomerulosclerosis

Zhou

Han

Shi

et al. 2018

Journal of Biological Chemistry

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Focal segmental glomerulosclerosis (FSGS) is a common kidney disease that results in nephrotic syndrome. FSGS arises from dysfunction and apoptosis of podocytes in the glomerulus of the kidney, leading to podocytopathy. The molecular mechanisms underlying podocyte apoptosis remain incompletely understood. Using an array of gene expression profiling, PCR, and in situ hybridization assay, we found here that the levels of the long noncoding RNA LOC105374325 were elevated in the renal podocytes of individuals with FSGS. We also observed that the microRNAs miR-34c and miR-196a/b down-regulated the expression of the apoptosis regulators BCL2-associated X, apoptosis regulator (Bax), and BCL2 antagonist/killer 1 (Bak) in podocytes. Competitive binding between LOC105374325 and miR-34c or miR-196a/b increased Bax and Bak levels and caused podocyte apoptosis. Of note, the mitogen-activated protein kinase P38 and the transcription factor CCAAT enhancer-binding protein ␤ (C/EBP␤) up-regulated LOC105374325 expression. P38 inhibition or C/EBP␤ silencing decreased LOC105374325 levels and inhibited apoptosis in adriamycin-treated podocytes. LOC105374325 overexpression decreased miR-34c and miR-196a/b levels, increased Bax and Bak levels, and induced proteinuria and focal segmental lesions in mice. In conclusion, activation of the P38/C/ EBP␤ pathway stimulates the expression of LOC105374325, which, in turn, increases Bax and Bak levels and causes apoptosis by competitively binding to miR-34c and miR-196a/b in the podocytes of individuals with FSGS.

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“…They modulate a lot of cell biological processes such as cell development, inflammatory responses, proliferation, and apoptosis . Several miRNAs including miR‐374b, miR‐146a, let‐7b, and miR‐29b‐3p were identified to act vital roles in the development of IgAN . However, the role of miRNAs in the IgAN is still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR‐320 promotes B cell proliferation and the production of aberrant glycosylated IgA1 in IgA nephropathy

Shi

Zhao

2018

J of Cellular Biochemistry

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IgA nephropathy (IgAN) is one of the most common primary glomerulonephritis. However, the etiology of this disease is complex and the pathogenesis of IgAN is still unknown. MicroRNAs (miRNAs) play important roles in a lot of pathological and physiological processes. In this study, we showed that the expression of miR-320 was significantly upregulated in renal tissues and urinary of IgAN patients. Moreover, the intra-renal expression level of miR-320 had significant correlation with miR-320 expression in the urinary of IgAN patients. Overexpression of miR-320 increased B cell proliferation and promoted cyclin D1 expression. Furthermore, we identified that PTEN was direct target gene of miR-320 in the B cell. Ectopic expression of miR-320 suppressed PTEN expression. Overexpression of miR-320 decreased Cosmc expression in the B cell. In addition, we demonstrated that Cosmc expression was significantly downregulated in the renal tissues and urinary of IgAN patients. The intra-renal expression level of Cosmc had significant correlation with Cosmc expression of urinary in IgAN patients. We proved that the expression level of Cosmc was negatively correlated with the expression of miR-320 in the renal tissues of IgAN patients. Overexpression of miR-320 promoted the B cell proliferation through suppressing PTEN expression. Taken together, these data suggested that miR-320 acted an important role in the development of IgAN.

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Increased miR‐374b promotes cell proliferation and the production of aberrant glycosylated IgA1 in B cells of IgA nephropathy

Cited by 51 publications

References 26 publications

CDG and immune response: From bedside to bench and back

CDG and immune response: From bedside to bench and back

The long noncoding RNA LOC105374325 causes podocyte injury in individuals with focal segmental glomerulosclerosis

MiR‐320 promotes B cell proliferation and the production of aberrant glycosylated IgA1 in IgA nephropathy

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