TRIM40 inhibits IgA1-induced proliferation of glomerular mesangial cells by inactivating NLRP3 inflammasome through ubiquitination

Shen, Jiaojiao; Qing, WU; Liang, Tingyu; Zhang, Jian; Bai, Jia-Yuan; Yuan, Meijie; Shen, Peicheng

doi:10.1016/j.molimm.2021.10.012

Cited by 14 publications

(8 citation statements)

References 30 publications

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“…A meta-analysis examining the association of anti-depressants with COVID-19 incidence and severity found that most either had no impact or had have slight protective effects [ 115 ]. TRIM40 —Tripartite motif (TRIM)-containing proteins are E3 ubiquitin ligases that possess crucial regulatory functions in innate immunity [ 116 ]. In particular, they attenuate antiviral immune response [ 117 ].…”

Section: Discussionmentioning

confidence: 99%

“…In particular, they attenuate antiviral immune response [ 117 ]. TRIM40 also has associations with IgA nephropathology, which causes kidney disease; it is thought to suppress IgA1-induced GMC proliferation by inhibiting the activation of NLRP3 inflammasome [ 116 ]. TRIM40′s associations with kidney disease and regulatory functions in immunity both align with a role in resistant hypertension and COVID-19, respectively.…”

Section: Discussionmentioning

confidence: 99%

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Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19

Kartchner,

McCoy,

Dubey

et al. 2023

Biology

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Multiple studies have reported new or exacerbated persistent or resistant hypertension in patients previously infected with COVID-19. We used literature-based discovery to identify and prioritize multi-scalar explanatory biology that relates resistant hypertension to COVID-19. Cross-domain text mining of 33+ million PubMed articles within a comprehensive knowledge graph was performed using SemNet 2.0. Unsupervised rank aggregation determined which concepts were most relevant utilizing the normalized HeteSim score. A series of simulations identified concepts directly related to COVID-19 and resistant hypertension or connected via one of three renin–angiotensin–aldosterone system hub nodes (mineralocorticoid receptor, epithelial sodium channel, angiotensin I receptor). The top-ranking concepts relating COVID-19 to resistant hypertension included: cGMP-dependent protein kinase II, MAP3K1, haspin, ral guanine nucleotide exchange factor, N-(3-Oxododecanoyl)-L-homoserine lactone, aspartic endopeptidases, metabotropic glutamate receptors, choline-phosphate cytidylyltransferase, protein tyrosine phosphatase, tat genes, MAP3K10, uridine kinase, dicer enzyme, CMD1B, USP17L2, FLNA, exportin 5, somatotropin releasing hormone, beta-melanocyte stimulating hormone, pegylated leptin, beta-lipoprotein, corticotropin, growth hormone-releasing peptide 2, pro-opiomelanocortin, alpha-melanocyte stimulating hormone, prolactin, thyroid hormone, poly-beta-hydroxybutyrate depolymerase, CR 1392, BCR-ABL fusion gene, high density lipoprotein sphingomyelin, pregnancy-associated murine protein 1, recQ4 helicase, immunoglobulin heavy chain variable domain, aglycotransferrin, host cell factor C1, ATP6V0D1, imipramine demethylase, TRIM40, H3C2 gene, COL1A1+COL1A2 gene, QARS gene, VPS54, TPM2, MPST, EXOSC2, ribosomal protein S10, TAP-144, gonadotropins, human gonadotropin releasing hormone 1, beta-lipotropin, octreotide, salmon calcitonin, des-n-octanoyl ghrelin, liraglutide, gastrins. Concepts were mapped to six physiological themes: altered endocrine function, 23.1%; inflammation or cytokine storm, 21.3%; lipid metabolism and atherosclerosis, 17.6%; sympathetic input to blood pressure regulation, 16.7%; altered entry of COVID-19 virus, 14.8%; and unknown, 6.5%.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19

Kartchner,

McCoy,

Dubey

et al. 2023

Biology

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show abstract

“…Experimental data reported by studies performed using different models of kidney injury, such as chronic glomerulonephritis [ 37 , 38 , 39 , 40 ], diabetic nephropathy [ 41 , 42 ], Lupus Nephritis [ 43 ], crystalline nephropathy [ 44 , 45 , 46 , 47 ] and hypertensive nephropathy [ 48 , 49 , 50 ], have shown that NLRP3 inflammasome activation participates in the underlying pathogenetic events involved in the onset and progression of kidney damage, regardless of the aetiology of kidney disease. The contribution of NLRP3 machinery activation in the pathogenetic events affecting renal tissue, leading to CKD/ESRD, have been attributed to different molecular mechanisms, occurring through both canonical and non-canonical pathways [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Association between NLRP3 rs10754558 and CARD8 rs2043211 Variants and Susceptibility to Chronic Kidney Disease

Russa

Lofaro

Montesanto

et al. 2023

IJMS

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Nod-like receptor protein 3 (NLRP3) is a multi-protein complex belonging to the innate immune system, whose activation by danger stimuli promotes inflammatory cell death. Evidence supports the crucial role of NLRP3 inflammasome activation in the transition of acute kidney injury to Chronic Kidney Disease (CKD), by promoting both inflammation and fibrotic processes. Variants of NLRP3 pathway-related genes, such as NLRP3 itself and CARD8, have been associated with susceptibility to different autoimmune and inflammatory diseases. In this study, we investigated for the first time the association of functional variants of NLRP3 pathway-related genes (NLRP3-rs10754558, CARD8-rs2043211), with a susceptibility to CKD. A cohort of kidney transplant recipients, dialysis and CKD stage 3–5 patients (303 cases) and a cohort of elderly controls (85 subjects) were genotyped for the variants of interest and compared by using logistic regression analyses. Our analysis showed a significantly higher G allele frequency of the NLRP3 variant (67.3%) and T allele of the CARD8 variant (70.8%) among cases, compared with the control sample (35.9 and 31.2%, respectively). Logistic regressions showed significant associations (p < 0.001) between NLRP3 and CARD8 variants and cases. Our results suggest that the NLRP3 rs10754558 and CARD8 rs2043211 variants could be associated with a susceptibility to CKD.

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“…Other members of this family, including the E3-ligase TRIM24 has been shown to interact with NLRP3, and mediate its ubiquitination although no ubiquitin chains types have been identified in the context of endometriosis context, a disease liked to inflammation that curses with abnormal growth of endometrial tissues outside the endometrium and myometrium of the uterus ( Hang et al, 2021 ). In IgA nephropathy, one of the most common primary glomerulonephritis, has been linked to aberrant activation of NLRP3 inflammasome, TRIM40 has been shown to suppress NLRP3 activation by inducing its ubiquitylation and degradation, consequently loss of TRIM40 leads to overactivation of NLRP3 and proliferation of glomerular mesangial cells ( Shen et al, 2021 ). Another negative regulator, TRIM31 directly binds to the PYD domain of NLRP3 via its N-terminal RING domain and induces Lys48-linked poly-ubiquitination and degradation of NLRP3 ( Song et al, 2016 ), and therefore, supresses NLRP3 inflammasome activation.…”

Section: Ubiquitylation Of Inflammasome Componentsmentioning

confidence: 99%

Posttranslational Regulation of Inflammasomes, Its Potential as Biomarkers and in the Identification of Novel Drugs Targets

Nanda

Vollmer²,

Pérez-Oliva

2022

Front. Cell Dev. Biol.

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In this review, we have summarized classical post-translational modifications (PTMs) such as phosphorylation, ubiquitylation, and SUMOylation of the different components of one of the most studied NLRP3, and other emerging inflammasomes. We will highlight how the discovery of these modifications have provided mechanistic insight into the biology, function, and regulation of these multiprotein complexes not only in the context of the innate immune system but also in adaptive immunity, hematopoiesis, bone marrow transplantation, as well and their role in human diseases. We have also collected available information concerning less-studied modifications such as acetylation, ADP-ribosylation, nitrosylation, prenylation, citrullination, and emphasized their relevance in the regulation of inflammasome complex formation. We have described disease-associated mutations affecting PTMs of inflammasome components. Finally, we have discussed how a deeper understanding of different PTMs can help the development of biomarkers and identification of novel drug targets to treat diseases caused by the malfunctioning of inflammasomes.

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TRIM40 inhibits IgA1-induced proliferation of glomerular mesangial cells by inactivating NLRP3 inflammasome through ubiquitination

Cited by 14 publications

References 30 publications

Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19

Literature-Based Discovery to Elucidate the Biological Links between Resistant Hypertension and COVID-19

Association between NLRP3 rs10754558 and CARD8 rs2043211 Variants and Susceptibility to Chronic Kidney Disease

Posttranslational Regulation of Inflammasomes, Its Potential as Biomarkers and in the Identification of Novel Drugs Targets

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