Monitoring of peripheral blood cluster of differentiation 4+ adenosine triphosphate activity and CYP3A5 genotype to determine the pharmacokinetics, clinical effects and complications of tacrolimus in patients with autoimmune diseases

Mizuno, Shugo; Nakatani, Kaname; Wakabayashi, Hiroki; Ishikawa, Eijiï¿1⁄2; Araki, Toshimitsu; Taniguchi, Akira; Isaji, Shuji; Okuda, Masahiro

doi:10.3892/etm.2017.5364

Cited by 5 publications

(5 citation statements)

References 15 publications

(27 reference statements)

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“…The results showed that in MN patients, TAC blood concentrations of CYP3A5 expressers are comparatively lower than those of CYP3A5 non-expressers at different time points (≤1 month, 1–6 months, and ≥6 months) after medication administration. The findings are consistent with the effect of different CYP3A5 * 3 genotypes on TAC in transplant patients ( Muraki et al, 2018 ). However, the impact of the CYP3A5*3 genetic polymorphism on the effectiveness of TAC therapy in patients with MN remains uncertain.…”

Section: Discussionsupporting

confidence: 89%

Meta-analysis of the effects of CYP3A5*3 gene polymorphisms on tacrolimus blood concentration and effectiveness in Chinese patients with membranous nephropathy

Dai,

Yuan,

Chai

2024

Front. Pharmacol.

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ObjectiveThe study aimed to systematically evaluate the relationship between CYP3A5*3 gene polymorphisms and the blood concentration and effectiveness of tacrolimus (TAC) in patients with membranous nephropathy (MN).MethodsPubMed, Cochrane Library, Embase, Web of Science, China Biomedical, China National Knowledge Infrastructure, Wanfang, Vipshop, ReadShow, Clinical Trials Registry, and other databases were searched. Studies on the relationship between CYP3A5*3 gene polymorphism and TAC blood concentration in MN patients were collected, and meta-analysis was performed using Stata 16 software. ResultsA total of eight publications were included in the study, including 498 MN patients. CYP3A5*3 gene polymorphisms are associated with tacrolimus blood levels in patients with MN. The results of the relationship between CYP3A5*3 genotype polymorphisms and tacrolimus blood trough concentrations of the AA + AG genotype were lower than those of the GG genotype at ≤1 month [WMD = −2.08, 95% CI (−2.57, −1.59), p < 0.001] and 1–6 months [WMD = −0.63, 95% CI (−0.98, −0.27), p < 0.001]; however, they were not statistically significant at ≥6 months (p = 0.211). Furthermore, the subgroup analysis revealed that the dose-adjusted concentration of tacrolimus (C0/D) of the AA + AG genotype was lower than that of the GG genotype at ≤1 month [SMD = −1.93, 95% CI (−2.79, −1.08), p < 0.001], 1–6 months [SMD = −2.25, 95% CI (−2.71, −1.79), p < 0.001], and ≥6 months [SMD = −2.36, 95% CI (−2.86, −1.86), p < 0.001]. In addition, there was no statistically significant difference in effectiveness between the two groups at 3, 6, and 12 months of TAC administration (p > 0.05).ConclusionSerum TAC concentrations in MN patients were correlated with CYP3A5*3 genotype polymorphisms. Detection of the CYP3A5*3 genotype before the administration of TAC may provide some clinical value for optimizing the treatment of MN patients.Systematic Review Registration:https://inplasy.com/, identifier [INPLASY202430083].

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Section: Discussionsupporting

confidence: 89%

Meta-analysis of the effects of CYP3A5*3 gene polymorphisms on tacrolimus blood concentration and effectiveness in Chinese patients with membranous nephropathy

Dai,

Yuan,

Chai

2024

Front. Pharmacol.

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“…These colorectal cancer responsible genes might be candidate genes for CD. Recently, increasing evidence demonstrated that CXCL5 [379], S100A8 [380], LCN2 [381], CXCL1 [382], S100A9 [383], CXCL9 [384], CXCL11 [385], CXCL10 [386], NCF2 [387], SLC11A1 [388], GDF15 [389], IL1RN [390], STAT1 [391], CYP27B1 [392], SOCS3 [393], TLR8 [394], CD55 [395], ADGRG3 [396], CCL3 [397], FCGR2A [398], CCL2 [399], CD14 [400], IGFBP2 [401], PCSK9 [402], IDO1 [403], FOXP3 [404], CD163 [405], CCL7 [406], TLR2 [407], CCR2 [408], IL20RA [409], S100P [410], ADAMTS1 [411], TIMP1 [412], ICAM1 [413], IFNG (interferon gamma) [414], TREM2 [415], APOE (apolipoprotein E) [416], CCR1 [417], IL6 [418], CTHRC1 [419], PDCD1LG2 [420], CCL4 [421], IL11 [422], COL1A1 [423], MMP2 [424], IL1A [425], CD24 [426], POSTN (periostin) [427], GZMB (granzyme B) [428], BCL2A1 [429], CSF2 [430], TDO2 [431], CTLA4 [432], PADI4 [433], MPO (myeloperoxidase) [434], HP (haptoglobin) [435], MUC5B [436], MMP7 [437], PON3 [438], ABHD6 [439], AICDA (activation induced cytidine deaminase) [440], UGT1A6 [441], CYP2D6 [442], CYP3A5 [443], DGAT1 [444], FCRL4 [445], SLC22A4 [446], DPP4 [447], ACE (angiotensin I converting enzyme) [448], SLC5A11 [449], VIPR1 [450], FCRL3 [451], CD160 [452] and IL22RA2 […”

Section: Discussionmentioning

confidence: 99%

Identification of hub genes and key pathways in pediatric Crohn’s disease using next generation sequencing and bioinformatics analysis

Vastrad¹,

Vastrad²

2022

Preprint

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Pediatric Crohn's Disease (CD) also known as inflammatory bowel diseases, affects millions of people all over the world. The aim of this investigation is to identify the key genes in CD and uncover their potential functions. We downloaded the next generation sequencing (NGS) dataset GSE73374 from the Gene Expression Omnibus (GEO) database. The NGS dataset GSE73374 was used to screen differentially expressed genes (DEGs) between samples from patients with CD and healthy controls. Gene ontology (GO) and REACTOME pathway enrichment analyses were applied for the DEGs. Subsequently, a protein - protein interaction (PPI) network, modules, miRNA- hub gene regulatory network and TF - hub gene regulatory network were constructed to identify hub genes, miRNAs and TFs. Receiver operating characteristic curve (ROC) analysis was applied to validate the hub genes. A total of 957 DEGs were identified, including 478 up regulated genes and 479 down regulated genes. GO and REACTOME results suggested that several Go terms and pathways are involved in response to stimulus, extracellular region, signaling receptor binding, small molecule metabolic process, membrane, transporter activity, immune system and biological oxidations. The top centrality hub genes MDFI, MNDA, FBXO6, TFRC, STAT1, DPP4, MME, SLC39A4, APOA1 and TMEM25 were screened out as the critical genes among the DEGs from the PPI network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network. This investigation identified key genes and signal pathways, which might help us improve our understanding of the molecular mechanisms of CD and identify some novel therapeutic targets for CD.

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“…Rheumatoid arthritis (RA) is a chronic systemic disease, mainly characterized by synovitis, synovial hyperplasia, pannus formation, and osteochondral destruction ( Muraki et al, 2018 ; Shiraishi et al, 2017 ). Due to the joint dysfunction caused by RA, patients often have limited activities, and the quality of life is seriously reduced ( Wang et al, 2020a ).…”

Section: Introductionmentioning

confidence: 99%

Mir204 and Mir211 suppress synovial inflammation and proliferation in rheumatoid arthritis by targeting Ssrp1

Wang

Fan

Teng

et al. 2022

eLife

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Rheumatoid arthritis (RA) is a chronic inflammatory joint disease characterized by synovial hyperplasia. Mir204 and Mir211 are homologous miRNAs with the same gene targeting spectrum. It is known that Mir204/211 play an important role in protecting osteoarthritis development; however, the roles of Mir204/211 in RA disease have not been determined. In the present study, we investigated the effects and molecular mechanisms of Mir204/211 on synovial inflammation and hyperproliferation in RA. The effects of Mir204/211 on the inflammation and abnormal proliferation in primary fibroblast-like synoviocytes (FLSs) were examined by Mir204/211 gain-of-function and loss-of-function approaches in vitro and in vivo. We identified the structure-specific recognition protein 1 (Ssrp1) as a downstream target gene of Mir204/211 based on the bioinformatics analysis. We overexpressed Ssrp1and Mir204/211 in FLS to determine the relationship between Ssrp1 and Mir204/211 and their effects on synovial hyperplasia. We created a collagen-induced arthritis (CIA) model in wild-type as well as Mir204/211 double knockout (dKO) mice to induce RA phenotype and administered adeno-associated virus (AAV)-mediated Ssrp1-shRNA (AAV-shSsrp1) by intra-articular injection into Mir204/211 dKO mice. We found that Mir204/211 attenuated excessive cell proliferation and synovial inflammation in RA. Ssrp1 was the downstream target gene of Mir204/211. Mir204/211 affected synovial proliferation and decelerated RA progression by targeting Ssrp1. CIA mice with Mir204/211 deficiency displayed enhanced synovial hyperplasia and inflammation. RA phenotypes observed in Mir204/211 deficient mice were significantly ameliorated by intra-articular delivery of AAV-shSsrp1, confirming the involvement of Mir204/211-Ssrp1signaling during RA development. In this study, we demonstrated that Mir204/211 antagonize synovial hyperplasia and inflammation in RA by regulation of Ssrp1. Mir204/211 may serve as novel agents to treat RA disease.

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Monitoring of peripheral blood cluster of differentiation 4+ adenosine triphosphate activity and CYP3A5 genotype to determine the pharmacokinetics, clinical effects and complications of tacrolimus in patients with autoimmune diseases

Cited by 5 publications

References 15 publications

Meta-analysis of the effects of CYP3A5*3 gene polymorphisms on tacrolimus blood concentration and effectiveness in Chinese patients with membranous nephropathy

Meta-analysis of the effects of CYP3A5*3 gene polymorphisms on tacrolimus blood concentration and effectiveness in Chinese patients with membranous nephropathy

Identification of hub genes and key pathways in pediatric Crohn’s disease using next generation sequencing and bioinformatics analysis

Mir204 and Mir211 suppress synovial inflammation and proliferation in rheumatoid arthritis by targeting Ssrp1

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