Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis

Li, Mingqiao; Wang, Weihua; Cheng, Ying; Zhang, Xiaoxun; Zhao, Nan; Tan, Ya Hwee; Zhang, Xiaoxun; Chai, Jin; Pan, Qiong

doi:10.1016/j.jbc.2021.101543

Cited by 8 publications

(5 citation statements)

References 29 publications

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“…As shown in the Figure S2, we found that the mRNA expressions of Ripk3 and Mlkl related to necroptosis did not change under bile acid stimulation, suggesting that bile acid stimulation alone might not induce necroptosis. In addition, based on previous studies on cholestatic liver disease and necroptosis, 25–27 TNF‐α is significantly elevated in cholestasis 24 . All these studies revealed that necroptosis was induced by TNF‐α.…”

Section: Resultsmentioning

confidence: 93%

“…As shown in the Figure S2, we found that the mRNA expressions of cholestatic liver disease and necroptosis, [25][26][27] TNF-α is significantly elevated in cholestasis. 24 All these studies revealed that necroptosis was induced by TNF-α. Therefore, bile acids may not directly induce necroptosis, but indirectly via increased TNF-α.…”

Section: Il-32 Inhibited Necroptosis In 1% Lcainduced and Anit-induce...mentioning

confidence: 99%

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Hepatic interleukin 32 attenuates liver injury through repression of necroptosis in cholestasis

Mao

Zhang

et al. 2023

J of Digest Diseases

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Objective: We aimed to evaluate the association between interleukin (IL)-32 and necroptosis in cholestatic liver injury.Methods: Levels of necroptosis-related markers in cholestatic and control patients, including the receptor-interacting serine-threonine kinase 3 (RIPK3), receptorinteracting serine-threonine kinase 1 (RIPK1), and mixed lineage kinase domain-like (MLKL) were measured. Animal experiments in C57BL/6J and transgenic mice with IL32β/γ overexpression were also conducted to confirm the effect of IL-32 on necroptosis in cholestasis, which was induced by α-naphthylisothiocyanate (ANIT) and 1% lithocholic acid (LCA). PLC/PRF/5-ASBT and primary mouse hepatocytes were utilized for the investigation of the regulation and mechanism of IL-32 in cholestasis.

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Section: Resultsmentioning

confidence: 93%

Section: Il-32 Inhibited Necroptosis In 1% Lcainduced and Anit-induce...mentioning

confidence: 99%

Hepatic interleukin 32 attenuates liver injury through repression of necroptosis in cholestasis

Mao

Zhang

et al. 2023

J of Digest Diseases

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“…Our data demonstrate numerous medulla-specific accessible chromatin regions associated with medullary chromatin loops across the SLCO3A1 promoter and gene body. SLCO3A1 has been implicated in Crohn's disease and experimental colitis 37,38 , cholestasis 39,40 , and Parkinson's disease 41 . Therefore, determining its role in the adult kidney medulla will be an intriguing future line of investigation.…”

Section: Discussionmentioning

confidence: 99%

Multi-omic Analysis of Primary Human Kidney Tissues Identifies Medulla-Specific Gene Expression Patterns

Haug

Muthusamy

et al. 2022

Preprint

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The renal medulla is a specialized region of the kidney with important homeostatic functions. It has also been implicated in genetic and developmental disorders and ischemic and drug-induced injuries. Despite its role in kidney function and disease, the medulla's baseline gene expression and epigenomic signatures have not been well described in the adult human kidney. Here we generate and analyze gene expression (RNA-seq), chromatin accessibility (ATAC-seq) and chromatin conformation (Hi-C) data from adult human kidney cortex and medulla. Using data from our carefully annotated specimens, we assign samples in the larger public GTEx database to cortex and medulla, thereby identifying several misassignments and extracting meaningful medullary gene expression signatures. Using integrated analysis of gene expression, chromatin accessibility and conformation profiles, we reveal insights into medulla development and function. Our datasets will also provide a valuable resource for researchers in the GWAS community for functional annotation of genetic variants.

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“…The gyration radii of 4 kDa, 70 kDa, 500 kDa, and 2000 kDa dextran are 2.2 nm, 9 nm, 10.5 nm, and 58 nm, respectively [224]. Therefore, the diameter of the pore created by FUS-MB treatment at an acoustic pressure of 0.51 Mpa is about 20 nm, which is of sufficient size for entry of plasma proteins and therapeutic antibodies, which have a diameter of 10-11 nm [225]. The opening of the BBB following FUS-MB is on the order of hours, and the BBBD is resolved by 6-24 h [226].…”

Section: Bbbd Following Intravenous Microbubble/focused Ultrasoundmentioning

confidence: 98%

Advanced Blood-Brain Barrier Drug Delivery

2023

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Commons Attribution (CC BY) license, which allows users to download, copy and build upon published articles, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. Preface to "Advanced Blood-Brain Barrier Drug Delivery"This Special Issue of Pharmaceutics, "Advanced Blood-Brain Barrier Drug Delivery", comprises 17 articles, which cover five areas of brain drug delivery, including receptor-mediated transport (RMT), carrier-mediated transport (CMT), active efflux transport (AET), Trojan horse lipid nanoparticles (LNP), and the in vivo measurement of drug transport across the blood-brain barrier (BBB). The articles on RMT describe the genetic engineering of IgG fusion proteins, wherein the IgG domain targets an endogenous peptide receptor at the BBB. The IgG domain of the fusion protein acts as a molecular Trojan horse to ferry the fused biologic agentinto the brain, which alone does not cross the BBB. Endogenous CMT systems for the brain drug delivery of small molecules include the GLUT1 glucose transporter, the LAT1 large neutral amino acid transporter, and others. AET systems at the BBB cause the active efflux of small-molecule drugs from brain to blood, and include carriers in the Solute Carrier (SLC) and the ATP binding cassette (ABC) transporter super-families. Trojan horse LNPs are formulated to access RMT systems at the BBB for the brain delivery of mRNA or plasmid DNA. Articles in this Special Issue critically evaluate the in vivo measurement of drug transport into brain.

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Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis

Abstract: Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis,

Cited by 8 publications

References 29 publications

Hepatic interleukin 32 attenuates liver injury through repression of necroptosis in cholestasis

Hepatic interleukin 32 attenuates liver injury through repression of necroptosis in cholestasis

Multi-omic Analysis of Primary Human Kidney Tissues Identifies Medulla-Specific Gene Expression Patterns

Advanced Blood-Brain Barrier Drug Delivery

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