Wildtype (wt) mouse cone transcriptome change with Txnip treatment
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ABSTRACT:
PROVIDER: PRJNA707576 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13895267_1.fastq.gz | Fastqsanger.gz | |||
| SRR13895267_2.fastq.gz | Fastqsanger.gz | |||
| SRR13895268_1.fastq.gz | Fastqsanger.gz | |||
| SRR13895268_2.fastq.gz | Fastqsanger.gz | |||
| SRR13895269_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: To identifiy mRNA changes in wt cone photoreceptors with Txnip overexpression treatment, which improved retinitis pigmentosa (RP) cone survival and visual acuity. Methods: two wt mouse strains, BALB/c and C57BL/6J were injected with AAV-Txnip or AAV-H2BGFP control subretinally at P0. Retinas were dissected out at P21 for BALB/c and P35 for C57BL/6J. 1,000 H2BGFP labeled cones per retina sample were FACS sorted out, and subject for RNA-sequencing. Results: only ~70 genes in P21 BALB/c and 1 genes in C57BL/6J were found differentially expressed with Txnip treatment. Only 1 genes (i.e. Txnip) were in commonly upregulated between the two lists. Conclusions: Txnip seems to be not changing RNA expression much in wt cones. Instead, its major function to rescue RP cones may lay in protein-protein interactions.
2021-03-15 | GSE168503 | GEO
Project description:Purpose: To identifiy mRNA changes in retinitis pigmentosa (RP) cone photoreceptors with Txnip overexpression treatment, which improved RP cone survival and visual acuity. Methods: two RP mouse strains, rd1 and Rho-/-, were injected with AAV-Txnip or AAV-H2BGFP control subretinally at P0. Retinas were dissected out at P21 for rd1 and P90 for Rho-/-. 1,000 H2BGFP labeled cones per retina sample were FACS sorted out, and subject for RNA-sequencing. Results: >1,400 genes in P21 rd1 and >700 genes in Rho-/- were found differentially expressed with Txnip treatment. Conclusions: 25 genes are in common between P21 rd1 and P90 Rho-/- with Txnip treatment. On this list, notably, three mitochondrial Electron Transport Chain (ETC) genes were up-regulated.
2021-01-20 | GSE161622 | GEO
Project description:Retinitis pigmentosa (RP) mouse cone transcriptom change with Txnip treatment
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Project description:Among vertebrate animals, mammals have retained a unique molecular change that allows an intracellular arrestin domain-containing protein to bind covalently to thioredoxin. This interaction of Thioredoxin-Interacting Protein (TXNIP) with thioredoxin can only occur when thioredoxin is in the reduced state, allowing TXNIP to "sense" the cellular oxidized environment1. Here we show that a single cysteine in TXNIP mediates the development of hepatic insulin resistance in the setting of a high fat diet (HFD). Mice with exchange of TXNIP Cysteine 247 for Serine (C247S) showed improved whole-body and hepatic insulin sensitivities compared to wildtype (WT) controls following an 8-week HFD. The inhibition of the TXNIP-thioredoxin interaction under chow and HFD also regulated plasma and liver lipids and reduced free fatty acid accumulation in the livers following HFD. These data show that mammals have a single amino acid enabling interaction of redox state with TXNIP that mediates insulin resistance in the setting of a high-fat diet. This reveals a potential evolutionarily-conserved mechanism for hepatic insulin resistance in metabolic syndromes.
2025-06-25 | GSE275407 | GEO
Project description:RNA samples were collected from LSECs isolated from TXNIP-/- and WT mice. High-throughput sequencing was performed as single-end 75 sequencing using NextSeq 550.
2024-01-10 | GSE217238 | GEO
Project description:Thioredoxin-interacting protein (TXNIP) is ubiquitously expressed in blood cells, including hematopoietic stem cells (HSCs), monocytes, and platelets. Here we report a novel finding that TXNIP plays a crucial role in megakaryopoiesis and platelet biogenesis via interacting with GATA1, a transcription factor for megakaryocyte-erythroid differentiation. Txnip-/- mice displayed immature megakaryocytes in the bone marrow with thrombocytopenia, which had gotten worse as the mice aged. Transcriptome analysis revealed that the transcriptional activity of GATA1 was significantly enhanced in the Txnip-/- megakaryocyte precursors (MkPs) than wild type (WT) cells. During megakaryopoiesis in ex vivo, Txnip-/- MkPs remained small in cell size with less mitochondrial mass, and more glycolysis for ATP production, as opposed to the normal megakaryocyte maturation. The effects of TXNIP in megakaryocytes were recapitulated in human cord blood CD34+ HSC-derived differentiation. Taken together, this study demonstrates the importance of spatiotemporal expression of TXNIP in platelet biogenesis. We propose for the first time that TXNIP might play a critical role in determining a lineage between megakaryocytes and erythroid cells from a common megakaryocyte-erythroid progenitor via regulation of transcriptional activity of GATA1.
2022-12-31 | GSE186400 | GEO
Project description:Quantseq 3'mRNA-seq in LESCs from WT and TXNIP-/- mice
| PRJNA898149 | ENA
Project description:Chemotherapy, the standard of care treatment for cancer patients with advanced disease, has been increasingly recognised to activate host immune responses to produce durable outcomes. Here, in colorectal adenocarcinoma (CRC) we identify oxaliplatin-induced Thioredoxin Interacting Protein (TXNIP), a MondoA-dependent tumor suppressor gene, as a negative regulator of Growth/Differentiation Factor 15 (GDF15). GDF15 is a negative prognostic factor in CRC and promotes the differentiation of regulatory T cells (Tregs), which inhibit CD8 T cell activation. Intriguingly, multiple models including patient-derived tumor organoids demonstrate that the loss of TXNIP and GDF15 responsiveness to oxaliplatin is associated with advanced disease or chemotherapeutic resistance, with transcriptomic or proteomic GDF15/TXNIP ratios showing potential as a prognostic biomarker. These findings illustrate a potentially common pathway where chemotherapy-induced epithelial oxidative stress drives local immune remodelling for patient benefit, with disruption of this pathway seen in refractory or advanced cases.
2024-08-12 | PXD051666 | Pride
Project description:Cone photoreceptors are the primary initiator of visual transduction in the human retina. Dysfunction or death of rod photoreceptors precedes cone loss in many retinal and macular degenerative diseases, suggesting a rod-dependent trophic support for cone survival. Rod differentiation and homeostasis are dependent on the basic motif leucine zipper transcription factor NRL. The loss of Nrl in mice (Nrl-/-) results in a retina with predominantly S-opsin containing cones that exhibit molecular and functional characteristics of WT cones. Here we report that Nrl-/- retina undergoes a rapid but transient period of degeneration in early adulthood, with cone apoptosis, retinal detachment, alterations in retinal vessel structure, and activation and translocation of retinal microglia. However, cone degeneration stabilizes by four months of age, resulting in a thinned but intact outer nuclear layer with residual cones expressing S- and M-opsins and a preserved photopic ERG. At this stage, microglia translocate back to the inner retina and reacquire a quiescent morphology. Gene profiling analysis during the period of transient degeneration reveals misregulation of stress response and inflammation genes, implying their involvement in cone death. The Nrl-/- retina illustrates the long-term viability of cones in the absence of rods and may serve as a model for elucidating mechanisms of cone homeostasis and degeneration that would be relevant to understanding diseases of the cone-dominant human macula. Targets were generated from a pair of retinas (one Nrl-/- mouse) per biological replicate. Four biological replicates were generated for each of the five aging timepoints (1, 2, 4, 6, and 10 months post natal).
2011-11-15 | E-GEOD-33674 | biostudies-arrayexpress