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Losartan controls immune checkpoint blocker-induced edema and improves survival in glioblastoma

ABSTRACT: Losartan controls immune checkpoint blocker-induced edema and improves survival in glioblastoma

PROVIDER: PRJNA874707 | ENA |

REPOSITORIES: ENA

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Losartan controls immune checkpoint blocker-induced edema and improves survival in glioblastoma

Project description:Immune checkpoint blockers (ICBs) have failed in all Phase III glioblastoma trials. Here, we found that ICBs induce cerebral edema in some patients and mice with glioblastoma. Through single-cell RNA sequencing, intravital imaging, and T cell blocking studies in mice, we demonstrated that this edema results from an inflammatory response following anti-PD1 antibody treatment that disrupts the blood-tumor-barrier. Used in lieu of immunosuppressive corticosteroids, the angiotensin receptor blocker losartan prevented this ICB-induced edema and reprogrammed the tumor microenvironment, curing 20% of mice which increased to 40% in combination with standard of care treatment. Using a bihemispheric tumor model, we identified a “hot” tumor immune signature prior to losartan+anti-PD1 therapy that predicted long-term survival. Our findings provide the rationale and associated biomarkers to test losartan with ICBs in glioblastoma patients.

2023-01-01 | GSE212246 | GEO

Gene expression profiling of aortic media after long-term treatment with an angiotensin II-receptor blocker, Losartan

Project description:Rats (Wag/Rij, females) were chronically treated with Losartan (20mg/d), an angiotensin II-receptor blocker during 9 months. Gene expression profiling was performed on aortic media to understand the long-term effect of this molecule on the cardiovascular system. Two-conditions experiment, Ctrl vs Losartan-treated animals. Biological replicates: 5 control replicates, 5 Losrtan-treated animals. All the RNA samples were pooled to provide a reference RNA for a two-color experiment.

2010-09-23 | E-GEOD-18298 | biostudies-arrayexpress

Gene expression profiling of aortic media after long-term treatment with an angiotensin II-receptor blocker, Losartan

2010-09-23 | GSE18298 | GEO

Edema Toxin-treated Macrophage Study

Project description:Edema toxin (EdTx), which is a combination of edema factor and a binding moiety (protective antigen), is produced by Bacillus anthracis, the etiological agent of anthrax. EdTx is an adenylyl cyclase enzyme that converts adenosine triphosphate to adenosine-3’,5’-monophosphate, resulting in interstitial edema seen in anthrax patients. We used GeneChip analysis to examine global transcriptional profiles of EdTx-treated RAW 264.7 murine macrophage-like cells at 3 and 6 hr. Keywords: Toxin response

2006-10-24 | GSE4712 | GEO

Carp edema virus

Project description:Genome sequence of carp edema virus

| PRJDB11353 | ENA

Carp edema virus

Project description:Carp edema virus Raw sequence reads

| PRJNA937218 | ENA

Transcriptome alterations of hiPSC-CMs after alcohol treatment, alcohol and losartan co-treatment

Project description:In order to investigate the changes of hiPSC-CMS transcriptome after alcohol treatment and whether losartan has an effect on the changes of hiPSC-CM transcriptome after alcohol treatment, RNAseq was performed on hiPSC-CMs treated with 100mM alcohol and 100mM alcohol co-treated with1uM losartan.

2022-02-05 | GSE195981 | GEO

Attenuation of SARS-CoV-2 Infection by Losartan in Human Kidney Organoids

Project description:COVID-19 associated acute kidney injury (COVID-AKI) is a common complication of SARS-CoV-2 infection in hospitalized patients. It is unclear how susceptible human kidneys are to direct SARS-CoV-2 infection and whether pharmacologic manipulation of the renin-angiotensin II signaling (RAS) pathway modulates this susceptibility. Using induced pluripotent stem cell derived kidney organoids, SARS-CoV-1, SARS-CoV-2 and MERS-CoV tropism, defined by the paired expression of a host receptor (ACE2, NRP1 or DPP4) and protease (TMPRSS2, TMPRSS4, FURIN, CTSB or CTSL), was identified primarily amongst proximal tubule cells. Losartan, an angiotensin II receptor blocker being tested in COVID-19 patients, inhibited angiotensin II mediated internalization of ACE2, upregulated interferon stimulated genes (IFITM1 and BST2) known to restrict viral entry, and attenuated the infection of proximal tubule cells by SARS-CoV-2. Our work highlights the susceptibility of proximal tubule cells to SARS-CoV-2 and reveals a putative protective role for RAS inhibitors during SARS-CoV-2 infection.

2022-01-23 | GSE149687 | GEO

Expression data from kidney tissues treated with vehicle, losartan and metformin

Project description:Chronic kidney disease (CKD) is one of the major global health problems with high incidence, poor prognosis and high medical cost. However, few pharmacological options are available for CKD. Metformin is widely used for treatment of type-2 diabetes, but recent works showed that metformin ameliorates tumor progression, inflammatory disease and tissue fibrosis. Whether metformin ameliorates non-diabetic chronic glomerular disease and CKD is unexplored. Here we showed that metformin or losartan (used as control) has protective effects against CKD by suppressing proteinuria, renal inflammation, fibrosis and glomerular injury in Alport syndrome mouse model, which spontaneously manifests chronic glomerular and kidney disease. Transcriptome analysis showed that metformin and losartan influenced molecular pathways of metabolism and inflammation, respectively. While metformin specifically affected genes that were classified as metabolic regulators, losartan specifically altered genes that were classified as inflammatory regulators. Metformin also induced multiple signaling pathways not affected by losartan. Overall, metformin ameliorates non-diabetic chronic glomerular diseases, and could be considered a therapeutic option for CKD. We used microarrays to investigate the global gene expression underlying the protective effects of metformin on Alport syndrome mice model

2021-01-30 | GSE109861 | GEO

Genomic alterations in Reinke's edema

Project description:Genomic alterations in Reinke's edema

| PRJNA736237 | ENA