Project description:Gene expression was determined for Male accessory gland and testes in different members of the Anopheles gambiae complex, including An. gambiae (Savannah, MRA-762), An. coluzzii (Mopti) [2], An. arabiensis [3], An. merus [4] and An. quadriannalatus [5. All the mosquito stocks were obtained from the Malaria Research and Reference Reagent Resource Center (MR4) in Atlanta (https://www.beiresources.org/Catalog/BEIVectors/MRA-762.aspx). References: 1. MR4 wild stocks information. Access Jenuary 2018. (Kisumu) https://www.beiresources.org/Catalog/BEIVectors/MRA-762.aspx 2. MR4 wild stocks information. Access Jenuary 2018. (Mopti) https://www.beiresources.org/Catalog/BEIVectors/MRA-763.aspx 3. MR4 wild stocks information. Access Jenuary 2018. (arabiensis) https://www.beiresources.org/Catalog/BEIVectors/MRA-856.aspx 4. MR4 wild stocks information. Access Jenuary 2018. (merus) https://www.beiresources.org/Catalog/BEIVectors/MRA-1156.aspx 5. MR4 wild stocks information. Access Jenuary 2018. (quadriannulatus) https://www.beiresources.org/Catalog/BEIVectors/MRA-1155.aspx
Project description:The objective of this study was to test the novel non-steroidal mineralocorticoid receptor antagonist (MRA) finerenone as a monotherapy in a preclinical Duchenne muscular dystrophy (DMD) model. Microarray was used to detail gene expression differences in ventricular heart tissue from finerenone-treated dystrophin-deficient, utrophin-haploinsufficient Het (utrn+/−; mdx) mice versus untreated Het mice.
Project description:Mineralocorticoids play a critical role in maintaining sodium and potassium homeostasis and pathophysiological processes including hypertrophy, inflammation and fibrosis. Mineralocorticoid antagonists (MRAs) have shown to protect from kidney and heart disease, however, their molecular mechanism of action is poorly understood. Here we performed single nuclei and bulk transcriptomics and chromatin accessibility analysis to characterize the mode of kidney protection by steroidal and non-steroidal MRA treatment in a rat model of mineralocorticoid-induced cardiorenal end-organ damage. We define mineralocorticoid sensitive cell types and gene network in the kidney. We show that in diseased kidneys specific proximal tubule cells develop an injured profibrotic phenotype expressing Spp1 and Il34. Nonsteroidal finerenone protects from profibrotic differentiation of proximal tubule cells. Profibrotic gene signature can classify human kidney tissue samples and predict prognosis. Our multi-omics approach elucidates target cell types and potential mechanisms of renal protection by finerenone.
2023-11-17 | GSE183840 | GEO
Project description:Identification of FLA and MRA from water of external anthropogenic and nosocomial environment
Project description:Mineralocorticoids play a critical role in maintaining sodium and potassium homeostasis and pathophysiological processes including hypertrophy, inflammation and fibrosis. Mineralocorticoid antagonists (MRAs) have shown to protect from kidney and heart disease, however, their molecular mechanism of action is poorly understood. Here we performed single nuclei and bulk transcriptomics and chromatin accessibility analysis to characterize the mode of kidney protection by steroidal and non-steroidal MRA treatment in a rat model of mineralocorticoid-induced cardiorenal end-organ damage. We define mineralocorticoid sensitive cell types and gene network in the kidney. We show that in diseased kidneys specific proximal tubule cells develop an injured profibrotic phenotype expressing Spp1 and Il34. Nonsteroidal finerenone protects from profibrotic differentiation of proximal tubule cells. Profibrotic gene signature can classify human kidney tissue samples and predict prognosis. Our multi-omics approach elucidates target cell types and potential mechanisms of renal protection by finerenone.
Project description:Mineralocorticoids play a critical role in maintaining sodium and potassium homeostasis and pathophysiological processes including hypertrophy, inflammation and fibrosis. Mineralocorticoid antagonists (MRAs) have shown to protect from kidney and heart disease, however, their molecular mechanism of action is poorly understood. Here we performed single nuclei and bulk transcriptomics and chromatin accessibility analysis to characterize the mode of kidney protection by steroidal and non-steroidal MRA treatment in a rat model of mineralocorticoid-induced cardiorenal end-organ damage. We define mineralocorticoid sensitive cell types and gene network in the kidney. We show that in diseased kidneys specific proximal tubule cells develop an injured profibrotic phenotype expressing Spp1 and Il34. Nonsteroidal finerenone protects from profibrotic differentiation of proximal tubule cells. Profibrotic gene signature can classify human kidney tissue samples and predict prognosis. Our multi-omics approach elucidates target cell types and potential mechanisms of renal protection by finerenone.