Project description:To compare the snRNA seq transcriptional profile in renal tubule cells after conditional deletion of Cpt1a to floxed littermate controls, in mice fed a high fat diet for 2 years, and to compare mice aged 2 years with high fat diet to young mice.

2025-06-16 | GSE277335 | GEO

Plasminogen activator inhibitor-2 regulates immune response in kidney injury and renal aging mpact of plasminogen activator inhibitor-2 in kidney injury and renal aging

Project description:The plasminogen activator inhibitor-2 (PAI-2; encoded by the SerpinB2 gene) has been described in the context of macrophage activation and in cellular senescence. As both mechanisms are important in kidney disease we tested a possible role of PAI-2 in renal injury and repair. Methods:Aging, ischemia/reperfusion injury and unilateral ureteral obstruction were performed on the mice. Bone marrow was transplantefrom SerpinB2-/- to wild-type littermates and vice versa. Primary tubular cells and macrophages from SerpinB2-/- and wildtype mice were used for functional studies and transcriptional profiling. Results: PAI-2 expression was up-regulated in cultured senescent tubular cells and in kidneys of aged mice. In the lack of PAI-2 in SerpinB2-/- mice was associated with enhanced renal fibrosis and an inflammatory phenotype during aging and in kidney injury models. While acute injury was associated with fewer monocytes/macrophages in SerpinB2-/- kidneys the subsequent resolution of inflammation seen in wildtype kidneys was lacking in knockout mice. Conclusion: PAI-2 regulates renal aging, tubular damage, and resolution of inflammation. PAI-2 is crucial for kidney repair in mice .

2019-10-22 | GSE139156 | GEO

Murine kidneys： WT Models vs METTL3-cKO Models

Project description:MeRIP and RNA Epitranscriptomic Microarray analysis in kidneys of conditional knockout (cKO) METTL3 mice and wild type mice following glyoxylate-induced CaOx nephrocalcinosis.In METTL3-cKO mice, METTL3 subjected the specific absence from renal tubular epithelial cells. Goal was to determine the effects of METTL3 gene knockout on the expression and N6-methyladenosine (m6A) modifications of global gene.

2025-09-05 | GSE212868 | GEO

Mitochondrial Calcium Uniporter Promotes Kidney Aging through Inducing Mitochondrial Calcium-Mediated Renal Tubular Cell Senescence

Project description:Kidney is a vital organ responsible for homeostasis in the body. To retard kidney aging is of great importance for maintaining body health. Whereas the therapeutic strategies targeting against kidney aging are not elucidated. Recent studies show mitochondrial dysfunction is critical for renal tubular cell senescence and kidney aging, however, the underlying mechanisms of mitochondrial dysfunction in kidney aging have not been demonstrated. Herein, we found calcium overload, and the mitochondrial calcium uniporter (MCU) was induced in renal tubular cells and aged kidney. To activate MCU not only triggered mitochondrial calcium overload, but also induced reactive oxygen species (ROS) production and cellular senescence and age-related kidney fibrosis. Inversely, to block MCU or chelate calcium diminished ROS generation, restored mitochondrial homeostasis, and retarded cell senescence and protected against kidney aging. These results demonstrate MCU plays a key role in promote renal tubular cell senescence, which provides a new insight on the therapeutic strategy for fighting against kidney aging.

2024-10-02 | GSE262514 | GEO

A role for CPT1A to prevent blood vessel permeability revealed by in depth proteomics

Project description:Endothelial cells (ECs) line the inner wall of blood vessels and maintain vascular stability. Vascular stability alteration is a hallmark of pathologies such as cancer and thrombosis. A role for fatty acid oxidation (FAO) in this process is unknown. Integrating MS-proteomics and metabolic modeling revealed that FAO increases when ECs cultured on matrigel are assembled into a fully formed network. Inhibition of CPT1A in ECs, a limiting enzyme in FAO, results in disruption of this network. Acute CPT1A inhibition reduces cellular ATP levels and oxygen consumption, which can be restored replenishing the tricarboxylic acid cycle (TCAc). Phosphoproteomic changes upon acute CPT1A inhibition evoked those triggered by thrombin, a potent inducer of EC permeability through calcium signaling. Indeed, CPT1A inhibition increased EC permeability and vascular leakage, which were restored replenishing the TCAc or, partially, inhibiting calcium influx. Our study shows the possibility of altering FAO to interfere with ECs in diseases.

2015-01-28 | PXD001186 | Pride

Genome-wide analysis of gene expression in normal and fibrotic mouse kidneys with and without Twist1 or with and without Snai1(Snail) expression in proximal tubular epithelial cells

Project description:In this study mice were engineered to specifically delete Twist1 or Snail expression in proximal tubular epithelial cells of the kidney (ggt-cre+;Twist flox/flox and ggt-cre+;Snail flox/flox ). These mice and control mice (ggtcre-;Twist flox/flox: these express Twist1, and ggtcre-;Snail flox/flox:these express Snail) were subjected to unilaterial ureteric obstruction. This experiment allows for the collection and analysis of expression in contralateral healthy (HK) kidney adn obstructed disease (DK) kidney. Total RNA was isolated from the contralateral healthy (HK) and obstructed disease (DK) kidneys of 3 mice with ggt-cre-;Twist flox/flox genotype (Wildtype like) and 4 mice with ggt-cre+;Twist flox/flox genotype (loss of Twist1 in proximal tubular epithelial cells), 3 mice with ggt-cre-;Snail flox/flox genotype (Wildtype like) and 3 mice with ggt-cre+;Snail flox/flox genotype (loss of Snail in proximal tubular epithelial cells). Total RNA was also isolated from kidneys of completely healthy mice: 3 mice ggt-cre-;WT, 3 mice ggt-cre+;WT, 3 mice ggt-cre+;Twist flox/flox and 3 ggt-cre+;Snail flox/flox

2015-08-03 | E-GEOD-60685 | biostudies-arrayexpress

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