Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA209132 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Animals were sc dosed with 5mg/kg anti-miR-214 or control anti-miR, had UUO performed and were sacrificed at 7 days. n=4 animals per group, 2 groups
2013-11-05 | E-GEOD-48194 | biostudies-arrayexpress
Project description:Animals were sc dosed with 5mg/kg anti-miR-214 or control anti-miR, had UUO performed and were sacrificed at 7 days.
2013-11-05 | GSE48194 | GEO
Project description:Purpose: Determine the differential gene expression pattern between wildtype, Pkd2-KO and Pkd2-miR-214 KO mice Methods: kidney mRNA profiles of Pkd2-KO and Pkd2-mir-214-KO mice was sequenced with N of 3 in each group Results: 972 differentially expressed transcripts were identified between Pkd2-KO kidneys and Pkd2-miR-214-KO kidneys Conclusion: Deletion of miR-214 promotes interstitial inflammation in mouse models of ADPKD
2019-09-25 | GSE137945 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Gene expression analysis in the kidney following disseminated candididiasis
| PRJNA348680 | ENA
Project description:Kidney fibrosis is a major hallmark of chronic kidney disease and is defined by an excessive accumulation of extracellular matrix, primarily collagens. While collagen synthesis has been extensively investigated, the contribution of impaired collagen degradation to the development of fibrosis remains poorly understood. Collagen degradation involves the activity of proteases producing collagen-derived peptides (CDPs). Here we tested the hypothesis whether reduced collagen degradation participates to the development of kidney fibrosis. For that, CDPs were quantified in pelvic urine of kidney undergoing fibrosis following unilateral ureteral obstruction (UUO). C57Bl6 male mice underwent UUO- or sham-surgery and were sacrificed after 3- or 7-days (3D or 7D). Fibrosis was evaluated by histology. Urinary CDP composition (qualitative-sequences and quantitative-abundances) was analysed by mass spectrometry (MS). Based on collagen protein deposition, UUO-induced fibrosis was detected at 7D and not at 3D. At both 3D and 7D, of the more than 300 significantly different CDPs were found in UUO-pelvic urine, 70% of them displaying a reduced abundance in UUO compared to sham-bladder. In UUO-bladder urine, significant CDPs were found only at 7D with 79% of them displaying increased abundance. CDPs derived from Col1a1, Col1a2 and Col3a1 were the most represented and distributed in clusters along their parental protein sequence. Most clusters were composed of seemingly decreasing length CDPs containing the entire sequence of the shortest CDP. Within the clusters, inter-CDP correlations of abundance were very different between UUO-pelvis and UUO-bladder at 3D and 7D post-UUO. In conclusion, using a mouse model of fibrosis that enables the specific study of CDPs from the fibrotic kidney, we observe that reduced collagen degradation could play a key role in the early stages of fibrosis development. Our research suggests a potential need for a shift in the development of anti-fibrotic strategies, emphasizing not only the inhibition of collagen synthesis but also the enhancement of its degradation.
2026-01-12 | PXD064569 | Pride
Project description:Chronic kidney disease is associated with progressive renal fibrosis, where perivascular cells give rise to the majority of α-SMA positive myofibroblasts. We sought to identify pericytic miRNAs that could serve as a target to decrease myofibroblast formation. We induced kidney fibrosis in FoxD1-GC;Z/Red-mice by unilateral ureteral obstruction (UUO) followed by FACS sorting of dsRed-positive FoxD1-derivative cells and miRNA profiling. MiR-132 selectively increased 21-fold during pericyte-to-myofibroblast formation whereas miR-132 was only 2.5-fold up in total kidney lysates (both in UUO and ischemia-reperfusion injury). MiR-132 silencing in UUO decreased collagen deposition (35%) and tubular apoptosis. Immunohistochemistry, western blot and qRT-PCR confirmed a similar decrease in interstitial α-SMA+ cells. Pathway analysis identified a rate-limiting role for miR-132 in myofibroblast proliferation that was confirmed in vitro. Indeed, antagomir-132 treated mice displayed a reduction in the number of proliferating, ki67+ interstitial myofibroblasts. Interestingly, this was selective for the interstitial compartment and did not impair the reparative proliferation of tubular epithelial cells, as evidenced by an increase in ki67+ epithelial cells, as well as increased (p-)RB1, Cyclin-A and decreased RASA1, p21 levels in kidney lysates. Taken together, silencing miR-132 counteracts the progression of renal fibrosis by selectively decreasing myofibroblast proliferation and could potentially serve as a novel antifibrotic therapy. Total RNA obtained from FACS sorted mouse renal FoxD1-derivatve interstitial cells from mice that were treated with antagomir-132 or scramblemir and underwent UUO (n=4)
2016-02-16 | E-GEOD-76548 | biostudies-arrayexpress