Effect of Smurf1 or Smurf2 deficiency on Gene Expression Profiling of aged mouse liver tissues
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PROVIDER: PRJNA454813 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptome analysis of RNAs extracted from livers of wild type or Smurf1 knock out (KO) or Smurf2 KO mice at age of 11 month old. We prepared RNA from the following groups: livers of Wild type (WT) or Smurf1 KO or Smurf2 KO mouse from mixed Black Swiss/129SvEv background at age of 11 month old. The gene expression profiles were compared, and selected genes that showed either increased or decreased expression by a cut-off of 1.5 folds, p< 0.05. The results showed that many genes that are involved in lipid metabolism were upregulated in Smurf1-/- livers. These results also indicate that Smurf1 plays a more prominent role in the liver than Smurf2.
2018-12-19 | GSE113995 | GEO
Project description:Purpose: TGF-β/BMP signaling pathway has a significant role in fibrotic cataract. Smurf1, a ubiquitin protein ligase, regulates the TGF-β/BMP signaling pathway through the ubiquitin-proteasome system (UPS). This study aims to investigate the role of Smurf1 in the progression of fibrotic cataract and its underlying mechanism.Method: We employed a mouse injury-induced anterior subcapsular cataract (ASC) model and administered Smurf1 inhibitor A01 through anterior chamber injection for in vivo investigation. RNA sequencing was performed to examine global gene expression changes. The volume of the subcapsular opacity was determined using whole-mount immunofluorescence of lens anterior capsules. Lentivirus was utilized to create cell lines with Smurf1 knockdown or overexpression in SRA01/04. Protein levels were assessed by Simple Western. Lens epithelial cell (LEC) proliferation was evaluated by CCK8 and EdU assays. LEC migration was measured by Transwell and wound healing assays.Results: The mRNA levels of genes associated with cell proliferation, migration, epithelial-mesenchymal transition (EMT), TGF-β/BMP pathway and UPS, including Smurf1, were upregulated in ASC model. The mRNA expression of Smurf1 was also upregulated in anterior lens capsules of age-related cataract patients. Anterior chamber injection of A01 inhibited ASC formation and EMT. In vitro knockdown of Smurf1 resulted in reduced proliferation, TGF-β2-induced migration and EMT of LECs. Smurf1 inhibition upregulated Smad1, Smad5 and pSmad1/5. Conversely, Smurf1 overexpression displayed the opposite phenotypes.Conclusion: Smurf1 regulated the progression of fibrotic cataract by influencing the proliferation, migration and EMT of LECs through regulation of Smad signaling pathway, offering a novel target for the treatment of fibrotic cataract.
2024-02-14 | GSE245411 | GEO
Project description:Purpose: TGF-β/BMP signaling pathway has a significant role in fibrotic cataract. Smurf1, a ubiquitin protein ligase, regulates the TGF-β/BMP signaling pathway through the ubiquitin-proteasome system (UPS). This study aims to investigate the role of Smurf1 in the progression of fibrotic cataract and its underlying mechanism.Method: We employed a mouse injury-induced anterior subcapsular cataract (ASC) model and administered Smurf1 inhibitor A01 through anterior chamber injection for in vivo investigation. RNA sequencing was performed to examine global gene expression changes. The volume of the subcapsular opacity was determined using whole-mount immunofluorescence of lens anterior capsules. Lentivirus was utilized to create cell lines with Smurf1 knockdown or overexpression in SRA01/04. Protein levels were assessed by Simple Western. Lens epithelial cell (LEC) proliferation was evaluated by CCK8 and EdU assays. LEC migration was measured by Transwell and wound healing assays.Results: The mRNA levels of genes associated with cell proliferation, migration, epithelial-mesenchymal transition (EMT), TGF-β/BMP pathway and UPS, including Smurf1, were upregulated in ASC model. The mRNA expression of Smurf1 was also upregulated in anterior lens capsules of age-related cataract patients. Anterior chamber injection of A01 inhibited ASC formation and EMT. In vitro knockdown of Smurf1 resulted in reduced proliferation, TGF-β2-induced migration and EMT of LECs. Smurf1 inhibition upregulated Smad1, Smad5 and pSmad1/5. Conversely, Smurf1 overexpression displayed the opposite phenotypes.Conclusion: Smurf1 regulated the progression of fibrotic cataract by influencing the proliferation, migration and EMT of LECs through regulation of Smad signaling pathway, offering a novel target for the treatment of fibrotic cataract.
2024-02-14 | GSE245407 | GEO
Project description:We aim to the investigate the role of SMURF1 in breast cancer progression. MCF-7 cells were used as the model and SMURF1 was silenced by siRNA.
2018-08-14 | GSE102653 | GEO
Project description:Comparison of aged wt, krt18+/- and krt18-/- non-tumorous liver tissues
| PRJNA320385 | ENA
Project description:Cerebral Cavernous Malformations (CCM), caused by loss of CCM1, CCM2 or CCM3 in endothelial cells (ECs), are leaky capillaries causing seizures and stroke. CCM protein loss gives overlapping changes in biomechanical and transcriptional properties of ECs, due to common RhoA-driven alterations in cytoskeletal organization and intracellular signaling. However, EC models of 3-D tube formation show loss of each CCM protein generates distinct morphological defects in tubular structures. Computational modeling, live-cell imaging and RNA sequencing revealed distinct functional roles of CCM1 and CCM3 in regulating EC-EC and EC-matrix interactions. CCM2 has an intermediate phenotype consistent with its interaction with CCM1 and CCM3. In ECs, CCM proteins regulate SMURF1 E3 ligase ubiquitination and degradation of RhoA. Loss of CCM proteins results in loss of SMURF1 and a concomitant increase of MEKK3, a negative regulator of SMURF1 expression. We propose CCM lesions develop because of dysregulated SMURF1 resulting in RhoA and MEKK3 gain-of-function.
2019-04-05 | GSE112882 | GEO
Project description:Effect of leptin deficiency in Bmal1 knockout mice across different tissues
| PRJNA631168 | ENA
Project description:GRSF1 deficiency in skeletal muscle reduces endurance in aged mice
| PRJNA722912 | ENA
Project description:Transcriptome analysis of metabolic tissues in young and aged mice
| PRJNA492410 | ENA
Project description:GRSF1 is a mitochondrial RNA-binding protein important for maintaining mitochondrial function. We found that GRSF1 is highly expressed in cultured skeletal myoblasts differentiating into myotubes. To understand the physiological function of GRSF1 in vivo, we generated mice in which GRSF1 was specifically ablated in skeletal muscle. The conditional knockout mice (Grsf1cKO) appeared normal until 7-9 months of age. Importantly, however, a reduction of muscle endurance compared to wild-type controls was observed in 16- to18-month old Grsf1cKO mice. Transcriptomic analysis revealed more than 200 mRNAs differentially expressed in Grsf1cKO muscle at this age. Notably, mRNAs encoding proteins involved in mitochondrial function, inflammatory reaction, and ion transport, including Mgarp, Cxcl10, Nfkb2, and Sln, were significantly elevated in aged Grsf1cKO muscle. Our findings suggest that GRSF1 deficiency exacerbates the functional decline of aged skeletal muscle, likely through multiple downstream genes.
2021-07-08 | GSE172311 | GEO