Ontology highlight
ABSTRACT:
PROVIDER: PRJNA891791 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The molecular mechanisms by which obesity increases the risk of cardiovascular diseases are poorly understood. The purpose of this study was to identify candidate biomarkers overexpressed in adipose tissue of obese subjects that could link expanded fat mass to atherosclerosis. We compared gene expression profile in subcutaneous adipose tissue (scWAT) of 28 obese and 11 lean subjects using microarray technology. This analysis identified 240 genes significantly overexpressed in scWAT of obese subjects. The genes were then ranked according to the correlation between gene expression and body mass index (BMI). In this list, the elastolytic cysteine protease cathepsin S was among the highly correlated genes. RT-PCR and Western blotting confirmed the increase in cathepsin S mRNA (P=0.006) and protein (P<0.05) in obese scWAT. The circulating concentrations of cathepsin S were also significantly higher in obese than in nonobese subjects (P<0.0001). Both cathepsin S mRNA in scWAT and circulating levels were positively correlated with BMI, body fat, and plasma triglyceride levels. In addition, we show that the proinflammatory factors, lipopolysaccharide, interleukin-1β, and tumor necrosis factor-α increase cathepsin S secretion in human scWAT explants. This study identifies cathepsin S as a novel marker of adiposity. Since this enzyme has been implicated in the development of atherosclerotic lesions, we propose that cathepsin S represents a molecular link between obesity and atherosclerosis. Keywords: disease state analysis
2007-09-26 | GSE9153 | GEO
Project description:Cathepsin L is a lysosomal protease that is secreted by several cancer cells. Cathepsin L upregulation has been widely associated with poor clinical outcome and increased metastatic incidence. However, whether Cathepsin L participates in tumor angiogenesis remains less studied. Our study showed a significant activation of angiogenic capacity of endothelial cells in presence of purified or tumor derived Cathepsin L. In addition, Cathepsin L exposure led to a significant increase in the proliferative capacity of endothelial cells. While the ability of Cathepsin L to promote endothelial cell sprouting, migration, invasion and tube formation can be attributed to its proteolytic effects on extracellular matrix, how it promotes endothelial cell proliferation remains obscure. The objective of this study was to test if Cathepsin L exposure can activate signaling cascades and gene expression leading to proliferation of endothelial cells.
2016-06-20 | GSE75744 | GEO
Project description:Primary outcome(s): Relationship with mRNA expression of B7 family molecules in blood of patients with colorectal cancer and clinicopathological factors
| 2623816 | ecrin-mdr-crc
Project description:Cisplatin-based chemotherapy is the most common treatment for unresectable bladder cancers and also increasingly used as neoadjuvant treatments before or after surgery and radiotherapy. Unfortunately, though many patients respond to the treatment, most of them develop resistance quickly with unclear mechanisms and few further treatment options. Here, we report that semi-squamazation is acquired during chemo treatment in both mice and human. Multi-omics analyses show that cathepsin H (CTSH), a direct target of p63, is associated with chemoresistance and semi-squamation. Treatment with the cathepsin inhibitor E64 specifically restrains chemoresistant but not chemosensitive cancer. Mechanistically, cathepsin inhibition induces fully squamous differentiation of bladder cancer cells, which requires TNF receptor 1alpha and is associated with pyroptosis. Our study suggests that semi-squamazation would be a diagnosistic marker for chemoresistance and differentiation therapy by targeting CTSH might be a potential treatment for chemoresistant bladder cancer.
2022-07-09 | GSE192575 | GEO
Project description:Cathepsin D deficiency in mammary epithelium transiently stalls murine breast cancer by interference with mTORC1 signaling
| PRJNA551126 | ENA
Project description:Interventions: Gold Standard:pathological diagnosis;Index test:AQP8
Primary outcome(s): mRNA of AQP8;AQP8 expression level
Study Design: Factorial
| 2704477 | ecrin-mdr-crc
Project description:mRNA Expression Changes with Cofilin-2 Deficiency
| PRJNA261010 | ENA
Project description:mRNA Expression Changes with Cofilin-2 Deficiency
2015-09-21 | E-GEOD-61404 | ExpressionAtlas
Project description:The neuroinflammation and peripheral immune response following subarachnoid hemorrhage (SAH) aggravates early brain injury and lead to poor prognosis. Cross-talk between brain and cervical lymph nodes (CLNs) plays a crucial role in neuroinflammation and neurological diseases-associated brain injury. However, whether CLNs participate in brain damage and how injured brain activates immune system in SAH remain unclear. Previously, we reported that extravasated erythrocytes are drained into CLNs early following SAH. Here, we demonstrated that the removal of CLNs attenuated neuroinflammation and neurological deficits in 2 mouse models of SAH. Interestingly, we found that extravasated erythrocytes in CLNs following SAH were significantly engulfed by LYVE-1+ lymphatic endothelial cells (LECs) in both mandibular and deep CLNs. Single-cell RNA sequencing of mandibular LNs revealed that the medullary LEC is the primary LEC subset to degrade erythrocytes via lysosome protease cathepsin S. LECs treated by erythrocytes in vitro leaded to increasing the expression of genes related to inflammatory response, chemokines and lysosome protease cathepsin S. Importantly, deficiency of cathepsin S specifically in LECs using transgenic mice or blockage of cathepsin S by its inhibitor reduced SAH-induced brain damage. These results revealed a mechanism of how extravasated erythrocytes triggers a CLN-mediated inflammatory response and the aggravation of brain injury in SAH, and target this process may become effective therapeutic strategies to alleviate SAH pathology.
2025-08-14 | GSE295771 | GEO