Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1097497 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease without effective medical therapies. Emerging evidences have suggested a crosstalk between adipose tissue and vascular cells and brown adipose tissue is beneficial for cardiovascular health. Nevertheless, whether brown remodeling of white adipose tissue would protect against AAA remains unclear. Here we showed that patients with AAA had a decreased browning level of adipose tissue and induction of adipose tissue browning significantly reduced AAA incidence and attenuated AAA development in mice. Using LC-MS/MS and proteomic analysis, we further identified Follistatin-like 1 (FSTL1) as a novel vessel-protective adipokine secreted by browning adipocytes. Mechanistically, FSTL1 inhibited VSMC apoptosis through DIP2A/AKT signaling. Furthermore, we demonstrated that adipocyte-specific deficiency of FSTL1 abrogated the protective effect of browning induction. Moreover, supplementation of FSTL1 either systemically or patched into hydrogel placing around abdominal aorta markedly limited aortic dilation and AAA progression. Our data suggest a protective role of adipose tissue browning and a novel batokine FSTL1 in the development of AAA, which may represent a novel intervention strategy for AAA.
2025-09-07 | PXD064197 | Pride
Project description:Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease without effective medical therapies. Emerging evidences have suggested a crosstalk between adipose tissue and vascular cells and brown adipose tissue is beneficial for cardiovascular health. Nevertheless, whether brown remodeling of white adipose tissue would protect against AAA remains unclear. Here we showed that patients with AAA had a decreased browning level of adipose tissue and induction of adipose tissue browning significantly reduced AAA incidence and attenuated AAA development in mice. Using LC-MS/MS and proteomic analysis, we further identified Follistatin-like 1 (FSTL1) as a novel vessel-protective adipokine secreted by browning adipocytes. Mechanistically, FSTL1 inhibited VSMC apoptosis through DIP2A/AKT signaling. Furthermore, we demonstrated that adipocyte-specific deficiency of FSTL1 abrogated the protective effect of browning induction. Moreover, supplementation of FSTL1 either systemically or patched into hydrogel placing around abdominal aorta markedly limited aortic dilation and AAA progression. Our data suggest a protective role of adipose tissue browning and a novel batokine FSTL1 in the development of AAA, which may represent a novel intervention strategy for AAA.
2025-09-06 | GSE296762 | GEO
Project description:Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease without effective medical therapies. Emerging evidences have suggested a crosstalk between adipose tissue and vascular cells and brown adipose tissue is beneficial for cardiovascular health. Nevertheless, whether brown remodeling of white adipose tissue would protect against AAA remains unclear. Here we showed that patients with AAA had a decreased browning level of adipose tissue and induction of adipose tissue browning significantly reduced AAA incidence and attenuated AAA development in mice. Using LC-MS/MS and proteomic analysis, we further identified Follistatin-like 1 (FSTL1) as a novel vessel-protective adipokine secreted by browning adipocytes. Mechanistically, FSTL1 inhibited VSMC apoptosis through DIP2A/AKT signaling. Furthermore, we demonstrated that adipocyte-specific deficiency of FSTL1 abrogated the protective effect of browning induction. Moreover, supplementation of FSTL1 either systemically or patched into hydrogel placing around abdominal aorta markedly limited aortic dilation and AAA progression. Our data suggest a protective role of adipose tissue browning and a novel batokine FSTL1 in the development of AAA, which may represent a novel intervention strategy for AAA.
2025-09-06 | GSE296628 | GEO
Project description:In order to investigate, at the mRNA level, the signaling pathways through which triiodothyronine (T3) affects osteoblast function, human mesenchymal stem cells derived from adipose tissue were subjected to a pre-established osteoinduction protocol, resulting in osteoblast-like cells, which were cultured with or without T3. RNA-Seq was performed using Illumina platform, and differential gene expression was assessed with DESeq2. Among differentially expressed genes, enrichment analysis was performed for biological processes against the Gene Ontology Consortium database, using both ClusterProfiler R package and STRING.
2022-06-20 | GSE205678 | GEO
Project description:As obesity has becoming an urged issue nowadays, delineation of the mechanisms of WAT tissue white-browning and beige adipose origin are of important topic. By the use of snRNA-seq, we can outline LepR cells play important role in the white-browning process and investigate the mechanisms participate at different white-browning treatments.
2022-11-06 | GSE216925 | GEO
Project description:Visceral white adipose tissue is closed correlated with obesity and metabolic dysfunction. Epididymal adipose tissue (eWAT) is considered as typical visceral white adipose tissue. Induction of browning of white adipose tissue improves metabolic dysfunction such as insulin resistance. In contrast to mice subcutaneous adipose tissue, visceral fat do not show significant browning under 4°C. However,under physiologically tolerable low temperature visceral adipose tissue can turn brown. We used microarrays to detail the global programme of gene expression in C57Bl/6 mice epididymal adipose tissue exposed to thermoneutral 30°C, 4°C and temperatures lower than 4°C.
2017-06-12 | GSE74062 | GEO
Project description:Cancer associated cachexia (CAC) causes white adipose tissue (WAT) lose by inhibiting adipogenesis, and promoting lipolysis, fat oxidation and browning. To uncover the specific lncRNAs and mRNAs involved in these processes, we used RNA microarray to identify the transcriptomes and found numerous lncRNAs and mRNAs differentially expressed in the fat tissue between CAC and normal mice.
2018-08-16 | GSE118611 | GEO
Project description:Differentiation of brown adipocytes is a crucial process for adaptive thermogenesis, which is stimulated by various factors. We found robust browning of inguinal white adipose tissue in UCP1/ApoE-DKO mice, but not in ApoE-KO mice, under high-fat diet condition. We used microarray to determine the genes specifically regulated in the browning white adipose tissue in UCP1/ApoE-DKO mice.
2018-10-01 | GSE95273 | GEO
Project description:Dataset containing multiple Hyptis and Artemisia spp. used for the discovery of natural products inhibiting aberrant signaling, namely MAPK/ERK and PI3K/AKT, in melanoma
2021-12-22 | MSV000088606 | GNPS
Project description:Oncogenic RAS activation, hypertranscription and transcription-replication conflicts (TRCs) are frequent features of cancer cells that are under investigation for therapeutic targeting. RAS oncogenes promote RNA polymerase activity and hypertranscription for cell growth and proliferation, which can the lead to TRCs. Here, we investigated hypertranscription and replication stress induced by the HRAS and KRAS oncogenes, and their downstream signalling through the MAPK and PI3K pathways. We show that HRAS causes more TRCs than KRAS because HRAS specifically hyperactivates the PI3K-AKT signalling pathway. MAPK signalling is insufficient to cause hypertranscription and TRCs, which require PI3K activity. PI3K hyperactivation was associated with increased E2F and MYC transcription programmes, increased S phase entry, increased nascent transcription of genes encoding ribosome biogenesis factors and expression of small nucleolar RNAs (snoRNAs). Inhibiting S phase entry alone did not rescue hypertranscription and replication stress, which required both MAPK and PI3K signalling. We report that a main downstream effector of PI3K-induced hypertranscription is AKT-mediated phosphorylation of GSK3b, which stabilises MYC. Cancer datasets further support that PI3K mutations may be associated with hypertranscription and replication stress signatures. Our findings suggest a mechanistic explanation for replication stress variability across RAS models and identify potential new predictors of TRCs in cancer.
2026-03-09 | GSE322525 | GEO