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Suppression of ANGPTL4 Reprograms Endothelial Cell Metabolism and Inhibits Angiogenesis

ABSTRACT: Suppression of ANGPTL4 Reprograms Endothelial Cell Metabolism and Inhibits Angiogenesis

PROVIDER: PRJNA869060 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21025304_1.fastq.gz	Fastqsanger.gz
	SRR21025304_2.fastq.gz	Fastqsanger.gz
	SRR21025305_1.fastq.gz	Fastqsanger.gz
	SRR21025305_2.fastq.gz	Fastqsanger.gz
	SRR21025306_1.fastq.gz	Fastqsanger.gz

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Suppression of ANGPTL4 Reprograms Endothelial Cell Metabolism and Inhibits Angiogenesis

Project description:Angiopoietin-like 4 (ANGPTL4) is known to regulate various cellular and systemic functions. However, its cell-specific role in endothelial cells (ECs) function and metabolic homeostasis remains to be elucidated. Here, using endothelial-specific Angptl4 knock-out mice (Angptl4iEC), and transcriptomics and metabolic flux analysis, we demonstrate that ANGPTL4 is required for maintaining EC metabolic function vital for vascular permeability and angiogenesis. Knockdown of ANGPTL4 in ECs promotes lipase-mediated lipoprotein lipolysis, which results in increased fatty acid (FA) uptake and oxidation. This is also paralleled by a decrease in proper glucose utilization for angiogenic activation of ECs. Mice with endothelial-specific deletion of Angptl4 showed decreased pathological neovascularization with stable vessel structures characterized by increased pericyte coverage and reduced permeability. Together, our study denotes the role of endothelial-ANGPTL4 in regulating cellular metabolism and angiogenic functions of EC.

2023-11-22 | GSE211128 | GEO

Contradictory Effect of ANGPTL4 on Hedgehog pathway by Galectin-7 and its Influence on Cancer metastasis and Angiogenesis

Project description:Background: Gastric cancer (GC) is a serious malignant disease of digestive system over the world. Angiopoietin-like protein 4 (ANGPTL4) was a secreted glycoprotein, which involved in multiple pathophysiological process, such as metabolic reprogramming, angiogenesis, proliferation and metastasis. Nevertheless, the expression, function, and prognostic significance of ANGPTL4 in GC are still contradictory. Methods: Bioinformatic analysis to confirm the expression and prognosis of ANGPTLs in GC. IF staining was used to detect ANGPTL4 protein in GC samples. The molecular biological effect of ANGPTL4 was confirmed by EdU, MTT, FCS, wound healing, transwell, tube formation chorioallantoic membrane model, and nude mice model assay in GC cell lines. RNA-seq was used to confirm the potential downstream mechanism of ANGPTL4, which verified by PCR, WB, IF, co-IP and molecular docking. Results: ANGPTL4, as an important ANGPTLs, was significantly correlated with poor diagnosis in GC patients. The proliferation, migration, invasion, apoptosis escaping, angiogenesis ability was enhanced by ANGPTL4 in SNU5 and MKN7, but repressed in AGS. LGALS7 could be upregulated in AGS transfected with ANGPTL4 OE, which was one of the key factors that cause ANGPTL4 to produce an anticancer phenotype. Conclusion: LGALS7 was a key factor for the contradictory effect of ANGPTL4 on activating hedgehog pathway to driving GC progression, including proliferation, migration, apoptosis escaping, angiogenesis and lymphangiogenesis.

2024-12-01 | GSE252074 | GEO

Characterization of ANGPTL4 function in macrophages and adipocytes using Angptl4-knockout and Angptl4-hypomorphic mice

Project description:ANGPTL4 regulates plasma lipids, making it an attractive target for correcting dyslipidemia. However, ANGPTL4 inactivation in mice fed a high fat diet causes chylous ascites, an acute-phase response, and mesenteric lymphadenopathy. Here, we studied the role of ANGPTL4 in lipid uptake in macrophages and in the above-mentioned pathologies using Angptl4-hypomorphic and Angptl4-/- mice. Angptl4 expression in peritoneal and bone marrow-derived macrophages was highly induced by lipids. Recombinant ANGPTL4 decreased lipid uptake in macrophages, whereas deficiency of ANGPTL4 increased lipid uptake, upregulated lipid-induced genes, and increased respiration. ANGPTL4 deficiency did not alter LPL protein levels in macrophages. Angptl4-hypomorphic mice with partial expression of a truncated N-terminal ANGPTL4 exhibited reduced fasting plasma triglyceride, cholesterol, and non-esterified fatty acid levels, strongly resembling Angptl4-/- mice. However, during high fat feeding, Angptl4-hypomorphic mice showed markedly delayed and attenuated elevation in plasma serum amyloid A and much milder chylous ascites than Angptl4-/- mice, despite similar abundance of lipid-laden giant cells in mesenteric lymph nodes. In conclusion, ANGPTL4 deficiency increases lipid uptake and respiration in macrophages without affecting LPL protein levels. Compared with the absence of ANGPTL4, low levels of N-terminal ANGPTL4 mitigate the development of chylous ascites and an acute-phase response in mice.

2019-08-24 | GSE136240 | GEO

Suppression of angiopoietin-like 4 reprograms endothelial cell metabolism and inhibits angiogenesis

Project description: Not available

| S-EPMC10716292 | biostudies-literature

MicroRNA-6084 orchestrates angiogenesis and liver metastasis in colorectal cancer via extracellular vesicles

Project description:The prognosis for colorectal cancer (CRC) patients with liver metastasis remains poor, and the molecular mechanisms driving CRC liver metastasis are still not fully understood. Hypoxia-induced extracellular vesicles (H-EVs) derived from tumors have emerged as key players in inducing angiogenesis by transferring non-coding RNAs. However, the specific role of CRC-derived hypoxic EVs (H-EVs) in regulating the formation of the pre-metastatic microenvironment (PMN) by inducing angiogenesis remains unclear. Our study demonstrates that H-EVs induce both angiogenesis and liver metastasis. Through microRNA microarray analysis, we identified a reduction in miR-6084 levels within H-EVs. We found that miR-6084 inhibits angiogenesis by being transferred to endothelial cells via EVs. In endothelial cells, miR-6084 directly targets ANGPTL4 mRNA, thereby suppressing angiogenesis through ANGPTL4-mediated JAK2/STAT3 pathway. Furthermore, we uncovered that SP1 acts as a transcription factor regulating miR-6084 transcription, while HIF1A decreases miR-6084 expression by promoting SP1 protein dephosphorylation and facilitating ubiquitin‒proteasome degradation in SW620 cells. In clinical samples, we observed low expression of miR-6084 in plasma-derived EVs from CRC patients with liver metastasis. In summary, our findings suggest that CRC-derived hypoxic EVs promote angiogenesis and liver metastasis through the HIF1A/SP1/miR-6084/ANGPTL4 axis. Additionally, miR-6084 holds promise as a potential diagnostic and prognostic biomarker for CRC liver metastasis.

2025-06-02 | GSE297674 | GEO

Apigenin inhibits tumor angiogenesis by suppressing microvesicle biogenesis

Project description:Apigenin inhibits tumor angiogenesis by suppressing microvesicle biogenesis

| PRJNA1055490 | ENA

COCO/DAND5 inhibits developmental and pathological ocular angiogenesis

Project description:COCO/DAND5 inhibits developmental and pathological ocular angiogenesis

| PRJNA671828 | ENA

Characterization of ANGPTL4 function in macrophages and adipocytes using Angptl4-knockout and Angptl4-hypomorphic mice

Project description:Characterization of ANGPTL4 function in macrophages and adipocytes using Angptl4-knockout and Angptl4-hypomorphic mice

| PRJNA561718 | ENA

COCO/DAND5 inhibits developmental and pathological ocular angiogenesis

Project description:Neovascularization contributes to multiple visual disorders including age-related macular degeneration (AMD). Current therapies for treating ocular angiogenesis are centered on the inhibition of vascular endothelial growth factor (VEGF). While clinically effective, some AMD patients are refractory or develop resistance to anti-VEGF and concerns of increased risks of developing geographic atrophy following long-term treatment have been raised. Identification of alternative pathways to inhibit pathological angiogenesis is thus important. We have identified a novel inhibitor of angiogenesis, COCO/DAND5, a member of the Cerberus-related DAN family. We demonstrate that COCO inhibits sprouting, migration and cellular proliferation of cultured endothelial cells. Intravitreal injections of COCO inhibited retinal vascularization during development and in models of retinopathy of prematurity and AMD. COCO equally abrogated angiogenesis in choroid explants and in a model of choroidal neovascularization. Mechanistically, COCO inhibited the expression of TGFβ and BMP pathwaysand altered ATP production, glucose uptake and redox balance of endothelial cells. Together, these data show that COCO is an inhibitor of retinal and choroidal angiogenesis, possibly representing a therapeutic option for the treatment of neovascular ocular diseases.

2020-12-22 | GSE160099 | GEO

Linoleic acid-induced ANGPTL4 inhibits C2C12 skeletal muscle differentiation by suppressing Wnt/β-catenin.

Project description:Linoleic acid-induced ANGPTL4 inhibits C2C12 skeletal muscle differentiation by suppressing Wnt/β-catenin.

| PRJNA874028 | ENA