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Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [I]

ABSTRACT: Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [I]

PROVIDER: PRJNA482455 | ENA |

REPOSITORIES: ENA

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Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway

Project description:Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway

| PRJNA482452 | ENA

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [II]

Project description:Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [II]

| PRJNA482461 | ENA

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [II]

Project description:To evaluate gene expression changes in response to low-density-lipoprotein related protein 1 (LRP1) depletion in endothelial cells, we performed mRNA-sequencing analysis with microvascular endothelial cells isolated from the liver LRP1 endothelial knockout mice and their littermate control wild type mice.

2021-06-11 | GSE117555 | GEO

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway [I]

Project description:To evaluate gene expression changes in response to low-density-lipoprotein related protein 1 (LRP1) depletion in endothelial cells, we performed mRNA-sequencing analysis with microvascular endothelial cells isolated from the lung, heart and liver LRP1 endothelial knockout mice and their littermate control wild type mice.

2021-06-11 | GSE117554 | GEO

Endothelium-specific depletion of LRP1 improves glucose homeostasis through the osteocalcin-IGF1R pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-11 | GSE117560 | GEO

Endothelium-specific depletion of LRP1 improves glucose homeostasis through inducing osteocalcin.

Project description: Not available

| S-EPMC8421392 | biostudies-literature

Decreased IGF1R Attenuates Senescence and Improves Function in Pancreatic beta-Cells

Project description:We previously reported that increased expression of IGF1R in mouse and human beta-cells is a marker of older beta-cells; however, its contribution to age-related dysfunction and cellular senescence remains to be determined. In this study, we explored the direct role of IGF1R in beta-cell function and senescence using inducible beta-cell specific IGF1R knockdown (betaIgf1rKD) mice. Adult betaIgf1rKD mice showed improved glucose clearance and glucose-induced insulin secretion, accompanied by decreased p21Cip1 protein expression in beta-cells. RNASeq of islets isolated from these betaIgf1rKD mice revealed restoration of 3 signaling pathways known to be downregulated by aging: sulfide oxidation, autophagy, and mTOR signaling. Additionally, deletion of IGF1R in mouse beta-cells increased transcription of genes important for maintaining beta-cell identity and function, such as Mafa, Nkx6.1, and Kcnj11, while decreasing senescence-related genes, such as Cdkn2a, Il1b, and Serpine 1. These results suggest that IGF1R signaling plays a causal role in aging-induced beta-cell dysfunction.

2023-06-19 | GSE229709 | GEO

Transcription profiling of mouse ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age vs. non transgenic littermate controls

Project description:IGF1 and IGF1 receptors (IGF1R) are present in the adult heart and have been shown to be essential for myocardial performance. Insulin-like growth factor 1 (IGF1) is produced in numerous tissues particularly by the liver in response to growth hormone stimulation and is an important factor in the regulation of post-natal growth and development. We have generated and characterized transgenic mice over-expressing the IGF1R. We crossed IGF1R transgenic mice with dominant negative (dn)PI3K (p110) and with constitutively active (ca)PI3K(p110) transgenic mice. Expression profiling was performed on the ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age. Non-transgenic littermates were used as controls.

2007-09-29 | E-GEOD-1143 | biostudies-arrayexpress

Celastrol targets LRP1 to inhibit fibroblast-macrophage crosstalk and ameliorates psoriasis progression

Project description:In the present study, we analyzed single-cell multi-omics data from psoriasis patients and healthy individuals and found that more fibroblast-macrophage communication was present in the dermis of psoriasis lesions, exacerbating psoriasis progression. A natural product library was used to screen for a small molecule compound, celastrol, that could interfere with fibroblast-macrophage communication. It was demonstrated that celastrol targeted low-denisity lipoprotein receptor-related protein 1 (LRP1) to inhibit fibroblast secretion of CCL2 and inhibited psoriasis progression by reducing its recruitment to macrophages, thereby blocking communication between the two cells. Moreover, conditional knockdown of LRP1 by fibroblasts significantly improved psoriasis in mice, suggesting that LRP1 may be an important target for the treatment of psoriasis.

2024-03-31 | GSE230842 | GEO

Effect of LRP1 deletion in vascular mural cells and APOE gentotype on gene expression in mouse brains

Project description:To investigate the apoE isoform-dependent role of vascular mural cell (VMC)-LRP1, we generated VMC-specific LRP1 knockout mice (smLrp1-/-), followed by breeding these mice with either APOE3-targeted replacement (TR) or APOE4-TR mice We then performed gene expression profiling analysis using data obtained from RNA-seq of cortical samples from 4 different mouse models

2023-05-12 | GSE225065 | GEO

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