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Expression data from LAM-associated fibroblasts and normal human lung fibroblasts co-cultured with TSC2-/- 621-101 cells

ABSTRACT: Expression data from LAM-associated fibroblasts and normal human lung fibroblasts co-cultured with TSC2-/- 621-101 cells

PROVIDER: PRJNA673807 | ENA |

REPOSITORIES: ENA

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Expression data from LAM-associated fibroblasts and normal human lung fibroblasts co-cultured with TSC2-/- 621-101 cells

Project description:Patients with Lymphangioleiomyomatosis (LAM) develop nodules of cells within the lung parenchyma. These lesions contain both TSC2-/- LAM cells, and wild type fibroblasts. We investigated the effect of TSC2-/- cells on the transcriptional profile of both normal fibroblasts and fibroblasts isolated from LAM patient tissue (LAFs) using Affymetrix Gene Chip arrays, to identify upregulated pathways which could contribute to LAM pathology. We used Affymetrix microarrays to detail the changes in the global profile of gene expression in fibroblasts following co-culture with 621-101 cells, and identified upregulation of several chemokines, indicating that the fibroblasts had adopted an inflammatory phenotype.

2021-12-31 | GSE160618 | GEO

Effect of the reduced mTORC1 activity on gene expression in LAM cells

Project description:mTORC1 is inhibited by rapamycin or Torin1 in lymphangioleiomyomatosis (LAM) 621-101 (TSC2-deficient) cells, in which mTORC1 activity is elevated, and we compared these effects to inhibition of S6K and its target SRPK2.

2024-11-20 | GSE273387 | GEO

Transcriptome profiles of LAM cell models exposed to oleic acid

Project description:RNA-seq profiling of Tsc2-deficient mouse embryonic fibroblasts (MEFs) and TSC2-deficient 621-101 human angiomyolipoma cells exposed to oleic acid or basal condition.

2025-07-10 | GSE301923 | GEO

Single-cell transcriptomic profile of LAM/AML cell model exposed to hydrocortisone

Project description:scRNA-seq profiling of TSC2-deficient 621-101 human angiomyolipoma cells exposed to hydrocortisone or DMSO.

2025-07-16 | GSE302428 | GEO

Gene expression profiling of 621-101 cells with rapamycin treatment and Rheb downregulation

Project description:621-101 cells were treated with rapamycin and rhebsiRna and samples were run in triplicates for each condition.

2018-01-01 | E-MTAB-3684 | biostudies-arrayexpress

Rapamycin-insensitive up-regulation of MMP2 and other genes in TSC2- deficient LAM-like cells

Project description:Rationale: Increased matrix metalloproteinase (MMP) activity has been implicated in the pathogenesis of lymphangioleiomyomatosis (LAM). Objectives: To investigate how TSC1 or TSC2 deficiency alters MMP expression and regulation. Methods: We studied immortalized cells that lack TSC2 derived from an angiomyolipoma (AML) of a LAM patient, and a TSC2 add back derivative; and murine embryonic fibroblast cells that lack Tsc1 or Tsc2 and respective controls. Global gene expression analysis was carried out in the AML and derivative cell lines. MMP levels in the conditioned media from these cells were analyzed by zymography and ELISA. Measurements and Main Results: We found increased MMP-2 expression in cells lacking TSC1/TSC2 compared to their respective controls by zymography. MMP-2 overproduction by these cells was not affected by rapamycin treatment. Gene expression analysis confirmed increased MMP-2 gene expression that was not affected by rapamycin. Furthermore, multiple other genes were found to be over-expressed in rapamycin-treated TSC2-deficient cells compared to TSC2+ cells. Conclusions: We conclude that TSC1/TSC2 deficiency leads to MMP-2 overproduction that is rapamycin insensitive, and that several genes exhibit similar patterns suggesting TSC1/TSC2 dependent but mTOR independent pathways may be involved in the pathogenesis of LAM.

2009-10-21 | GSE16944 | GEO

Whole transcriptome (gene expression and splice isoform changes) profiling using Affymetrix Human Transcriptome Array 2.0

Project description:Transcriptome analysis of total RNA samples from human cell line (LAM 621-101, female) Global gene and splice isoform expression profiling was performed to get a comprehensive view of transcriptome changes in human Lymphangioleiomyomatosis (LAM 621-101, female) cell line after inhibition of mTORC1 and SRPK2 proteins.

2017-09-28 | GSE104335 | GEO

LAM cell mTOR dysregulation induces IL6 and paracrine AT2 cell senescence impeding lung repair in lymphangioleiomyomatosis.

Project description:LAM is a rare disease which causes lung cysts and respiratory failure. TSC2 deficient ‘LAM cells’ with dysregulated mTOR signalling form nodules with fibroblasts causing lung injury. We examined if mTOR dysregulation could induce senescence and impair responses to lung injury. Senescence markers p21 and p16 were increased in LAM lungs and co-localised with alveolar type 2 cells. The SenMayo senescence gene panel was upregulated in LAM alveolar type 2 cells with senescence supressed by mTOR inhibition in patients. LAM cell / fibroblast spheroid cultures induced senescence markers in alveolar type 2 cell organoids, altered their growth and delayed epithelial scratch wound repair. Upstream regulator analysis predicted alveolar type 2 cell IL6 receptor activation. IL6 was produced by LAM cells, was overexpressed in LAM serum and related to lung function, induced p16 and p21 in alveolar type 2 cells and inhibited epithelial wound resolution. Wound repair in the presence of TSC2 null but not TSC2 addback LAM cell / fibroblast spheroids was enhanced by the IL6 receptor antagonist Tocilizumab. Our findings show TSC2 loss induces senescence and IL6 production which are associated with impaired lung repair. Targeting IL6 signalling in parallel with mTOR inhibition, may reduce lung damage in LAM.

2025-08-05 | GSE265851 | GEO

Transcriptomic Differences Associated with TSC2 Gene Expression Loss in Lymphangioleiomyomatosis [mouse cells]

Project description:Pulmonary Lymphangioleiomyomatosis (LAM), a rare lung disease that affects predominantly women, is characterized by proliferation of smooth muscle-like cells in the lungs, destruction of lung tissue, upregulation of VEGF-D, and growth of lymphatic vessels inducing a loss of pulmonary function. TSC2 gene mutations that render TSC2 inactive are a common finding associated with LAM. To better understand the function of the TSC2 gene, we sought to characterize differences in the transcriptome of cells where TSC2 is inactivated. RNA-Seq was used to measure transcript expression differences between TSC2-null mouse embryonic fibroblasts and TSC2-expressed mouse embryonic fibroblasts. The Illumina TruSeq method was used to prepare stranded poly(A)-selected RNA-Seq libraries, and 100bp paired-end reads were generated with an Illumina Hi-Seq 2500 instrument in high output mode. RNA-Seq data was analyzed using kallisto (http://pachterlab.github.io/kallisto/) and R.

2018-05-23 | GSE84477 | GEO

Transcriptomic Differences Associated with TSC2 Gene Expression Loss in Lymphangioleiomyomatosis [human cells]

Project description:Pulmonary Lymphangioleiomyomatosis (LAM), a rare lung disease that affects predominantly women, is characterized by proliferation of smooth muscle-like cells in the lungs, destruction of lung tissue, upregulation of VEGF-D, and growth of lymphatic vessels inducing a loss of pulmonary function. TSC2 gene mutations that render TSC2 inactive are a common finding associated with LAM. To better understand the function of the TSC2 gene in LAM , we sought to characterize differences in the transcriptome of cells where TSC2 is inactivated. RNA-Seq was used to measure transcript expression differences between a human TSC2-null angiolipoma cell line derived from an individual with LAM, and the same cell line with re-expressed TSC2 to serve as a control. The Illumina TruSeq method was used to prepare poly(A)-selected stranded RNA-Seq libraries, and 100bp paired-end reads were generated with an Illumina Hi-Seq 2500 instrument in high output mode. RNA-Seq data was analyzed using kallisto (http://pachterlab.github.io/kallisto/) and R.

2018-05-23 | GSE84476 | GEO

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