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Human Amniotic membrane modulates collagen production and deposition in vitro

ABSTRACT: Human Amniotic membrane modulates collagen production and deposition in vitro

PROVIDER: PRJNA1036675 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26705671_1.fastq.gz	Fastqsanger.gz
	SRR26705671_2.fastq.gz	Fastqsanger.gz
	SRR26705672_1.fastq.gz	Fastqsanger.gz
	SRR26705672_2.fastq.gz	Fastqsanger.gz
	SRR26705673_1.fastq.gz	Fastqsanger.gz

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Human Amniotic membrane modulates collagen production and deposition in vitro

Project description:Pathological fibrosis, an excessive accumulation of collagen, compromises tissue architecture, impedes its function and represents a medical complication. Properties of the amniotic membrane have demonstrated potential to regulate fibrotic processes. RNA sequencing analysis evaluated the effects of dehydrated human amnion/chorion membrane (DHACM) on fibrotic events using in vitro macromolecular crowding to mimic a physiologically relevant microenvironment. Functional enrichment with Reactome pathway analysis indicated that the function of a subset of these dysregulated genes was associated with the composition and function of the extracellular matrix. Further use of macromolecular crowding in vitro was used to evaluate the effects of DHACM and a lyophilized human amnion/chorion membrane (LHACM) on type 1 collagen production and deposition under profibrotic conditions (addition of TGFβ1). In the continued presence of TGFβ1, LHACM and DHACM regulated the intracellular production and extracellular deposition of type 1 collagen. In addition, results suggest that the effect on collagen deposition could in part be modulated through the regulation of proteins responsible for the extracellular post-translational modifications of collagen. These observations may support the use of DHACM and LHACM in the regulation collagen production/deposition in profibrotic environments.

2024-05-06 | GSE247237 | GEO

Hypoxia induced ATF3 escalates breast cancer invasion by increasing collagen deposition

Project description:Hypoxia induced ATF3 escalates breast cancer invasion by increasing collagen deposition

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Impact of fibrillar collagen scaffold on corneal stromal fibroblasts protein expression

Project description:The human cornea relies on its extracellular matrix (ECM) properties, with corneal stromal fibroblasts (CSFs) crucial for ECM remodeling. We studied the effects of nanofibrillar materials on CSFs using a decellularized human amniotic membrane (dHAM) and fibrillar collagen scaffold (FCS). FCS enhances focal adhesions (FAs), activating mechanotransduction signals through FAK autophosphorylation and YAP1 nuclear translocation. Nanofibrillar topography induces gene expression changes related to tissue remodeling and collagen production. Here, we performed shotgun proteomics analysis (DDA-PASEF in TimsToF Pro) to analyze the impact of FCS topography on CSFs protein expression.

2024-09-02 | PXD048096 | Pride

Nf1 Deficiency Increases Mammary Collagen Deposition and Restricts Adipocyte Differentiation Before Tumor Formation

Project description:Nf1 Deficiency Increases Mammary Collagen Deposition and Restricts Adipocyte Differentiation Before Tumor Formation

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Hypoxia induced ATF3 escalates breast cancer invasion by increasing collagen deposition

Project description:Activating transcription factors (ATFs), members of the adaptive-response gene family, participate in cellular processes to aid adaptations in response to extra- and/or intracellular changes. In this study, we observed that one of the ATFs Activating transcription factor 3 (ATF3) is upregulated under hypoxia via alterations in the epigenetic landscape of its promoter, followed by transcriptional upregulation. Under hypoxic conditions, Hypoxia-inducible factor 1-alpha (HIF1ɑ) alleviates methylation at the ATF3 promoter by recruiting TET1 and induces ATF3 transcription. Additionally, our RNA-seq analysis showed that ATF3 globally affects transcription under hypoxia and controls the processes of EMT and cancer invasion by stimulating the transcription of Prolyl 4-Hydroxylase Subunit Alpha 1 (P4HA1), an enzyme which enhances invasion conducive extracellular matrix (ECM) under hypoxic condition. Prolyl hydroxylases play a critical role in the hydroxylation and deposition of collagen in the extracellular matrix (ECM) during the evolution of cancer, which is necessary for metastasis. Importantly, P4HA1 undergoes alternative splicing under hypoxia, where the inclusion of exon 9a is increased. It is interesting to note that ATF3's involvement in P4HA1 splicing was also evident, as binding of ATF3 at intron 9a led to demethylation of this DNA region via recruitment of TET1. Further, we also show that the demethylated DNA region of intron 9a then becomes accessible to CTCF. Thus, a cascade of demethylation via ATF3 recruited TET1, followed by increased RNA PolII pause via CTCF at the intron 9a leads to inclusion of exon 9a. The P4HA1 9a isoform leads to enhanced invasion under hypoxic conditions by increasing deposition of collagen in the ECM. These results provide a novel hypoxia-induced HIF1ɑ-ATF3-P4HA1 axis which can be potentially exploited as a therapeutic target to impede EMT and ultimately breast cancer invasion.

2024-12-31 | GSE274936 | GEO

Nf1 Deficiency Increases Mammary Collagen Deposition and Restricts Adipocyte Differentiation Before Tumor Formation

Project description:BACKGROUND: The NF1 tumor suppressor gene is the main negative regulator of the RAS pathway and is frequently mutated in various cancers. Women with Neurofibromatosis Type I (NF1) – a tumor predisposition syndrome caused by a germline NF1 mutation – have an increased risk of developing aggressive breast cancer with poorer prognosis. The mechanisms by which NF1 mutation leads to breast cancer tumorigenesis are not well understood. Therefore, the objective of this work was to identify stromal alterations before tumor formation that result in the increased risk and poorer outcome seen among NF1 patients with breast cancer. METHODS: To accurately model the germline monoallelic NF1 mutations in NF1 patients, we utilized an Nf1-deficient rat model with accelerated mammary development and develops highly penetrant breast cancer. RESULTS: We identified increased collagen content in Nf1-deficient rat mammary glands before tumor formation that correlated with age of tumor onset. Additionally, gene expression analysis revealed that Nf1-deficient rat mammary mature adipocytes have increased collagen expression and shifted to a fibroblast and preadipocyte expression profile. This alteration in lineage commitment was also observed with in vitro differentiation but flow cytometry analysis did not show a change mammary adipose-derived mesenchymal stem cell abundance. CONCLUSION: Collectively, these studies uncovered the previously undescribed role of Nf1 in mammary collagen deposition and regulating adipocyte differentiation. In addition to unraveling the mechanism of tumor formation, further investigation of adipocytes and collagen modifications in preneoplastic mammary gland will create a foundation for developing early detection strategies of breast cancer among NF1 patients.

2023-05-08 | GSE231603 | GEO

Proteomic analysis of collagen membrane and matrix

Project description:High-resolution shotgun proteomic analysis on two porcine collagen-based biomaterials designed for guided bone regeneration and soft tissue augmentation was perfomed. A porcine-derived collagen membrane and a collagen matrix derived from peritoneum and/or skin were digested, separated by nano-reverse-phase high-performance liquid chromatography, and peptides subjected to mass spectrometric detection and analysis

2021-09-09 | PXD019298 | Pride

Enhanced Collagen Secretion in Epithelial Cancer Cells is associated with L1CAM Deficiency

Project description:Collagen, a critical component of the tumor microenvironment (TME), significantly influences cancer-associated fibrosis, tissue stiffness, immune response, and metastasis. Pancreatic ductal adenocarcinoma (PDAC) is characterized by excessive collagen deposition, and effective therapies remain limited. Our research challenges conventional understanding by highlighting the remarkable ability of specific tumor epithelial populations, particularly those with low levels of L1 cell adhesion molecule (L1CAM) expression (L1low), to actively modulate collagen dynamics within the TME. Transcriptome analysis of PDAC cells with varying L1 expression reveals shifts in collagen-related pathways, with heightened expression of collagen 17A1 (COL17A1) in L1low cells. Alongside, L1low cells exhibit enhanced migratory capacity. In an orthotopic mouse model, L1low cancer cells demonstrate increased collagen deposition, resistance to gemcitabine treatment, and an elevated propensity for liver metastases. Treatment with Tranilast, an anti-fibrotic drug, significantly reduces tumor volume and collagen deposition while enhancing L1 expression. This, in turn, mitigates tumor invasiveness and suppresses metastases formation. Overall, our study uncovers a novel role for L1CAM in PDAC aggressiveness and fibrosis, revealing a new epithelial population capable of collagen secretion and challenging the traditional notion that this function is solely attributed to stromal cells.

2024-06-11 | GSE268948 | GEO

Gene expression in amniotic menbrane-derived cells (mesenchymal stromal cells and epithelial cells) and expression signatures of these two types of cells after IL-10 stimulation

Project description:To further cell therapy, we have investigated gene expression profile of amniotic membrane-derived, two types of cells: mesenchymal stromal cells and epithelial cells. We previously reported that amniotic membrane derived cells are immunologically privileged and produced only minimal immune reactivity and that these cells, when stimulated by immunosuppressive agent IL-10, had higher differential potential for cardiomyocyte and more immunotolerance. To analysis these phenomenons, we performed gene expression profile of two types of cells after IL10 stimulation.

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RNA sequencing reveals distinct immune responses in the chorioamniotic membranes of women with preterm labor and microbial or sterile intra-amniotic inflammation

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2021-02-01 | GSE155526 | GEO

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