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Mmp14-Dependent Remodeling of the Pericellular-Dermal Collagen Interface Governs Fibroblast Survival

ABSTRACT: Mmp14-Dependent Remodeling of the Pericellular-Dermal Collagen Interface Governs Fibroblast Survival

PROVIDER: PRJNA1108711 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28927783_1.fastq.gz	Fastqsanger.gz
	SRR28927783_2.fastq.gz	Fastqsanger.gz
	SRR28927784_1.fastq.gz	Fastqsanger.gz
	SRR28927784_2.fastq.gz	Fastqsanger.gz
	SRR28927785_1.fastq.gz	Fastqsanger.gz

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Mmp14-Dependent Remodeling of the Pericellular-Dermal Collagen Interface Governs Fibroblast Survival

Project description:Dermal fibroblasts deposit type I collagen, the dominant extracellular matrix molecule found in skin, during early postnatal development. Coincident with this biosynthetic program, fibroblasts proteolytically remodel pericellular collagen fibrils by mobilizing the membrane-anchored matrix metalloproteinase, Mmp14. Unexpectedly, dermal fibroblasts in Mmp14-/- mice commit to a large-scale apoptotic program that leaves skin tissues replete with dying cells. A requirement for Mmp14 in dermal fibroblast survival is recapitulated in vitro when cells are embedded within, but not cultured atop, 3-dimensional hydrogels of cross-linked type I collagen. In the absence of Mmp14-dependent pericellular proteolysis, dermal fibroblasts fail to trigger β1 integrin activation and instead actuate a TGF-β1/phospho-JNK stress response that leads to apoptotic cell death in vitro as well as in vivo. Taken together, these studies identify Mmp14 as a requisite cell survival factor that maintains dermal fibroblast viability in postnatal dermal tissues.

2024-05-24 | GSE266914 | GEO

Mmp14 is essential for circadian clock rhythmicity in fibroblasts

Project description:Membrane type I-matrix metalloproteinase (MT1-MMP/Mmp14) is an unusual MMP because it is essential for survival in mice with multiple organ systems being affected for reasons that are unclear. Here, we show that the protein (MT1-MMP) and gene (Mmp14) are under strict circadian clock control and conditional knockout in fibroblasts leads to ~16% of the proteome losing or inverting circadian rhythmicity. The result is loss of the actin cytoskeleton and cell-matrix adhesions and major imbalance of the matrisome. Lack of collagen-I monomer turnover results in excess fibril formation in the absence of Mmp14. In the absence of Mmp14, paired-like homeodomain transcription factor 2 (Pitx2) is upregulated and remains in the nucleus where it drives Plod2 expression. The overall result is accumulation of collagen fibrils and elevated pyridinoline crosslinking that renders collagen fibrils insoluble. In conclusion, Mmp14 is a master regulator of circadian rhythms affecting the actin cytoskeleton and cell microenvironment.

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Chromatin remodeling governs postnatal maturation in dermal fibroblasts

Project description:Chromatin remodeling governs postnatal maturation in dermal fibroblasts

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Expression data from Skeletal Stem Cells cultured in 3-dimensional (3D) Collagen

Project description:Skeletal stem cells (SSCs) reside in a 3-dimensional extracellular matrix (ECM) compartment and differentiate into multiple cell lineages, thereby controlling tissue maintenance and regeneration. Within this environment, SSCs can proteolytically remodel the surrounding ECM in response to growth factors that direct lineage commitment. In the bone tissue, type I collagen is the most abundant ECM. The dominant type I collagenolytic proteinase found in mammals is the type I transmembrane MMP, MMP14. Therefore, SSCs from Mmp14+/+ or Mmp14-/- mice were cultured in collagen hydrogels to explore the gene expression regulated by ECM remodeling. Microarrays were used to detail the gene expression underlying ECM remodeling process in SSCs.

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Transcription profiling of human dermal fibroblasts after 3 hours of cyclic mechanical loading compared with ni loading - collagen 1 hydrogel dynamic loading tests

Project description:Cell viability and global gene expression was anayzed from collagen 1 hydrogel scaffolds following 3 hours of cyclic mechanical loading and compared with non-loaded scaffolds. Experiment Overall Design: 6 samples are analyzed (2 sets in triplicate). The first set is the Loaded condition in which Collagen 1 hydrogels seeded with Human dermal fibroblasts underwent cyclic loading of 0.1Hz for 180 minutes at 37 degrees Celsius. The second set is the control Unloaded condition in which the Collagen 1 hydrogels seeded with Human dermal fibroblasts are incubated at 37 degrees Celsius with no loading.

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Chromatin remodeling governs postnatal maturation in dermal fibroblasts [scRNA-Seq]

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Project description:Systemic sclerosis (SSc) is a devastating disease affecting the skin and internal organs. Dermal fibrosis manifests early and Modified Rodnan Skin Scores (MRSS) correlate with disease progression. Transcriptomics of SSc skin biopsies suggest the role of the in vivo microenvironment in maintaining the pathological myofibroblasts. Therefore, defining the structural changes in dermal collagen in SSc patients could inform our understanding of fibrosis pathogenesis. Here, we report a method for quantitative whole-slide image analysis of dermal collagen from SSc patients, and our findings of more aligned dermal collagen bundles in diffuse cutaneous SSc (dcSSc) patients. Using the bleomycin-induced mouse model of SSc, we identified a distinct high dermal collagen bundle alignment gene signature, characterized by a concerted upregulation in cell migration, adhesion, and guidance pathways, and downregulation of spindle, replication, and cytokinesis pathways. Furthermore, increased bundle alignment induced a cell migration gene signature in fibroblasts in vitro, and these cells demonstrated increased directed migration on aligned ECM fibers that is dependent on expression of Arhgdib (Rho GDP-dissociation inhibitor 2). Our results indicate that increased cell migration is a cellular response to the increased collagen bundle alignment featured in fibrotic skin. Moreover, many of the cell migration genes identified in our study are shared with human SSc skin and may be new targets for therapeutic intervention.

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Increased dermal collagen bundle alignment in Systemic Sclerosis is associated with a cell migration signature and role of Arhgdib in directed fibroblast migration on aligned ECMs [bleomycin]

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Transcriptional profile in dermal fibroblasts from patients with collagen VI related muscular dystrophy

Project description:Objectives: The collagen VI related muscular dystrophies (COL6-RD), Ullrich congenital muscular dystrophy (UCMD) and Bethlem myopathy (BM) are among the most common congenital muscular dystrophies, but the pathogenesis, including the role of mutant collagen VI in the matrix is poorly understood. To better define the pathways disrupted by mutations in collagen VI, we have used a transcriptional profiling approach with RNA-Seq to identify differentially expressed genes in COL6-RD patients from controls. Methods: We have used RNA-Seq to identify differentially expressed genes in cultured dermal fibroblasts from 13 COL6-RD patients (8 dominant negative and 5 null) and 6 controls. Sequence reads were analyzed using the TopHat/Cufflinks pipeline. Results: Differentially expressed transcripts between COL6-RD patient and control fibroblasts include upregulation of ECM components and downregulation of factors controlling matrix remodeling and repair. DN and null samples are differentiated by downregulation of genes involved with DNA replication and repair in null samples

2017-12-04 | GSE103270 | GEO

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