Quiescent Fibroblasts
Quiescent Fibroblasts - Related Videos
07:03
Determining Genome-wide Transcript Decay Rates in Proliferating and Quiescent Human Fibroblasts
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Cited by 4 •
2018
We describe a protocol for generating proliferating and quiescent primary human dermal fibroblasts, monitoring transcript decay rates, and identifying differentially decaying genes.
10:56
Confocal Imaging of Confined Quiescent and Flowing Colloid-polymer Mixtures
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Cited by 4 •
2014
Confocal microscopy is used to image quiescent and flowing colloid-polymer mixtures, which are studied as model systems for attractive suspensions. Image analysis algorithms are used to calculate structural and dynamic metrics for the colloidal particles that measure changes due to geometric confinement.
15:43
Experimental Generation of Carcinoma-Associated Fibroblasts (CAFs) from Human Mammary Fibroblasts
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Cited by 25 •
2011
Carcinoma-associated fibroblasts (CAFs) rich in myofibroblasts present within the tumour stroma, play a major role in driving tumour progression. We developed a coimplantation tumour xengraft model for experimentally generating CAFs from human mammary fibroblasts. The protocol describes how to establish CAF myofibroblasts that acquire an ability to promote tumourigenesis.
05:54
Rapid Culturing of Primary Murine Melanocytes and Fibroblasts: Isolating Melanocytes and Fibroblasts from Whole Murine Skin Sample
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2023
This video describes the rapid method to isolate and culture the melanocytes and fibroblast simultaneously from the postnatal mouse pup’s skin. These cells can be maintained and manipulated in vitro to study skin cell biology, wound healing, and melanoma.
06:04
Murine Dermal Fibroblast Isolation by FACS
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Cited by 28 •
2016
Fibroblast behavior underlies a spectrum of clinical entities, but they remain poorly characterized, largely due to their inherent heterogeneity. Traditional fibroblast research relies upon in vitro manipulation, masking in vivo fibroblast behavior. We describe a FACS-based protocol for the isolation of mouse skin fibroblasts that does not require cell culture.
FAQs
Quiescence is maintained through coordinated regulation rather than a single molecular switch. Reduced expression of cell-cycle genes limits progression through proliferation, while genetic and epigenetic mechanisms stabilize the G0 state and restrain proliferative signaling. This regulatory arrangement allows fibroblasts to remain viable yet responsive, making cell-state control central to understanding how connective tissues balance maintenance with repair.
Growth factors and matrix cues can shift fibroblasts away from quiescence by changing the signals that control proliferation and matrix production. Their effects show that the state depends on communication between regulatory pathways and the surrounding tissue environment. Studying these inputs helps explain how local damage or altered matrix conditions can trigger fibroblast activity during tissue remodeling.
Reversible arrest distinguishes quiescence from a loss of cellular capacity. Fibroblasts in G0 can retain the ability to respond when environmental or growth-related signals change, so researchers must interpret low proliferation together with potential reactivation. This feature makes quiescent fibroblasts useful for examining transitions between tissue maintenance, repair-associated activity, and excessive remodeling.
A useful analysis connects several readouts: expression of cell-cycle genes, activity of proliferative signaling, responsiveness to growth factors or matrix cues, and changes in matrix production. Comparing these features before and after altered environmental signals can reveal which regulatory networks maintain quiescence and which changes accompany reactivation. The approach links molecular regulation with observable cell-state transitions.
They are particularly informative in studies of wound repair, fibrosis, and tumor-associated stroma. In wound repair, reactivation supports tissue remodeling; in fibrosis, altered regulation may sustain excessive matrix production; and in tumors, fibroblast state can contribute to changes in the surrounding stroma. These applications connect cell-cycle control with broader effects on tissue structure and disease.
Genetic analysis can relate inherited or acquired changes in signaling pathways to altered fibroblast behavior. Such changes may affect how cells maintain quiescence, respond to growth factors or matrix cues, resume proliferation, or produce extracellular matrix. This perspective helps distinguish normal state transitions from dysregulated remodeling and clarifies how pathway changes may contribute to fibrosis or tumor-associated stromal changes.