Myofibroblast Development
Myofibroblast Development - Related Videos
06:59
Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue
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Cited by 43 •
2013
The myofibroblast is an influential stromal cell of the gastrointestinal tract that regulates important physiologic processes in both normal and disease states. We describe a technique that allows for the isolation of primary myofibroblasts from both mouse and human colon tissue, which can be utilized for in vitro experimentation.
06:02
Isolation of CD 90+ Fibroblast/Myofibroblasts from Human Frozen Gastrointestinal Specimens
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Cited by 17 •
2016
Here, a protocol to isolate and establish primary fibroblast/myofibroblast (MF) cultures from frozen gastric, small intestinal, and colonic tissue-yielding cells with a MF phenotype-is presented. These cells express CD90, α-SMA and vimentin. MFs can be used for a variety of functional assays including enzymatic activity and cytokine production.
08:59
Human Dupuytren's Ex Vivo Culture for the Study of Myofibroblasts and Extracellular Matrix Interactions
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Cited by 3 •
2015
Dupuytren’s disease (DD) is a fibroproliferative disease of the palm of the hand. Here, we present a protocol to culture resection specimens from DD in a three-dimensional (3D) culture system. Such short-term culture system allows preservation of the 3D structure and molecular properties of the fibrotic tissue.
11:18
Isolation of Myofibroblasts from Mouse and Human Esophagus
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Cited by 9 •
2015
We present a protocol to generate primary cultures of murine and human esophageal stromal cells with a myofibroblast phenotype. Cultured cells have spindle shaped morphology, express α-SMA and vimentin, and lack epithelial, hematopoietic and endothelial cell surface markers. Characterized stromal cells can be used in functional studies of epithelial-stromal interactions.
10:45
Isolation and Characterization of Adult Cardiac Fibroblasts and Myofibroblasts
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Cited by 20 •
2020
Obtaining a pure population of fibroblasts is crucial to studying their role in wound repair and fibrosis. Described here is a detailed method to isolate fibroblasts and myofibroblasts from uninjured and injured mouse hearts followed by characterization of their purity and functionality by immunofluorescence, RTPCR, fluorescence-assisted cell sorting, and collagen gel contraction.
FAQs
These signals promote coordinated changes rather than acting as isolated triggers. Transforming growth factor beta and mechanical tension stimulate cytoskeletal remodeling, helping precursor cells acquire features associated with contraction. Their influence is important because it links biochemical signaling with physical forces at an injured site, shaping how effectively damaged tissue can be stabilized during repair.
Increased alpha-smooth muscle actin reflects cytoskeletal remodeling associated with the contractile phenotype. This change helps cells generate contraction, which supports the approximation and strengthening of damaged tissue. Because its expression accompanies activation, alpha-smooth muscle actin can also serve as a useful marker when researchers investigate myofibroblast development in repair or fibrosis.
Extracellular matrix production gives repaired tissue structural reinforcement, complementing the contractile activity of activated cells. This contribution can be beneficial when it strengthens a wound, but excessive matrix-associated remodeling may participate in fibrosis. The balance between sufficient matrix production and overactive remodeling therefore influences whether healing remains restorative or becomes pathological.
The outcome depends on the extent and persistence of activation. Contractility and extracellular matrix production can strengthen damaged tissue during normal repair, while excessive activation can drive scar formation, organ fibrosis, or abnormal tissue remodeling. This dual role makes regulation important: interventions must reduce pathological activity without eliminating the repair functions needed for recovery.
Medical research examines this process to clarify how scars form, how organ fibrosis develops, and how tissues undergo abnormal remodeling. These applications extend beyond wound closure because they connect cellular activation with clinically important structural changes. Understanding the process can help explain why repair becomes excessive and identify mechanisms relevant to disease-focused investigation.
Research can track features associated with activation, including increased alpha-smooth muscle actin, cytoskeletal remodeling, and extracellular matrix production. These changes provide a basis for investigating biomarkers that reflect the process. The same knowledge supports therapies designed to limit excessive myofibroblast activation while preserving the contractile and tissue-strengthening activities required for effective repair.