Myofibroblast Formation
Myofibroblast Formation - Related Videos
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.
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.
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 push fibroblasts and related precursor cells toward a more contractile, matrix-producing state. The cells reorganize their cytoskeleton, begin expressing alpha-smooth muscle actin, and increase production of collagen and other extracellular matrix components. Together, these changes allow them to generate force, modify the surrounding tissue, and contribute to wound closure and strengthening during repair.
A key change is cytoskeletal reorganization accompanied by alpha-smooth muscle actin expression. The cells also increase synthesis of collagen and other extracellular matrix components, indicating a shift toward active tissue remodeling. These features distinguish the activated state from a less contractile, less matrix-producing condition and provide measurable indicators when studying the process in biological research.
Temporary activation supports wound closure, tissue strengthening, and controlled matrix remodeling during repair. If activation persists, continued contractile activity and extracellular matrix production can promote excessive scarring and organ fibrosis. This difference makes the duration and resolution of the response biologically important, because the same repair-associated capabilities can become damaging when they remain active.
Researchers can examine whether cells reorganize their cytoskeleton, express alpha-smooth muscle actin, and increase collagen or other extracellular matrix production. They can also evaluate changes in the surrounding matrix and the cells’ contractile behavior. Assessing these features together gives a broader view of phenotype acquisition than relying on a single molecular or structural change.
During repair, their contractile properties help draw damaged tissue together, while increased extracellular matrix production helps strengthen the repaired area. Their remodeling activity also changes the surrounding matrix as healing progresses. These combined functions connect cellular force generation with structural rebuilding, making myofibroblast formation relevant to how tissues close wounds and regain support after injury.
The process provides a biological link between tissue repair and pathological scarring. Studying how signals activate cells, how matrix production changes, and why activation persists can support research into antifibrotic therapies. At the same time, understanding these mechanisms is relevant to regenerative medicine, where effective repair must be encouraged without producing excessive scar tissue or organ fibrosis.