Myofibroblast Differentiation
Myofibroblast Differentiation - 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 provide cues that encourage fibroblasts and related precursor cells to adopt a more contractile, matrix-producing state. Their effects are reflected in cytoskeletal reorganization, increased alpha-smooth muscle actin expression, and greater production of extracellular-matrix proteins. The resulting cellular response can support tissue closure during repair, although prolonged signaling may contribute to pathological remodeling.
Alpha-smooth muscle actin marks a major cytoskeletal change as cells acquire contractile properties. Its increased expression indicates that fibroblasts are reorganizing internal structures to generate forces involved in wound contraction. Measuring this feature helps researchers characterize cellular state and distinguish repair-associated activation from less contractile fibroblast behavior.
Greater extracellular-matrix production can strengthen and remodel the damaged tissue during repair, but persistent production may cause excessive matrix accumulation. This imbalance changes the character of healing from temporary tissue restoration toward scar formation and fibrosis. The consequences are especially important when remodeling continues in organs such as the lung, liver, heart, or kidney.
The duration and context of activation are central. A controlled response supports wound contraction and tissue repair, whereas persistent activation maintains contractile activity and extracellular-matrix deposition after the immediate repair need. Studying this difference helps explain how a process that is useful during healing can become pathological when tissue remodeling does not resolve.
Medical research can examine cellular morphology, alpha-smooth muscle actin expression, cytoskeletal organization, and extracellular-matrix protein production as indicators of activation. These observations help characterize scar formation and identify biomarkers associated with remodeling. Researchers can then use the measured response to evaluate whether a therapy limits excessive activation or matrix deposition.
The same repair-associated cellular program can influence remodeling in multiple tissues, including the lung, liver, heart, and kidney. Persistent activation in any of these organs may promote fibrosis through excessive extracellular-matrix deposition. Comparing the process across organs gives medicine a framework for connecting cellular behavior with organ-specific scar formation and therapeutic research.