Myofibroblast Activity
Myofibroblast Activity - 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
Transforming growth factor beta and mechanical stress act as injury-associated signals that activate fibroblasts. This activation induces alpha-smooth muscle actin expression, promotes formation of contractile stress fibers, and increases collagen production. Together, these changes strengthen cellular contraction and matrix remodeling, helping coordinate repair while also creating mechanisms that can contribute to excessive scarring if activation continues.
Alpha-smooth muscle actin marks a major structural change during fibroblast activation. Its expression accompanies the development of contractile stress fibers, enabling cells to generate forces that support wound contraction. Because this marker appears alongside increased collagen production and remodeling behavior, researchers can use it to examine whether repair-associated cellular activation has occurred.
Repair requires coordinated contraction and matrix deposition, but prolonged activation shifts this response toward excessive extracellular matrix accumulation. Continued collagen production can thicken and stiffen repaired tissue rather than allowing remodeling to resolve. This imbalance links sustained myofibroblast activity with pathological fibrosis, including fibrotic disease affecting pulmonary, hepatic, and cardiac tissues.
Evaluation can focus on several connected outcomes: alpha-smooth muscle actin expression, contractile stress-fiber formation, collagen production, wound contraction, and extracellular-matrix remodeling. Examining these features together distinguishes a broader repair response from a single molecular change. The resulting profile helps researchers relate cellular behavior to tissue strengthening or excessive matrix deposition.
The activity provides a cellular framework for comparing how persistent repair responses affect different organs. In pulmonary, hepatic, and cardiac fibrosis, researchers can relate sustained contractile behavior and matrix deposition to tissue remodeling and disease progression. This cross-organ perspective helps connect common biological mechanisms with the distinct tissues in which pathological scarring develops.
Research can identify points at which repair-associated activation becomes excessive, including signaling by transforming growth factor beta, responses to mechanical stress, contractile changes, and collagen deposition. These findings support investigation of therapies designed to regulate scar formation and tissue remodeling rather than simply promoting contraction. The goal is to preserve wound repair while limiting pathological fibrosis.