Myofibroblast Accumulation
Myofibroblast Accumulation - Related Videos
06:59
Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue
0 Views •
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
0 Views •
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
0 Views •
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
0 Views •
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.
01:27
Cost Accumulation and Flow
0 Views •
2026
In manufacturing, production costs are accumulated and tracked to understand how resources are consumed and how they contribute to the final product. This process, known as cost accumulation, involves recording material, labor, and overhead costs and linking them to specific cost objects, such as individual products or production processes.Costs flow through inventory accounts in a sequence that mirrors the physical movement of goods. Initially, raw materials are recorded in the raw materials...
FAQs
Transforming growth factor beta, inflammatory cytokines, and mechanical stress can stimulate fibroblasts during infection or immune-mediated inflammation. These signals encourage fibroblasts to adopt a contractile, matrix-producing phenotype associated with alpha-smooth muscle actin expression and increased collagen deposition. The balance, intensity, and persistence of these signals help determine whether tissue remodeling supports repair or progresses toward fibrosis.
Mechanical stress is one of the signals that can sustain fibroblast activation during tissue injury and inflammation. As matrix production increases, the tissue may become stiffer, creating a physical environment associated with continued remodeling. This relationship helps explain why persistent myofibroblast activity can extend beyond initial repair and contribute to progressive changes in organ architecture.
Excessive accumulation can alter tissue architecture and increase extracellular matrix deposition, changing the physical environment through which immune cells move. These changes may influence local pathogen control by modifying immune-cell access to affected tissue. Consequently, remodeling that begins as a repair response can also shape the effectiveness of immune surveillance and inflammatory activity at the infection site.
Researchers can evaluate myofibroblast abundance together with indicators of matrix production, including alpha-smooth muscle actin expression and collagen deposition. Interpreting these measurements in the context of tissue architecture and stiffness helps distinguish a repair-associated response from excessive remodeling. The combined assessment is more informative than examining cell abundance alone because it captures both cellular persistence and structural consequences.
It becomes especially relevant when accumulation persists and produces excessive extracellular matrix, stiffens organs, or disrupts normal tissue architecture. These features identify remodeling as a potential pathological process rather than a transient repair response. Measuring the cellular and matrix changes can help researchers identify targets for antifibrotic therapies designed to limit damaging remodeling while preserving useful healing activity.
During infection or immune-mediated inflammation, signals from the inflammatory environment can reshape fibroblast behavior and the surrounding matrix. That remodeling may affect immune-cell movement and local pathogen control, linking tissue repair to infectious-disease outcomes. Because the process influences host tissue as well as inflammatory responses, it provides a rationale for investigating host-directed therapies that modify pathological remodeling rather than targeting pathogens alone.