Myofibroblast

J Cell Sci 1 July ; 13 : jcs

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Tissue healing is one of the mysteries of modern medicine. Healing involves complex processes and many cellular types, amongst which the myofibroblast plays a major role. In the eye, when needed, myofibroblasts can be found from the cornea to the retina, derived from a wide variety of different cells, and aimed at effectively repairing tissue damage.

Myofibroblast

Fibroblasts are cells present throughout the human body that are primarily responsible for the production and maintenance of the extracellular matrix ECM within the tissues. They have the capability to modify the mechanical properties of the ECM within the tissue and transition into myofibroblasts, a cell type that is associated with the development of fibrotic tissue through an acute increase of cell density and protein deposition. This transition from fibroblast to myofibroblast—a well-known cellular hallmark of the pathological state of tissues—and the environmental stimuli that can induce this transition have received a lot of attention, for example in the contexts of asthma and cardiac fibrosis. Recent efforts in understanding how cells sense their physical environment at the micro- and nano-scales have ushered in a new appreciation that the substrates on which the cells adhere provide not only passive influence, but also active stimulus that can affect fibroblast activation. These studies suggest that mechanical interactions at the cell—substrate interface play a key role in regulating this phenotype transition by changing the mechanical and morphological properties of the cells. Here, we briefly summarize the reported chemical and physical cues regulating fibroblast phenotype. We then argue that a better understanding of how cells mechanically interact with the substrate mechanosensing and how this influences cell behaviors mechanotransduction using well-defined platforms that decouple the physical stimuli from the chemical ones can provide a powerful tool to control the balance between physiological tissue regeneration and pathological fibrotic response. Fibroblasts are cells belonging to the mesenchyme that are capable of producing and modifying extracellular matrix ECM components such as fibronectin and collagen Kanekar et al. They are present in various tissues. For example, in neonatal and adult heart tissues, fibroblasts arise from endogenous cell populations via epithelial to mesenchymal transition EMT and from bone marrow derived cells Visconti et al. Cardiac fibroblasts play a crucial role during fetal development and neonatal growth by contributing ECM to several specific structures of the heart Figure 1 Manso et al. In general, fibroblasts are flat and spindle shaped and can be easily distinguished from other cell types residing in the tissues, as fibroblasts lack tissue-specific functional hallmarks. Returning to the example of the heart tissue, the cardiac fibroblasts lack the basement membrane typical of the other cardiac resident cells Kanekar et al. Figure 1. Fibroblast-to-myofibroblast transition FMT.

Feng H. Single-cell analysis reveals fibroblast heterogeneity and myofibroblasts in systemic sclerosis-associated interstitial lung disease, myofibroblast.

A myofibroblast is a cell phenotype that was first described as being in a state between a fibroblast and a smooth muscle cell. In the gastrointestinal and genitourinary tracts, myofibroblasts are found subepithelially in mucosal surfaces. Here they not only act as a regulator of the shape of the crypts and villi, but also act as stem-niche cells in the intestinal crypts and as parts of atypical antigen-presenting cells. They have both support as well as paracrine function in most places. Myofibroblasts were first identified in granulation tissue during skin wound healing. They also line the gastrointestinal tract, wherein they regulate the shapes of crypts and villi. They are positive for other smooth muscle markers, such as intermediate filament type desmin in some tissues, but may be negative for desmin in other tissues.

Intestinal fibrotic stenosis is a major reason for surgery in Crohn's disease [CD], but the mechanism is unknown. Thus, we asked whether intestinal adipocytes contribute to intestinal fibrosis. Adipocytes were found to transdifferentiate into myofibroblasts and confirmed to be involved in mesenteric fibrosis in our recent study. Here, we investigated the role and possible mechanisms of intestinal adipocytes in intestinal fibrosis in CD. The intestinal tissue of patients with CD with or without fibrotic stenosis [CD S or CD N ] and normal intestinal tissue from individuals without CD were obtained to assess alterations in submucosal adipocytes in CD S and whether these cells transdifferentiated into myofibroblasts and participated in the fibrotic process. Human primary adipocytes and adipose organoids were used to evaluate whether adipocytes could be induced to transdifferentiate into myofibroblasts and to investigate the fibrotic behaviour of adipocytes. Submucosal adipocytes were reduced in number or even absent in CD S tissue, and the extent of the reduction correlated negatively with the degree of submucosal fibrosis. Interestingly, submucosal adipocytes in CD S tissue transdifferentiated into myofibroblast-like cells and expressed collagenous components, possibly due to stimulation by submucosally translocated bacteria. LPS-stimulated human primary adipocytes and adipose organoids also exhibited transdifferentiation and profibrotic behaviour.

Myofibroblast

Federal government websites often end in. The site is secure. Cardiac myocytes, although large enough to make up most of the heart volume, are only a minority of cells within the heart with fibroblasts and blood vessel components endothelial and smooth muscle cells making up the remainder of the heart. In recent years, there has been increasing interest in the non-myocyte population within the heart. This is due, in part, to our increasing understanding of the biology of the non-myocyte cell types and additionally it is due to our awakening realization that these cells are not static but rather, that they are dynamic in nature indicating that they play a more active role in cardiac function than previously imagined.

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A high-affinity human monoclonal antibody specific to the alternatively spliced EDA domain of fibronectin efficiently targets tumor neo-vasculature in vivo. Wang, K. Scientific advances at the cellular and molecular level have led to a better understanding of the biological and pathophysiological mechanisms of wound healing. Myofibroblast proliferation and heterogeneity are supported by macrophages during skin repair. Decoding myofibroblast origins in human kidney fibrosis. Irani A. Fibrotic extracellular matrix activates a profibrotic positive feedback loop. Understanding the factors involved in healing and its signalling pathways, will potentially enable us to control corneal healing in the future, and thus avoid fibrotic ocular surface disease and the blindness that this may induce. Schmid, H. To address these issues, Zhang et al.

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Elesclomol upregulated intracellular levels of ROS, caspase-3, and cytochrome-c proteins, resulting in reduced myofibroblast numbers and a lower scar elevation in vivo [ ]. Vierhout M. The myofibroblast, a key cell in normal and pathological tissue repair. There is a controversial issue whether or not, routine methods of cancer management may stimulate myofibroblasts and enhance invasion and metastasis. Amanda Goodwin , Amanda Goodwin. This growth factor has a dual role in epithelial—mesenchymal transdifferentiation in various fibrotic diseases and in normal physiological healing, making it an ideal target. Epigenetic regulation of myofibroblast phenotypes in fibrosis. Unraveling SSc pathophysiology; the myofibroblast. Duterme C. In general, the mold must present precisely defined topographies that are transferred to the substrate. Fitzgerald A. C Different fibroblast activation pathways through biochemical and mechanical factors in asthmatic AS and not asthmatic NA patients.