Myofibroblasts are special cells that are an intermediate form of connective tissue cells (fibroblasts) and smooth muscle cells. Myo comes from the Greek and is a word phrase meaning muscle. This part designation takes into account the fact that myofibroblasts contain contractile elements giving them properties similar to those of smooth muscle cells. They have the capacity for long-lasting contractions (tensions) that occur involuntarily.
Fibroblasts are cells that are responsible for the formation of connective tissue in the active state. They produce collagen fibers and molecular components of the matrix in the extracellular space. Myofibroblasts are capable of generating large quantities of collagen when stimulated by appropriate factors. They occur in different tissues where they take on different functions. Accordingly, their formation and differentiation in different ways is possible.
They can arise from embryonic stem cells through direct differentiation, from smooth muscle cells or from certain connective tissue cells in capillary walls (pericytes). Most often, however, they arise in the presence of specific growth factors and signal cells in tissue from not yet fully differentiated fibroblasts.
The cells of myofibroblasts are divided into two parts by their functional structure. The connective tissue portion contains much rough endoplasmic reticulum where a large amount of type III collagen can be produced. This is a type I collagen precursor responsible for the assembly and the regulated fiber structure in intact connective tissue.
The large Golgi apparatus forms the membranes necessary for the construction of the canal system by which the collagen components are transported to their site of action.
The second part of myofibroblast cells has an actin myosin complex similar to that in smooth muscle cells. Actin and myosin are protein strands that are linked to each other in such a way that they contract (contract) through an adequate stimulus and consumption of energy. Unlike skeletal muscle, smooth muscle cells are not striated and can not contract as quickly. For this they are able to sustain strong tensions over a long time. A special feature of myofibroblasts is the direct connection with the fibronectin threads in the extracellular matrix.
These protein chains form a bridge system with which the cells are networked with each other. Through the connection, the contraction can be transferred to the entire system and thus to larger tissue structures.
Myofibroblasts are found in the subcutaneous layer of almost all mucous membranes. There they are responsible for maintaining the voltage and the physiognomy of special tissue forms. The formation of crypts (recoveries) and protuberances in the small intestine is largely determined by their contractility.
The maintenance of tension and volume in vessels is also one of their tasks, for example in the seminiferous tubules and the capillaries. These fine tubes, unlike the large arterial blood vessels, do not contain a muscle layer of smooth muscle cells. Due to the presence of myofibroblasts, however, there is a residual function with which the tension of the vessel walls can be adapted to different requirements. Perhaps the most important function of myofibroblasts is involvement in wound healing. The body tries to close tissue defects caused by injuries or other pathological processes as soon as possible.
The myofibroblasts play an important role here. The immune defense is significantly involved when it comes to tissue damage. Among other things, macrophages (phagocytes) are increasingly sent to the damaged area to absorb and phagocytose dead tissue particles. The emergence of these cells provides the initial stimulus to the conversion of fibroblasts into myofibroblasts. These produce large quantities of collagen fibers that reticulate over the defect site and form a temporary wound closure. At the same time they are connected with each other and with the wound edges via the fibronectin threads.
The contraction of all myofibroblasts causes them to be pulled together, an important process for accelerating wound closure. In further steps, this network-like structure is rebuilt. Type III collagen becomes Type I, the fibers line up along the pulling direction. The myofibroblasts become inactive and cease their tension activity.
The ability to act of the myofibroblasts is basically constitution-related and diminishes with increasing age. Bindegewebsschwächen are largely determined by these specifications and developments. Although regular physical activity can not completely halt or reverse this process, it can positively influence the process in the long term.
The presence of myofibroblasts is dependent on mediators that initiate their differentiation. If these are absent or only present in small numbers, not enough cells are converted. They can not or do not sufficiently fulfill the functions they normally assume. In particular, weaknesses of the immune system can have such consequences, but also genetic defects that affect the growth factors that are important for differentiation.
Increased myofibroblast activity, in turn, may be involved in morbid processes called fibrosis. These are diseases in which there is an increase in the connective tissue framework of organs. They are usually caused by the absorption of toxins over a longer period of time or by autoimmune diseases. As a result, in the course of the disease process, the extensibility of the connective tissue is significantly reduced and the functioning of the affected organs significantly affected. Typical examples of diseases caused by toxins are pulmonary fibrosis as a result of increased exposure to coal dust, asbestos or flour dust.
Scleroderma is an autoimmune disease in which the skin and fascia are affected by connective tissue remodeling. Frequently, the significant limitation of pulmonary function due to the involvement of the pulmonary fascia is the reason for the limited lifespan.Tags: