Synonyms for myofibroblasts or Related words with myofibroblasts

myofibroblast              fibrocytes              smcs              osteoblasts              cardiomyocytes              osteocytes              pericytes              chondrocytes              vsmc              microglia              myocytes              ascs              adipocytes              osteoclasts              cardiomyocyte              keratocytes              fibroblastic              vsmcs              fibrogenesis              preadipocytes              keratinocytes              astrocytes              macrophages              chondroblasts              chondrocyte              fibroblasts              hscs              synoviocytes              mesenchyme              fibrogenic              nscs              oligodendrocytes              hmscs              myocyte              myotubes              myoblasts              chondrocytic              osteoblastic              lipofibroblasts              myofibers              glomeruli              pmns              myogenic              stroma              mscs              lipofibroblast              epcs              hepatocytes              podocytes              neutrophils             

Examples of "myofibroblasts"
One example of further differentiation of dermal fibroblasts is that upon injury, dermal fibroblasts can give rise to myofibroblasts, fibroblast cells with smooth muscle characteristics. Dermal cells differentiate into myofibroblasts by altering their actin gene expression (which is silenced in dermal fibroblasts). When dermal fibroblasts express actin,the cells can slowly contract. This contraction plays a critical role in wound healing and fibrosis. By pulling tissues closed differentiated myofibroblasts, seal the skin after an injury (thereby, preventing infection but inducing scar formation. Interestingly, myofibroblasts can also be derived from non-fibroblast sources. Based on evidence of α-SMA expression from lung injuries, myofibroblasts can "arise de novo" directly from mesenchymal stem cells.
At first, contraction occurs without myofibroblast involvement. Later, fibroblasts, stimulated by growth factors, differentiate into myofibroblasts. Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction. Myofibroblasts contain the same kind of actin as that found in smooth muscle cells.
Some myofibroblasts (especially if they have a stellate form) may also be positive for GFAP.
More recently it has been shown that fibroblasts can transform into myofibroblasts with photobiomodulation.
As the actin in myofibroblasts contracts, the wound edges are pulled together. Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract. The contraction stage in proliferation ends as myofibroblasts stop contracting and commit apoptosis. The breakdown of the provisional matrix leads to a decrease in hyaluronic acid and an increase in chondroitin sulfate, which gradually triggers fibroblasts to stop migrating and proliferating. These events signal the onset of the maturation stage of wound healing.
Deep fascia can contract. What happens during the fight-or-flight response is an example of rapid fascial contraction. In response to a real or imagined threat to the organism, the body responds with a temporary increase in the stiffness of the fascia. Bolstered with tensioned fascia, people are able to perform extraordinary feats of strength and speed under emergency conditions. How fascia contracts is still not well understood, but appears to involve the activity of myofibroblasts. Myofibroblasts are fascial cells that are created as a response to mechanical stress. In a two step process, fibroblasts differentiate into proto-myofibroblasts that with continued mechanical stress, become differentiated myofibroblasts. Fibroblasts cannot contract, but myofibroblasts are able to contract in a smooth muscle-like manner.
Clinical presentation of a lump in the breast is histologically viewed as a collagenous tumor or desmoplastic response created by myofibroblasts of the tumor stroma. Proposed mechanisms of activation of myofibroblasts are by immune cytokine signaling, microvascular injury, or paracrine signaling by tumor cells.
The myofibroblasts make up a high proportion of the fibroblasts proliferating in the postembryonic wound at the onset of healing. In the rat model, for instance, myofibroblasts can constitute up to 70% of the fibroblasts, and is responsible for fibrosis on tissue.
The myofibroblasts in the lamina propria make it a very important contributor of inflammation and wound healing responses. Myofibroblasts are capable of releasing cytokines and chemokines in response to stress. Also their contractile capacity may help pull tissue together in the wound healing mechanism.
Similarly, in wounds that fail to resolve and become keloids or hypertrophic scars, myofibroblasts may persist, rather than disappearing by apoptosis.
Generally, the myofibroblasts disappear from the wound within 30 days, but can stay around in pathological cases in hypertrophy, such as keloids.
CYGB expression can be used as a specific marker with which hepatic stellate cells can be distinguished from portal myofibroblasts in the damaged human liver.
Fibroblastic foci are dense collections of myofibroblasts and scar tissue and, together with honeycombing, are the main pathological findings that allow a diagnosis of UIP.
Fibrosis of the liver is the accumulation of ECM proteins, such as collagen, that occurs in many chronic liver diseases. Increased liver stiffness (of existing collagen) has actually been shown to precede fibrosis and to be required for the activation of fibrogenic myofibroblasts. Fibroblasts move towards the stiffer tissue via durotaxis, and upon reaching it, will differentiate into fibrogenic myofibroblasts. This vicious positive feedback loop of durotaxis-dependent fibrosis could potentially be a therapeutic target for the prevention of liver fibrosis.
Myofibroblasts may interfere with the propagation of electrical signals controlling heart rhythm, leading to arrhythmia in both patients who have suffered a heart attack and in foetuses. Ursodiol is a promising drug for this condition.
Theophylline has been shown to inhibit TGF-beta-mediated conversion of pulmonary fibroblasts into myofibroblasts in COPD and asthma via cAMP-PKA pathway and suppresses COL1 mRNA, which codes for the protein collagen.
The pathophysiology of portal hypertension is indicated by increasing vascular resistance via different causes; additionally, stellate cells and myofibroblasts are activated. Increased endogenous vasodilators in turn promote more blood flow in the portal veins.
Myofibroblasts can contract by using smooth muscle type actin-myosin complex, rich in a form of actin called alpha-smooth muscle actin. These cells are then capable of speeding wound repair by contracting the edges of the wound.
Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges. They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes. Also, at an adhesion called the fibronexus, actin in the myofibroblast is linked across the cell membrane to molecules in the extracellular matrix like fibronectin and collagen. Myofibroblasts have many such adhesions, which allow them to pull the ECM when they contract, reducing the wound size. In this part of contraction, closure occurs more quickly than in the first, myofibroblast-independent part.
Hepatic stellate cells can be selectively stained with gold chloride, but their distinguishing feature in routine histological preparations is the presence of multiple lipid droplets in their cytoplasm. Cytoglobin expression has been shown to be a specific marker with which hepatic stellate cells can be distinguished from portal myofibroblasts in the damaged human liver. In murine liver, Reelin expressed by Ito cells has been shown to be a reliable marker in discerning them from other myofibroblasts. The expression of reelin is increased after liver injury.