Bleb (cell biology)

Initiation and expansion Bleb growth is driven by intracellular pressure (abnormal growth) generated in the cytoplasm when the actin cortex undergoes actomyosin contractions. The disruption of the membrane-actin cortex interactions are dependent on the activity of myosin-ATPase. Bleb initiation is affected by three main factors: high intracellular pressure, decreased amounts of cortex-membrane linker proteins, and deterioration of the actin cortex. The integrity of the connection between the actin cortex and the membrane are dependent on how intact the cortex is and how many proteins link the two structures. This generates a weak spot through which the cytoplasm flows, leading to the expansion of the bulge of membrane by increasing the surface area through tearing of the membrane from the cortex, during which time, actin levels decrease. Before the bleb is able to expand, pressure must build enough to reach a threshold. By inserting a micropipette into a cell, the cell can be aspirated rapidly until destruction of cortex-membrane bonds causes blebbing. ==Cellular function==

Apoptotic function Blebbing is one of the defined features of apoptosis. These bulges may separate from the cell, taking a portion of cytoplasm with them, to become known as apoptotic blebs. Phagocytic cells eventually consume these fragments and the components are recycled. Two types of blebs are recognized in apoptosis. Initially, small surface blebs are formed. During later stages, larger so-called dynamic blebs may appear, which may carry larger organelle fragments such as larger parts of the fragmented apoptotic cell nucleus. Function in cell migration Along with lamellipodia, blebs serve an important role in cell migration. The types of blebs vary greatly, including variations in bleb growth rates, size, contents, and actin content. It also plays an important role in all five varieties of necrosis, a generally detrimental process. However, cell organelles do not spread into necrotic blebs. ==Inhibition==

In 2004, a chemical known as blebbistatin was shown to inhibit the formation of blebs. This agent was discovered in a screen for small molecule inhibitors of nonmuscle myosin IIA. This interaction stabilizes a form of myosin II that is not bound to actin, thus lowering the affinity of myosin with actin. By interfering with myosin function, blebbistatin alters the contractile forces that impinge on the cytoskeleton-membrane interface and prevents the build up of intracellular pressure needed for blebbing. Blebbistatin has been investigated for its potential medical uses to treat fibrosis, cancer, and nerve injury. However, blebbistatin is known to be cytotoxic, photosensitive, and fluorescent, leading to the development of new derivatives to solve these problems. Some notable derivatives include , , and . == References ==