blebs

Blebs are bulbous protrusions of the plasma membrane that form on many cell types. They arise when a portion of the cell membrane temporarily detaches from the underlying actin cortex, allowing cytoplasmic fluid to push the membrane outward under pressure. Blebbing can occur during normal cellular processes, as well as in disease states.

Mechanism and dynamics: Blebs begin with local weakening or rupture of the cortex, coupled with intracellular pressure, leading to outward membrane expansion. The process is driven by actomyosin contractility, regulated in part by Rho-associated kinase (ROCK) and myosin II. Blebs are typically transient: a protrusion enlarges, then reassembles cortical actin under its edge and retracts. In many cells, blebbing is followed by stabilization of the cortex and, depending on context, may contribute to locomotion or be part of programmed cell death.

Contexts and roles: In apoptosis, blebbing is a hallmark morphological change often driven by caspase activity that alters cytoskeletal linkages; blebs can fragment into apoptotic bodies that are cleared by phagocytes. In cell migration, especially in amoeboid movement, cells extend blebs to propel themselves through tissue by rapid, pressure-driven protrusions. Blebbing also appears during development and wound healing in some cell types. In pathology, excessive or dysregulated blebbing can accompany cancer cell motility and metastasis.

Other contexts: The term bleb also appears in clinical descriptions of lung pathology. Subpleural or intrapulmonary blebs are small air-filled spaces that can rupture, potentially causing pneumothorax.

Observation and study: Blebs are observed via light and fluorescence microscopy, and their dynamics are analyzed to understand cytoskeletal organization, cell mechanics, and migratory behavior.