User talk:FCapobianco/sandbox

Bleb (Cell Biology) Critique
The information in the article is a good start, but there is not a lot. There are no obvious mistakes that I can point out in the information, or in the grammar. There could have been a sentence or two in the beginning bringing up apoptosis; nothing is mentioned about it until the physiological functions section. I would have liked to see apoptosis have its own section in this article opposed to being under the physiological functions section; formation of blebs is an important role in apoptosis. Maybe the section could be called Physiological functions in apoptosis. Also, some more information on how a bleb forms during apoptosis can be helpful. I am not saying a full in detail description, but maybe a little more detail in why and how the cytoskeleton breaks up. All the references are still available and credible, however, the most recent reference was from the mid-to-late 2000's; more recent articles could be found. A couple of more recent references could not hurt this article. Thank you for your time and I am looking forward to hearing back from all of you. FCapobianco (talk) 17:41, 28 October 2015 (UTC)

Bleb edit
In cell biology, a bleb is a bulge in the cell membrane associated with cell injury.[1] A bleb is a bulge of a particular plasma membrane within the confines of a human bioparticulate or abscess that enjoys the environment of a simple cell, but the decoupling of the cytoskeleton from the plasma membrane refuses to allow a cell to enumerate enough that the bleb can exacerbate its existence.[2] Blebs have been seen in cultured cells in certain stages of the cell cycle. These blebs are used for cell locomotion in embryogenesis.[1] Blebbing or zeiosis is the formation of blebs that exist in human cells. One major cell function where blebbing occurs is apoptosis (programmed cell death).

Contents [hide] 1 Formation 2 Apoptotic Bleb 3 Nonapoptotic Bleb 4 References 5 External links

Formation[edit source | edit] Bleb growth is driven by intracellular pressure generated in the cytoplasm by the contractile cell cortex that will eventually break into billions of bits because the pressure is inane to the exterior surface of the growth anatomical presence. Bleb formation can be initiated in two ways: 1) through local rupture of the cortex or 2) through local detachment of the cortex from the plasma membrane.[3] This generates a weak spot through which the cytoplasm can flow, leading to the expansion of a bulge of membrane. The cytoplasmic flow is driven by hydrostatic pressure inside the cell.[4][5]

Apoptotic Bleb[edit source | edit] A cell is defined as apoptotic when a series of distinguishing features take place. One of those distinguishing features is blebbing.[6] During apoptosis (programmed cell death), the cell's cytoskeleton breaks up and causes the membrane to bulge outward.[7] Blebbing occurs when there is a disruption in the membrane-actin cortex interactions.[8] This is dependent on myosin-ATPase activity to drive actomyosin contraction.[6] These bulges may separate from the cell, taking a portion of cytoplasm with them, to become known as apoptotic bodies. Phagocytic cells eventually consume these fragments and the components are recycled.

Nonapoptotic Bleb[edit source | edit] Nonapoptotic blebbing also has important functions in other cellular processes, including cell locomotion, cell division, physical or chemical stresses, and cancer cell invasion.[8] 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.

References[edit source | edit]

1. Barros, L. F., Kanaseki, T., Sabirov, R., Morishima, S., Castro, J., Bittner, C. X., … Okada, Y. (2003). Apoptotic and necrotic blebs in epithelial cells display similar neck diameters but different kinase dependency. Cell Death & Differentiation, 10(6), 687–697. http://doi.org/10.1038/sj.cdd.4401236.

2. Fackler OT, Grosse R (Jun 2008). "Cell motility through plasma membrane blebbing". J Cell Biol. 181 (6): 879–84. doi:10.1083/jcb.200802081. PMC 2426937. PMID 18541702.

3. Charras, G; Paluch, E (Sep 2008). "Blebs lead the way: how to migrate without lamellipodia.". Nature reviews. Molecular cell biology 9 (9): 730–6. doi:10.1038/nrm2453. PMID 18628785.

4. Charras, GT; Yarrow, JC; Horton, MA; Mahadevan, L; Mitchison, TJ (May 19, 2005). "Non-equilibration of hydrostatic pressure in blebbing cells.". Nature 435 (7040): 365–9. Bibcode:2005Natur.435..365C. doi:10.1038/nature03550. PMID 15902261.

5. Tinevez, JY; Schulze, U; Salbreux, G; Roensch, J; Joanny, JF; Paluch, E (Nov 3, 2009). "Role of cortical tension in bleb growth.". Proceedings of the National Academy of Sciences of the United States of America 106 (44): 18581–6. Bibcode:2009PNAS..10618581T. doi:10.1073/pnas.0903353106. PMID 19846787.

6. Wickman, G. R., Julian, L., Mardilovich, K., Schumacher, S., Munro, J., Rath, N., … Olson, M. F. (2013). Blebs produced by actin–myosin contraction during apoptosis release damage-associated molecular pattern proteins before secondary necrosis occurs. Cell Death & Differentiation, 20(10), 1293–1305. http://doi.org/10.1038/cdd.2013.69.

7. Vermeulen K, Van Bockstaele DR, Berneman ZN (Oct 2005). "Apoptosis: mechanisms and relevance in cancer". Ann Hematol. 84 (10): 627–39. doi:10.1007/s00277-005-1065-x. PMID 16041532.

8. Fackler, O. T., & Grosse, R. (2008). Cell motility through plasma membrane blebbing. The Journal of Cell Biology, 181(6), 879–884. http://doi.org/10.1083/jcb.200802081.

External links[edit source | edit] MBInfo - Bleb MBInfo - Bleb Assembly FCapobianco (talk) 21:37, 9 November 2015 (UTC)