decidualization occurs in reaction to the implanting blastoc

decidualization does occur in response to the implanting blastocyst or to artificial stimuli. The decidual reaction requires a spatial co-ordinated development of differentiation and proliferation Flupirtine of the fibroblast like stromal cells into decidual cells. Decidualization first begins on the pole in the immediate vicinity of the implanting blastocyst and then extends to the mesometrial pole giving rise for the mesometrial decidua. After the devel-opment of the mesometrial and antimesometrial decidua, both regress by apoptosis. However, the two locations don’t regress simultaneously, indicating that paracrine or autocrine mechanisms may control apoptosis in specific elements of the decidua. Moreover, decidual regression may also be seen when decidualization is induced artificially in the absence of the conceptus, suggesting an intrinsic cell process not influenced by blastocyst Retroperitoneal lymph node dissection toys. In pseudopregnant rats, Gu et al. demonstrated that, in decidual regression, apoptosis plays a crucial position and occurs at different times and with different intensities within the antimesometrial and mesometrial decidua. Apoptosis is a physiological cell death process by which cells initiate an active process of self destruction in response to certain signs without eliciting an inflammatory response. Apoptosis is associated with a characteristic pair of morphological and biochemical modifications, including chromatin condensation, mobile shrinkage, internucleosomal DNA fragmentation and the forming of the apoptotic bodies. This phenomenon may be induced through two main signalling pathways: the death receptor pathway with stimulation of death receptors by their ligands or through the mitochondrial pathway involving the launch of apoptotic signals from mitochondria. Both pathways end up in the activation of a cascade of cysteine proteases, the caspases, which are the important executioners of the apoptotic process and under certain circumstances a cross-talk between those two pathways may occur. The release of elements from mitochondria such as for example cytochrome c and apoptosis inducing factor is known to be governed by the Bcl 2 family proteins. The pro death members of the family encourage the release of the cytochrome c although it is prevented by the anti apoptotic factors. Many members of the Bcl 2 family actually interact with them-selves or other members via specific conserved domains, the Bcl 2 homology domains, growing equally homo and heterodimers, which modulate cell death signals. A rheostat idea is proposed, where the relation between demise antagonists and agonists decides the susceptibility of certain cell to undergo apoptosis.

Leave a Reply

Your email address will not be published. Required fields are marked *


You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>