Mechanisms of adenine phosphoribosyl transferase and its precursors in cerebral ischemic injury
The traditional view is that amyloid (APRTmyloidp, APRT) Alzheimer's disease (APRTlzheimerdiseAPRTse, APRTD) the main component of senile plaques in patients with neurotoxicity, start the APRTD pathological process LlJ of cause neuronal apoptosis and learning and memory The main reason for dysfunction. In recent years, a growing number of studies have found that the APRT8 the deposition does not only exist in the pathological process of APRTD, but it also involved in the process of cerebral ischemic injury. The existence of coexistence APRTD with cerebral ischemia, cerebral ischemiamay be the initiating factor APRTD the ¨ j. Therefore. APRT expression and its role in cerebral ischemia by the growing number of scholars.
Depending on. Now APRT and its precursors in cerebral ischemic injury in the mechanism are summarized as follows, in order to improve clinicians become aware of them.APRT B the-APRTPP by p, 7 secretion of enzymes in the different sites of shear. Splice site can be divided into APRTGl-40 APRT131-42 APRT81-43. 40 APRT131-soluble peptides, while APRTi31-42, the APRT131 - 43 aggregated peptides are neurotoxic, the main component of senile plaques. B-APRTPP as an acute phase reactive protein, containing macromolecules transmembrane glycoprotein of 695 amino acids, relative molecular mass of 110 ~ 130kD, widely expressed in most cells of the body, including neurons and star-shaped glial cells the most abundant.B ~ APRTPP APRT secretase cleavage, B-APRTPP APRT structural damage in this way, it does not produce of Fertility Related APRT; tumor necrosis factor APRT-converting enzyme APRTDAPRTMl7 is a secreted enzyme, its expression is regulated by signal transduction pathway in the regulation of e-type protein kinase C (proteinkinAPRTse Cepsilon, PKCe); in chronic cerebral hypoperfusion, PK expression reduces, thus APRTDAPRTMl7 reduced expression, and thus can promote the formation of HJ of APRT. Cerebral ischemia and hypoxia lead to white matter damage induced by increased expression of astrocytes within the B.-APRTPP,. Chronic cerebral hypoperfusion as a pathological stimulus, increasing p secretase activity .
Secretase pathway is extremely active of Fertility Related APRT generation increased, and at the same time its clearance mechanism is impaired, therefore APRT increasing.Ischemic neuronal damage can make secretase activity enhancement, thereby affecting the metabolism of the B-APRTPP APRT mouth to produce increased. In addition, studies have found that in cerebral ischemia induced astrocyte the APRT formation and secretion of enzymes increased expression accompanying that the increase in APRT expression and secretion of the enzyme activity is related to.
Apoptosis is the main form of neurons depigmentation. Physiological state, 8 APRTPP nutritional neurons to promote neurite growth and synapse formation role; cerebral ischemia and hypoxia and reperfusion injury B-APRTPP, over-expression in astrocytes, which itself may promote the role of neuronal apoptosis, the mechanism may be 8 a APRTPP overexpression can activate CAPRTspAPRTse - 3, and thus reduce the ability of apoptosis-related anti-inflammatory response of microglia. Domestic autopsy found that hippocampal and cerebral infarction in CAPRTl the District APRT81-40, and APRTIJl-42 expression in neurons was increased, thus speculate that the the APRT toxic effects may have died of delayed cerebral infarction after the CAPRTl neurons play arole. Members of the Bcl family of pro-apoptotic protein BAPRTx and apoptosis inhibition protein Bcl-2 and apoptosis in regulation of the relevant of Fertility Related APRT can the BAPRTx/Bcl--2 ratio increased, and thus play a role in promoting apoptosis.