Autocrine mechanism

Rong, S., and G. F. Vande Woude. 1994. Autocrine mechanism for met protooncogene tumorigenicity. Cold Spring Harb Symp Quant Biol 59 629-36. 

Gualandris, A., Rusnati, M., Belled, M., Nelli, E. E., Bastaki, M Molinari-Tosatti, M. P., Bonardi, F., Parolini, S., Albini, A., Morbidelli, L., Ziche, M., Corallini, A., Possati, L., Vacca, A., Ribatti, D. and Presta., M. (1996). Basic fibroblast growth factor overexpression in endothelial cells an autocrine mechanism for angiogenesis and angioproliferative diseases. Cell Growth Differentiation 7, 147-160. 

In autocrine signaling, cells of the same type communicate with one another. The hormone produced by the signaling cell affects a cell of the same type by binding to receptors on these cells and initiating an intracellular signal cascade. If an autocrine hormone is secreted simultaneously by many cells then a strong response occurs in the cells. Autocrine mechanisms are of particular importance in the immune response (see Chapter 11). 

Bochkov, V.N. et al. Oxidized phospholipids stimulate angiogenesis via autocrine mechanisms, implicating a novel role for lipid oxidation in the evolution of atherosclerotic lesions. Circ. Res. 99 (2006) 900-8. 

In mature T cells, activation of the TCR induces proliferation via an autocrine mechanism by stimulating the synthesis of both IL-2 and IL-2 receptor (Meuer et al., 1984). On withdrawal of IL-2 these cell undergo apoptosis by a mechanism that requires synthesis of both protein and RNA (Duke and Cohen, 1986). However, if IL-2 or other growth factors are available, these cells proliferate for 3-4 days, after which time they undergo apoptosis, a phenomenon referred to as activation-induced cell death (AICD). Protein and RNA synthesis is required at the time of activation for AICD to proceed (Shi et al., 1989 Ucker et al., 1989 Green and Scott, 1994). Although not strictly developmental cell death, AICD has been used to study the involvement of molecules such as Fas (see Section 3.2) and Myc (see Section 5.2) in the T cell. 

Johnson PR, Burgess JK, Underwood PA, An W, Poniris MH, Tamm M, Ge Q, Roth M, Black JL. Extracellular matrix proteins modulate asthmatic airway smooth muscle cell proliferation via an autocrine mechanism. J Allergy Clin Immunol 2004 113 690-696. 

Overexpression of Met in some cancers can result in its own activation and does not depend on an autocrine mechanism. Overexpression of HGF and Met has been observed in a large portion of human NSCLC, ° and this has been chnically suggested... 

Voss MJ, MoUer MF, Powe DG, Niggemann B, Zanker KS, Entschladen F. Luminal and basal-Uke breast cancer cells show increased migration induced by hypoxia, mediated by an autocrine mechanism. BMC Cancer. 2011 11 158. doi 10.1186/1471-2407-ll-158. 

The secretion of catecholamines in the adrenal tissue is controlled by the splanchnic nerve and influenced by a number of factors, including circulating hormones and paracrine and autocrine mechanisms. 

The existence of multiple layers of control is consistent with the observed responses to hypoxia, in which initial fetal adaptations are altered over time in an organ-specific manner and dependent upon the severity and initial cause of the hypoxia. It is believed that these secondary changes are effected by paracrine and autocrine mechanisms and occur as the needs of the local tissues overcome centrally controlled drives to protect the most vital fetal systems. The local mechanisms are needed to prevent ischemic damage to vulnerable tissues, such as the gut. 

Active oxygen species, especially hydrogen peroxide and probably hydroxyl radical, play a role in particle uptake in the tracheobronchial epithelium and possibly in the alveolar epithelium. Surface iron on the particle is one important factor in this process. The normal production of small amounts of hydrogen peroxide by pulmonary epithelial cells may serve as an accidental autocrine mechanism that increases uptake, and release of AOS ITom particle-evoked inflammatory cells may well have the same effect. Exogenous sources of AOS (e.g., ozone and cigarette smoke) greatly enhance uptake of many particles and probably potentiate mineral dust-induced pathological reactions. 

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