autocrine loop

autocrine loop

A type of interaction between growth factors, cytokines and target cells, in which a cell produces the same growth factors and cytokines for which it has receptors, allowing the cell to stimulate itself, as occurs in smooth muscle cell production and IL-1 response.
References in periodicals archive ?
Tumour co-expression of apelin and its receptor is the basis of an autocrine loop involved in the growth of colon adenocarcinomas.
These data would suggest that FL-RAGE might increase in astrocytes when motor neuron death becomes significant, consistently with the possibility that an autocrine loop of RAGE activation in astrocytes, dependent on signals released by dying motor neurons, may occur.
Gonzalez Torres et al., "S100B protein activates a RAGE-dependent autocrine loop in astrocytes: implications for its role in the propagation of reactive gliosis," Journal of Neurochemistry, vol.
[sup][26] Interestingly, mast cells are known to release and respond to TNF-a, indicating a positive autocrine loop that leads to the augmentation of mast cell activation.
It has been shown that VEGF-A induces proliferation, survival, and protection of AML cells against apoptosis by an autocrine loop via VEGFR signaling (31), (32), (33).
Blockade of the insulin-like growth factor-I receptor inhibits growth of human colorectal cancer cells: evidence of a functional IGF-II-mediated autocrine loop. Int J Cancer 1994; 58 : 452-9.
It increases production of vascular endothelial growth factor (VEGF), the main angiogenic factor, which in turn enhances the expression of CXCR4 receptor in endothelial cells, in an autocrine loop (3).
[46] The exuberant endothelial proliferation involves an autocrine loop of endothelial secretion of basic fibroblast growth factor.
Ethier, "Altered EGFR localization and degradation in human breast cancer cells with an amphiregulin/EGFR autocrine loop," Cellular Signalling, vol.
The differential sensitivity of prostate cancer cells to TGF-[alpha] suggests that the autocrine loop involving TGF-[alpha] in prostate cancer cell lines may be further regulated by other unknown factors.
The results indicated that macrophages could establish the adaptation to LPS stimulation partly via their innate nonneuronal cholinergic autocrine loop.
Constitutive endothelin-1 overexpression promotes smooth muscle cell proliferation via an external autocrine loop. J Biol Chem 1994;269:10112-8.