Muscarinic receptors participation in angiogenic response induced by macrophages from mammary adenocarcinoma-bearing mice

Torre, Eulalia de la; Davel, L; Jasnis, María A.; Gotoh, Tomomi; Lustig, Eugenia Sacerdote de; Sales, Marı́a Elena

doi:10.1186/bcr1005

Cited by 26 publications

(15 citation statements)

References 23 publications

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“…Particularly M 1 and M 2 receptors participate in the angiogenic response exerted by CARB modulating arginine metabolism via arginase II. These results are coincident with previous reports published by our laboratory that demonstrated M 1 and M 2 collaborative actions on urea production by arginase II in the angiogenic pro-tumor effects exerted by macrophages purified from LMM3 tumor bearers (de la Torre et al, 2005).…”

Section: Discussionsupporting

confidence: 94%

Role of non-neuronal cholinergic system in breast cancer progression

Español¹,

Torre²,

Fiszman³

et al. 2007

Life Sciences

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Section: Discussionsupporting

confidence: 94%

Role of non-neuronal cholinergic system in breast cancer progression

Español¹,

Torre²,

Fiszman³

et al. 2007

Life Sciences

Self Cite

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“…Muscarinic receptors are expressed on immune cells, including macrophages (15,31,32), which produce TNF during endotoxemia (33,34). Vagal efferents, distributed throughout the reticuloendothelial system and other peripheral organs are positioned to rapidly transmit the antiinflammatory signal to these cells.…”

Section: Discussionmentioning

confidence: 99%

Central muscarinic cholinergic regulation of the systemic inflammatory response during endotoxemia

Pavlov

Ochani

Gallowitsch-Puerta

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

300

215

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TNF has a critical mediator role in inflammation and is an important therapeutic target. We recently discovered that TNF production is regulated by neural signals through the vagus nerve. Activation of this ''cholinergic antiinflammatory pathway'' inhibits the production of TNF and other cytokines and protects animals from the inflammatory damage caused by endotoxemia and severe sepsis. Here, we describe a role for central muscarinic acetylcholine receptors in the activation of the cholinergic antiinflammatory pathway. Central muscarinic cholinergic activation by muscarine, the M1 receptor agonist McN-A-343, and the M2 receptor antagonist methoctramine inhibited serum TNF levels significantly during endotoxemia. Centrally administered methoctramine stimulated vagus-nerve activity measured by changes in instantaneous heart-rate variability. Blockade of peripheral muscarinic receptors did not abolish antiinflammatory signaling through the vagus nerve, indicating that peripheral muscarinic receptors on immune cells are not required for the cytokine-regulating activities of the cholinergic antiinflammatory pathway. The role of central muscarinic receptors in activating the cholinergic antiinflammatory pathway is of interest for the use of centrally acting muscarinic cholinergic enhancers as antiinflammatory agents. muscarinic receptors ͉ systemic inflammation ͉ TNF ͉ vagus nerve T he overproduction of cytokines, including TNF, mediates tissue damage during the response to injury or pathogenic invasion (1). Physiological and molecular mechanisms that control TNF production maintain cytokine homeostasis and minimize or prevent damage during the host response to infection, injury, arthritis, and other disorders (1-3). Recently, we found (4-6) that electrical or pharmacological activation of the efferent vagus nerve inhibits the release of TNF and attenuates the development of endotoxin-induced shock in rodents. Stimulation of the efferent vagus nerve activates the release of acetylcholine. Although the vagus nerve is a ''classical'' cholinergic regulator of visceral functions in which peripheral muscarinic acetylcholine receptors have a major mediating role, the vagusnerve cytokine-inhibiting activity (which is termed ''the cholinergic antiinflammatory pathway'') requires signaling through nicotinic ␣ 7 subunit-containing receptors (4, 5).Studies have implicated muscarinic receptor-dependent mechanisms in the central modulation and integration of vagal regulation of visceral functions. For example, vagus nerve control of glycogen synthesis in the liver, the Bezold-Jarish cardiovascular reflex and the regulation of exocrine pancreatic secretion are modulated centrally by brain muscarinic receptor mechanisms (7-10). Thus, we reasoned that brain muscarinic receptors could be involved in the central regulation of the vagus-nerve immunomodulatory function. Our results indicate that central cholinergic activation by selective muscarinic receptor ligands significantly inhibits systemic TNF in endotoxemic rats and activates th...

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“…It has been suggested that Mps could participate in this process, but little is known about the mechanisms involved in it (Nucera et al, 2011). We had previously reported that peritoneal Mps from tumor‐bearing mice are able to induce a strong neovascular response in the skin of singeneic mice (de la Torre et al, 2005). Similar results accompanied by the increment of VEGF‐A and MMP‐9 are observed when LPS‐treated Mps are inoculated in the skin of singeneic mice (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Liver biopsy interpretation in liver cancer

Balabaud

2011

Hepatology

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Muscarinic receptors participation in angiogenic response induced by macrophages from mammary adenocarcinoma-bearing mice

Cited by 26 publications

References 23 publications

Role of non-neuronal cholinergic system in breast cancer progression

Role of non-neuronal cholinergic system in breast cancer progression

Central muscarinic cholinergic regulation of the systemic inflammatory response during endotoxemia

Liver biopsy interpretation in liver cancer

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