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GEOFFREY BURNSTOCK AN. R. ACAD. NAC. FARM.

P2Y2 and P2Y4 receptors activated by UTP and ATP, whereas
activated cells express P2Y6 receptors activated by UDP and ATP.
It has been speculated that the P2Y receptors on satellite cells may
be an attractive target to prevent or treat liver fibrosis, via regulation
of procollagen-1 transcription. ATP has been shown recently to
rapidly activate multiple components of the c-jun N-terminal kinase
(JNK) cascade, a central player in hepatocyte proliferation and liver
regeneration. This study identifies extracellular ATP as a hepatic
mitogen with implications about the regulation of liver growth and
repair.

The effect of ATP on salivary glands has been recognised since
1982. Both P2X and P2Y subtypes are expressed and opportunities
for utilization of these receptors as pharmaceutical targets for
diseases involving salivary gland dysfunction appear promising.

IMMUNE SYSTEM AND INFLAMMATION

ATP and adenosine are released at sites of inflammation.
ATP is involved in the development of inflammation through a
combination of actions: release of histamine from mast cells,
provoking production of prostaglandins, and the production and
release of cyokines from immune cells. In contrast, adenosine exerts
anti-inflammatory actions. P2X7 and P2Y1 and P2Y2 receptors located
on inflammatory and immune cells play a pivotal role in
inflammation and immunomodulation (13).

In addition to the roles of purines in inflammation, they have a
broad range of functions carried out through purinergic receptors
on immune cells, including killing intracellular pathogens by
inducing apoptosis of host macrophages, chemoattraction and cell
adhesion. Purinergic compounds may turn out to be useful for the
treatment of neurogenic inflammation, rheumatoid arthritis and
periodontitis.

ATP-induced apoptosis in macrophages via P2X7 receptors, also
results in killing of the mycobacteria contained within them, in
contrast, to the macrophage apoptoses produced by other agents;
elucidation of the bacterial killing mechanism initiated by the P2X7

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