| Literature DB >> 24717577 |
César L Araujo1, Ileana B Quintero1, Anja Kipar2, Annakaisa M Herrala1, Anitta E Pulkka1, Lilli Saarinen3, Sampsa Hautaniemi3, Pirkko Vihko4.
Abstract
We have previously shown that in addition to the well-known secreted isoform of prostatic acid phosphatase (sPAP), a transmembrane isoform exists (TMPAP) that interacts with snapin (a SNARE-associated protein) and regulates the endo-/exocytic pathways. We have also shown that PAP has 5'-ectonucleotidase and thiamine monophosphatase activity and elicits antinociceptive effects in mouse models of chronic inflammatory and neuropathic pain. Therefore, to determine the physiological role of PAP in a typical exocrine organ, we studied the submandibular salivary gland (SMG) of PAP(-/-) and wild-type C57BL/6J mice by microarray analyses, microRNA sequencing, activity tests, immunohistochemistry, and biochemical and physiological analyses of saliva. We show that PAP is the main acid phosphatase in the wild-type male mouse saliva, accounting for 50% of the total acid phosphatase activity, and that it is expressed only in the granular convoluted tubules of the SMGs, where it is the only 5'-ectonucleotidase. The lack of PAP in male PAP(-/-) mice was associated with a significant increase in the salivation volume under secretagogue stimulation, overexpression of genes related to cell proliferation (Mki67, Aurkb, Birc5) and immune response (Irf7, Cxcl9, Ccl3, Fpr2), and upregulation of miR-146a in SMGs. An increased and sustained acinar cell proliferation was detected without signs of glandular hyperplasia. Our results indicate that in PAP(-/-) mice, SMG homeostasis is maintained by an innate immune response. Additionally, we suggest that in male mice, PAP via its 5'-ectonucleotidase activity and production of adenosine can elicit analgesic effects when animals lick their wounds.Entities:
Keywords: 5′-ectonucleotidase activity; TMPase activity; acid phosphatase; submandibular salivary gland; transmembrane prostatic acid phosphatase
Mesh:
Substances:
Year: 2014 PMID: 24717577 DOI: 10.1152/ajpcell.00062.2014
Source DB: PubMed Journal: Am J Physiol Cell Physiol ISSN: 0363-6143 Impact factor: 4.249