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Dysfunction of salivary glands and decrease in saliva are serious problems in clinical dentistry since saliva maintains oral health. Tissue injuries caused by γ-irradiation or autoimmune syndromes induce atrophy of salivary acinar cells. We have previously reported that cell isolation processes from rat parotid glands by digestion with enzymes mimic tissue injuries and result in decrease of expression of amylase, which indicates dysfunction of acinar cells. In this study, we found that a non-selective PKC inhibitor, Ro31-8220, and an inhibitor of MEK1/2, U0126, suppressed the decrease of amylase activity caused by cell isolation. Gö6983, an inhibitor for novel PKC, also suppressed its decrease although Gö6976, a specific inhibitor for conventional PKC, did not. Time-dependent increase in phosphorylation of novel PKCs during culture was detected. Their phosphorylation was inhibited by addition of Ro31-8220 or Gö6983, but not by Gö6976. Phosphorylation of novel PKC was inhibited by U0126 while Erk1/2 activation was not suppressed by Ro31-8220, which suggests that activation of Erk1/2 is upstream of phosphorylation of novel PKCs. Addition of diphenyleneiodonium suppressed the activation of Erk1/2. Therefore, tissue injury during cell isolation generates reactive oxygen species, which causes dysfunction of parotid acinar cells via activation of Erk1/2 and novel PKCs.

Tissue Injury-induced Reactive Oxygen Species Cause Dysfunction of Parotid Acinar Cells via Erk-novel PKC Activation