Upregulation of BAG3 with apoptotic and autophagic activities in maggot extractpromoted rat skin wound healing

Maggot extract (ME) accelerates rat skin wound healing, however its effect on cell maintenance in wound tissues remains unclear. Bcell lymphoma (Bcl) 2associated athanogene (BAG)3 inhibits apoptosis and promotes autophagy by associating with Bcl2 or Beclin 1. Bcl2, the downstream effector of signal transducer and activator of transcription 3 signaling, is enhanced in MEtreated wound tissues, which may reinforce the Bcl2 antiapoptotic activity and/or cooperate with Beclin 1 to regulate autophagy during wound healing. The present study investigated expression levels of BAG3, Bcl2, Beclin 1 and light chain (LC)3 levels in rat skin wound tissues in the presence and absence of ME treatment. The results revealed frequent TUNELnegative cell death in the wound tissues in the early three days following injury, irrespective to ME treatment. TUNELpositive cells appeared in the wound tissues following 4 days of injury and 150 µg/ml ME efficiently reduced apoptotic rate and enhanced BAG3 and Bcl2 expression. Elevated Beclin 1 and LC3 levels and an increased LC3 II ratio were revealed in the MEtreated tissues during the wound healing. The results of the present study demonstrate the antiapoptotic effects of BAG3 and Bcl2 in MEpromoted wound healing. Beclin 1/LC3 mediated autophagy may be favorable in maintaining cell survival in the damaged tissues and MEupregulated BAG3 may enhance its activity.