Abstract
Botulinum toxin type A (BTXA) is a neurotoxic protein produced by Clostridium botulinum. Our previous studies demonstrated that BTXA inhibits the secretory function of submandibular gland (SMG) and changes its structure. Several studies reported that SMG damage and repair often occur with autophagy in the rat. However, no studies reported whether secretory inhibition and structural changes of SMG after BTXA injection is related with autophagy. The present study was carried out to explore the association between BTXA injection and autophagy in rat SMG. Western blotting and immunofluorescence were used to detect the expression and distribution of light chain 3 (LC3) in rat SMG. MTS was used to detect the toxicity of BTXA on rat SMG-C6 cell line. GFP-LC3 and Lyso-Tracker Red fluorescence probe were used to assess the levels of autophagosomes and lysosome fusion and the effect of BTXA on autophagic flux in SMG-C6. Western blotting and immunofluorescence results showed that BTXA temporarily increased autophagosomes in rat SMG. MTS results showed that BTXA exerted its toxicity on SMG-C6 in a dose-dependent manner. BTXA increased the number of autophagosomes in SMG-C6; however, most autophagosomes did not colocalize with lysosome. Therefore, we presume that BTXA can change autophagic flux of SMG cells, the mechanism of which might relate with BTXA’s disturbing autophagosome-lysosome fusion.
Highlights
Botulinum toxin (BTX) is a neurotoxic protein produced by Clostridium botulinum [1,2,3]
These results suggested that Botulinum toxin type A (BTXA) can temporarily increase the autophagosomes in rat submandibular gland (SMG) cells
Our previous studies proved that BTXA decreased the salivation via inducing SMG cell apoptosis and changing aquaporin 5 (AQP5) expression and distribution, but the hidden mechanism has not been fully illustrated
Summary
Botulinum toxin (BTX) is a neurotoxic protein produced by Clostridium botulinum [1,2,3]. Autophagy plays in the development of eukaryotic cells and related diseases [9,10,11]. It has four stages, namely the formation of a separation membrane, the formation of autophagosomes, the fusion of autophagosomes and lysosomes, and the degradation of autophagic products. Autophagic flux is a process by which phagosomes fuse into lysosomes and degrade their contents [12,13]. This process occurs not when autophagy is going, but when autophagy is completed [12]. Autophagy is currently considered to be closely related to tumors, cardiovascular diseases, neurodegenerative diseases, aging, autoimmune diseases, and tissue fibrosis [10,14,15,16,17,18,19]
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