Molybdenum and cadmium co-exposure induces CaMKKβ/AMPK/mTOR pathway mediated-autophagy by subcellular calcium redistribution in duck renal tubular epithelial cells

Role of PLC/IP3/IP3R axis in excess molybdenum exposure induced apoptosis in duck renal tubular epithelial cells

“…Our experimental results showed that Mo could dramatically improve PLC activity, IP 3 content, and IP 3 R expression level, which indicated that Mo could activate PLC/IP 3 /IP 3 R axis. And according to our previous in vivo research results, excess Mo could cause Ca homeostasis imbalance by improving the expression levels of relevant factors (CaMKII, CaN, CRT, GRP78 and so on) in duck kidneys 8 . GRP78, GRP94 and CRT are the most abundant Ca buffer proteins in the ER.…”

“…Evidence has revealed that cytoplasmic Ca 2+ overload is one of the dominant factors triggering apoptosis 15,23,24 . According to our previous research, the nephrotoxicity caused by excess Mo was closely interrelated with Ca 2+ homeostasis disorder, cytoplasmic Ca 2+ concentration ([Ca 2+ ] c ) overload and apoptosis 8,9 . However, the role of ER in adjusting the increase of [Ca 2+ ] c and whether the rise of [Ca 2+ ] c in subcellular Ca 2+ reallocation can be used as a link to regulate apoptosis need to be further explored.…”

“…Some reports have indicated that high levels of Mo can be deposited in the epithelial cells of the proximal renal tubule, eliciting calcium (Ca) homeostasis imbalance, apoptosis, pyroptosis and autophagy, thus resulting in irreversible nephrotoxic damage. [8][9][10][11][12] The essence of Ca homeostasis imbalance is the Huiling Guo and Caiying Zhang are the equal first authors. destruction of intracellular calcium ion (Ca 2+ ) homeostasis.…”

“…15,23,24 According to our previous research, the nephrotoxicity caused by excess Mo was closely interrelated with Ca 2+ homeostasis disorder, cytoplasmic Ca 2+ concentration ([Ca 2+ ] c ) overload and apoptosis. 8,9 However, the role of ER in adjusting the increase of [Ca 2+ ] c and whether the rise of [Ca 2+ ] c in subcellular Ca 2+ reallocation can be used as a link to regulate apoptosis need to be further explored. Hence, this experiment investigated the effect of PLC/IP 3 /IP 3 R axis in regulating [Ca 2+ ] c -mediated apoptosis triggered by excess Mo exposure in the duck renal tubular epithelial cells.…”

Clostridium perfringens α toxin damages the immune function, antioxidant capacity and intestinal health and induces PLCγ1/AMPK/mTOR pathway-mediated autophagy in broiler chickens

“…PLCγ1 plays a crucial role in the pathogenesis induced by α toxin [ 17 ]. Recent studies have shown that PLC could modulate the AMP-activated protein kinase (AMPK) pathway in inflammation [ 18 ] and autophagy [ 19 ]. AMPK, a key regulator of cell metabolism, is triggered by the induction of cellular stress (such as an increase in Ca 2+ concentration or the production of reactive oxygen species) [ 20 ].…”