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10.1038/cdd.2013.177 http://scihub22266oqcxt.onion/10.1038/cdd.2013.177 C3950320!3950320!24336047     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24336047&cmd=llinks): Failed to open stream: HTTP request failed! 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Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation |pdf=|usr=}}{{24336047}} gab.com Text Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=24336047 #FOAvip Calcium deficiency causes abnormal colonic growth and increases colon cancer risk with poorly understood mechanisms. Here we elucidate a novel signaling mechanism underlying the Ca2+ deficiency-induced epithelial proliferation using a unique animal model. The zebrafish larval yolk sac skin contains a group of Ca2+-transporting epithelial cells known as ionocytes. Their number and density increases dramatically when acclimated to low [Ca2+] environments. BrdU pulse-labeling experiments suggest that low [Ca2+] stimulates pre-existing ionocytes to re-enter the cell cycle. Low [Ca2+] treatment results in a robust and sustained activation of IGF1R-PI3K-Akt signaling in these cells exclusively. These ionocytes specifically express Igfbp5a, a high-affinity and specific binding protein for insulin-like growth factors (IGFs) and the Ca2+-selective channel Trpv5/6. Inhibition or knockdown of Igfbp5a, IGF1 receptor, PI3K, and Akt attenuates low [Ca2+]-induced ionocyte proliferation. The role of Trpv5/6 was investigated using a genetic mutant, targeted knockdown, and pharmacological inhibition. Loss-of-Trpv5/6 function or expression results in elevated pAkt levels and increased ionocyte proliferation under normal [Ca2+]. These increases are eliminated in the presence of an IGF1R inhibitor, suggesting that Trpv5/6 represses IGF1R-PI3K-Akt signaling under normal [Ca2+]. Intriguingly, blockade of Trpv5/6 activity inhibits the low [Ca2+]-induced activation of Akt. Mechanistic analyses reveal that the low [Ca2+]-induced IGF signaling is mediated through Trpv5/6-associated membrane depolarization. Low extracellular [Ca2+] results in a similar amplification of IGF-induced PI3K-PDK1-Akt signaling in human colon cancer cells in a TRPV6-dependent manner. These results uncover a novel and evolutionarily conserved signaling mechanism that contributes to the abnormal epithelial proliferation associated with Ca2+ deficiency. Twit Text FOAVip Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=24336047 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24336047 #FOAvip English Wikipedia <ref>{{Cite pmid|24336047}}</ref> Calcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt signaling regulates abnormal epithelial cell proliferation #MMPMID24336047 Dai W; Bai Y; Hebda L; Zhong X; Liu J; Kao J; Duan C Cell Death Differ 2014[Apr]; 21 (4): 568-81 PMID24336047show ga Calcium deficiency causes abnormal colonic growth and increases colon cancer risk with poorly understood mechanisms. Here we elucidate a novel signaling mechanism underlying the Ca2+ deficiency-induced epithelial proliferation using a unique animal model. The zebrafish larval yolk sac skin contains a group of Ca2+-transporting epithelial cells known as ionocytes. Their number and density increases dramatically when acclimated to low [Ca2+] environments. BrdU pulse-labeling experiments suggest that low [Ca2+] stimulates pre-existing ionocytes to re-enter the cell cycle. Low [Ca2+] treatment results in a robust and sustained activation of IGF1R-PI3K-Akt signaling in these cells exclusively. These ionocytes specifically express Igfbp5a, a high-affinity and specific binding protein for insulin-like growth factors (IGFs) and the Ca2+-selective channel Trpv5/6. Inhibition or knockdown of Igfbp5a, IGF1 receptor, PI3K, and Akt attenuates low [Ca2+]-induced ionocyte proliferation. The role of Trpv5/6 was investigated using a genetic mutant, targeted knockdown, and pharmacological inhibition. Loss-of-Trpv5/6 function or expression results in elevated pAkt levels and increased ionocyte proliferation under normal [Ca2+]. These increases are eliminated in the presence of an IGF1R inhibitor, suggesting that Trpv5/6 represses IGF1R-PI3K-Akt signaling under normal [Ca2+]. Intriguingly, blockade of Trpv5/6 activity inhibits the low [Ca2+]-induced activation of Akt. Mechanistic analyses reveal that the low [Ca2+]-induced IGF signaling is mediated through Trpv5/6-associated membrane depolarization. Low extracellular [Ca2+] results in a similar amplification of IGF-induced PI3K-PDK1-Akt signaling in human colon cancer cells in a TRPV6-dependent manner. These results uncover a novel and evolutionarily conserved signaling mechanism that contributes to the abnormal epithelial proliferation associated with Ca2+ deficiency. äCalcium deficiency-induced and TRP channel-regulated IGF1R-PI3K-Akt si(epmc).pdf DeepDyve Pubget Overpricing