Short communicationAndrographolide reduces proliferation and migration of lens epithelial cells by modulating PI3K/Akt pathway
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Acknowledgments
Forum Kayastha is the recipient of the INSPIRE Fellowship (IF110617) and is thankful to the Department of Science and Technology (DST), New Delhi, INDIA. The authors would like to thank Darshini Ganatra for cell culture assistance and Dr. Devarshi Gajjar for helpful comments on the manuscript.
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2020, Experimental Eye ResearchCitation Excerpt :What's more, miR-221–3p was confirmed to be a target of circHIPK3, and miR-221–3p overexpression reversed circHIPK3 up-regulation-induced protection in HLECs. Previous studies have identified that PI3K/AKT pathway is an important underlying mechanism of HLEC dysfunction, and its inactivation attenuated HLEC proliferation, spreading and migration (Jiang et al., 2006; Kayastha et al., 2014; Liegl et al., 2014). In this study, we found miR-221–3p inhibition up-regulated p-PI3K and p-AKT expression, which was abolished by simultaneous treatment of LY294002, and LY294002 treatment reversed miR-221–3p inhibition-mediated inhibition on HLEC damage.
Dichloroacetate prevents TGFβ-induced epithelial-mesenchymal transition of retinal pigment epithelial cells
2020, Experimental Eye ResearchCitation Excerpt :For treatment, cells were grown in 10 cm culture dishes up to 90% confluence and then cells were divided as per the requirement. Cell survival was assessed by MTT assay as previously described (Mosmann, 1983; Kayastha et al., 2014). Cells were plated at a concentration of 1 × 104 cells per well into 96-well culture plate in medium supplemented with 10% FBS.
Andrographolide, a diterpene lactone from Andrographis paniculata and its therapeutic promises in cancer
2018, Cancer LettersCitation Excerpt :Andrographolide was found to reduce growth factor (TGF-β and bFGF), and induce cell proliferation and migration of lens epithelial cell line (FHL 124). Andrographolide also reduced the level of phosphorylated Akt (Ser473) and Akt (Thr308) in the treated cells [103]. Matrix metallo-proteins (MMPs) mediated inhibition of cell proliferation and migration by andrographolide was also observed in T47D and MDA-MB-231 cells [104].
Ionizing radiation induced cataracts: Recent biological and mechanistic developments and perspectives for future research
2016, Mutation Research - Reviews in Mutation ResearchCitation Excerpt :This may result in aberrant cell division, cell migration and differentiation potentially leading to cataract in vivo [44,110,111]. However, in vitro studies also suggest that lens cells are able to modify their microenvironment, further promoting aberrant behavior such as the expression of transforming growth factor β (TGFβ) and fibroblast growth factor 2 (FGF2) which may promote migration (e.g. [112]), and release of MMPs [74]. Other in vitro studies have investigated oxidative stress without IR exposure, and also noted the change in expression of certain proteins that could be involved in premature senescence, potentially inhibiting successful differentiation into LFCs (e.g. [113]).
Role of carcinogenesis related mechanisms in cataractogenesis and its implications for ionizing radiation cataractogenesis
2015, Cancer LettersCitation Excerpt :Consideration of mechanisms behind posterior LEC migration is also crucial. FGF2 and TGFβ induce LEC migration by activation of the phosphatidyl inositol 3-kinase (PI3K)/Akt pathway [229], and a gradient of concentration of FGF2, TGFβ and other growth factors has been proposed to play critical roles in determining LEC proliferation and posterior migration [230]. IR induces FGF2 in human LECs [231], and NTEs involve TGFβ (see subsection ‘Cortical cataracts’).