Impact of polyvinyl chloride (PVC) microplastic on growth, photosynthesis and nutrient uptake of Solanum lycopersicum L. (Tomato).

Microplastics (MPs) pollution and their impact on plants have become a global threat, but their effect at the molecular level remains scarce. This study aims to gain insight into the effects of polyvinylchloride microplastic (PVC-MP) on tomato plants at the genetic and protein levels. In this study, we found that increasing concentrations of PVC-MP (2.5, 5,7.5, and 10% w/w) in the soil did not cause any phytotoxic (chlorosis or necrosis) symptoms but it did result in a dose-dependent reduction in plant growth-related parameters, such as height, leaf area, stem diameter, and plant fresh and dry weight. Additionally, the number of secondary roots was reduced while the primary roots were elongated. Furthermore, PVC-MP also caused a significant decrease in light-harvesting pigments chlorophylls, and carotenoids while increasing the level of reactive oxygen species (ROS) and lipid peroxidation in plants. Microscopic analysis of the roots revealed the uptake of PVC-MP of size less than 10 µm. Micro- and macro-element analysis showed changes in concentrations of Ca, Cu, Fe, Mg, Mn, Ni, and Zn, upon PVC-MP exposure. Results from western blotting and q-PCR showed that higher doses of PVC-MP significantly reduced the CO2-fixing enzyme RuBisCO and D1 proteins of PSII at both protein and transcript levels. These findings suggest that lower levels of light-harvesting pigments, D1 protein, RuBisCO, and modulation of nutrient absorption are among the factors responsible for growth suppression in tomato plants upon exposure to PVC-MP. As tomato plants are economically significant crops, an increase in PVC-MP in agricultural fields may have a detrimental influence on crop production, resulting in economic loss.

Integrin ß4 induced epithelial-to-mesenchymal transition involves miR-383 mediated regulation of GATA6 levels.

BACKGROUND: The process of transdifferentiating epithelial cells to mesenchymal-like cells (EMT) involves cells gradually taking on an invasive and migratory phenotype. Many cell adhesion molecules are crucial for the management of EMT, integrin ß4 (ITGB4) being one among them. Although signaling downstream of ITGB4 has been reported to cause changes in the expression of several miRNAs, little is known about the role of such miRNAs in the process of EMT. METHODS AND RESULTS: The cytoplasmic domain of ITGB4 (ITGB4CD) was ectopically expressed in HeLa cells to induce ITGB4 signaling, and expression analysis of mesenchymal markers indicated the induction of EMT. ß-catenin and AKT signaling pathways were found to be activated downstream of ITGB4 signaling, as evidenced by the TOPFlash assay and the levels of phosphorylated AKT, respectively. Based on in silico and qRT-PCR analysis, miR-383 was selected for functional validation studies. miR-383 and Sponge were ectopically expressed in HeLa, thereafter, western blot and qRT-PCR analysis revealed that miR-383 regulates GATA binding protein 6 (GATA6) post-transcriptionally. The ectopic expression of shRNA targeting GATA6 caused the reversal of EMT and ß catenin activation downstream of ITGB4 signaling. Cell migration assays revealed significantly high cell migration upon ectopic expression ITGB4CD, which was reversed upon ectopic co-expression of miR-383 or GATA6 shRNA. Besides, ITGB4CD promoted EMT in in ovo xenograft model, which was reversed by ectopic expression of miR-383 or GATA6 shRNA. CONCLUSION: The induction of EMT downstream of ITGB4 involves a signaling axis encompassing AKT/miR-383/GATA6/ß-catenin.

Horizontal Transfer of miR-643 from Cisplatin-Resistant Cells Confers Chemoresistance to Recipient Drug-Sensitive Cells by Targeting APOL6.

Acquisition of resistance to cisplatin is a major impediment to the success of cisplatin-based combination therapies for cancer. Recent studies indicate that exosomal miRNAs derived from drug-resistant tumour cells can confer resistance properties to recipient cells by a horizontal transfer mechanism. Although the role of horizontal transfer of a few miRNAs has been described, little is known about the concerted action of horizontal transfer of miRNAs in conferring cisplatin resistance. The present study was designed to identify the role of miR-643, which is one of the most significantly increased miRNA in exosomes released from cisplatin-resistant Heptocarcinoma cells, in altering the cisplatin resistance properties of recipient cells. Drug-sensitivity assays involving miR-643 revealed that ectopic expression of miR-643 can desensitise the cells towards cisplatin. Furthermore, we identified APOL6 as a major target of miR-643. Further mechanistic studies showed that miR-643 can modulate APOL6 mRNA and protein levels, leading to a reversal of APOL6-mediated apoptosis. Altogether, our results suggest an APOL6-dependent mechanism for miR-643 mediated cisplatin resistance upon the horizontal transfer across cell types.