rno-mir-127: In this work, rno-mir-127 blockade leads to KIF3B overexpression and endocytic activity increase [PMC3433485][PMC3433485]. Therefore, rno-mir-127 induction during I/R and H/R could protect cell-matrix and cell-cell adhesions trough KIF3B downregulation, among other mechanisms not yet identified, contributing to cell structure maintenance and epithelial barrier function [PMC3433485][PMC3433485]. rno-mir-127 overexpression by pre-miR transfection in NRK-52E cells promotes cell adhesion not only during normoxia but also after hypoxia (Figure 4A) [PMC3433485][PMC3433485]. In any case, our results indicate a great correlation between the expression of rno-mir-127 in both the in vitro and in vivo model in rat [PMC3433485][PMC3433485]. On the other hand, we identified here for the first time KIF3B as a real target of rno-mir-127 in rat proximal tubule cells during H/R [PMC3433485][PMC3433485]. Moreover, we have identified KIF3B, a component of kinesin II complex , as a real target of rno-mir-127 in proximal tubule cells, with potential implications in cell trafficking [PMC3433485][PMC3433485]. The rno-mir-127 was the most consistent and significantly modulated miRNA showing an increased expression during minimum medium hypoxia (mimicking ischemia) and 1 hour of reperfusion (Figure 1A) [PMC3433485][PMC3433485]. On the other hand, tight junctions (TJ) are essential for epithelial barrier impermeability, thus we investigated rno-mir-127 modulation effects in these structures [PMC3433485][PMC3433485]. Regarding a potential protective role of miR-127 in response to I/R, this work describes for the first time the effects of rno-mir-127 modulation in actin cytoskeleton organization and adhesive structures integrity during I/R injury [PMC3433485][PMC3433485]. All these data demonstrate that rno-mir-127 induction promotes cell adhesion and cytoskeleton structure maintenance during H/R [PMC3433485][PMC3433485]. These results demonstrate that KIF3B is a target gene for rno-mir-127 in NRK-52E cells during H/R, both regulating proximal tubule cell function [PMC3433485][PMC3433485]. rno-mir-127 is increased during hypoxia and Ischemia and at 1h and 24 hours of reperfusion respectively, time points where cellular damage or renal tissue damage is maximum in this model [PMC3433485][PMC3433485]. To go further into the biological significance of rno-mir-127 induction, we performed a bioinformatics target prediction for this miRNA using different databases available online, such as microcosm (www.pictar.mdc-berlin.de) [PMC3433485][PMC3433485]. In this work, we have identified rno-mir-127 and its human homologous hsa-miR-127-3p as important mediators of the proximal tubule response to I/R [PMC3433485][PMC3433485]. Moreover, rno-mir-127 is also induced during ischemia and 24 hours of reperfusion in our in vivo rat model of I/R (Figure 1B) [PMC3433485][PMC3433485]. rno-mir-127 induction during I/R is a cytoskeleton protection mechanism which prevents actin depolimerization and promotes cell adhesion by preventing FAC disassembly and TJ disorganization [PMC3433485][PMC3433485]. Furthermore, rno-mir-127 blockade by anti-miR aggravates cytoskeleton and adhesion structures disorganization caused by hypoxia [PMC3433485][PMC3433485]. Following renal ischemia and reperfusion in rats, an increased expression of rno-mir-127 was found, and Kinesin Family Member 3B (KIF3B), which is involved in cellular endocytosis, was identified as a novel target of miR-127 [PMC4442302][PMC4442302].