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Glass substrate, a new type of substrate with excellent mechanical and electrical properties of glass itself, has great potential to become an ideal platform for heterogeneous integration in chiplet systems for high-performance computing applications. The residual stress of the metal layer generated on the glass surface during the electroplating process is one of the major bottlenecks of glass packaging technologies, resulting in glass-metal layer delamination and glass breakage. This paper demonstrated for the first time a method to regulate the residual stress by manipulating the nanotwin directions of the electroplated Cu. The experimental results show that nanotwins with three different directions (non-directional, vertical, and horizontal) can be manipulated by controlling electroplating conditions (concentration of Cl− and gelatin, stirring speed). The orientations of non-directional, vertical, and horizontal nanotwinned Cu are non-oriented, 110 and 111, respectively. After electroplating, the 111-oriented nanotwinned Cu has the smallest residual stress (39.7 MPa). Annealing can significantly reduce the residual stress of nanotwinned Cu, which has been attributed to the decrease in the geometric necessity dislocation density. 110-oriented nanotwinned Cu had drastic recrystallization, while 111-oriented nanotwinned Cu and non-oriented nanotwinned Cu had only slight recrystallization. After annealing, the residual stress of 111-nt-Cu remains the lowest (29.1 MPa). [ABSTRACT FROM AUTHOR]

The stem cell niche is thought to affect cell cycle quiescence, proliferative capacity, and communication between stem cells and their neighbors. How these activities are controlled is not completely understood. Here we define a microRNA family (miRs-103/107) preferentially expressed in the stem cell-enriched limbal epithelium that regulates and integrates these stem cell characteristics. miRs-103/107 target the ribosomal kinase p90RSK2, thereby arresting cells in G0/G1 and contributing to a slow-cycling phenotype. Furthermore, miRs-103/107 increase the proliferative capacity of keratinocytes by targeting Wnt3a, which enhances Sox9 and YAP1 levels and thus promotes a stem cell phenotype. This miRNA family also regulates keratinocyte cell-cell communication by targeting: (a) the scaffolding protein NEDD9, preserving E-cadherin-mediated cell adhesion; and (b) the tyrosine phosphatase PTPRM, which negatively regulates connexin 43-based gap junctions. We propose that such regulation of cell communication and adhesion molecules maintains the integrity of the stem cell niche ultimately preserving self-renewal, a hallmark of epithelial stem cells. S tem C ells 2015;33:1642-1656 [ABSTRACT FROM AUTHOR]

A distinct boundary exists between the progenitor cells in the basal limbal epithelium and the more differentiated corneal epithelial basal cells. We have shown that reciprocal expression patterns of EphA2 and Ephrin-A1 are likely to contribute to normal limbal-corneal epithelial compartmentalization as well as play a role in response to injury. How this signaling axis is regulated remains unclear. We have demonstrated that microRNAs (miRNAs) play critical roles in corneal epithelial wound healing and several miRNAs (e.g. miR-210) have been predicted to target ephrins. Previous expression profiling experiments demonstrated that miR-210 is prominently expressed in corneal epithelial cells. RNA-seq data acquired from miR-210-depleted HCECs showed up-regulation of genes involved in cellular migration. In addition, miR-210 is decreased after corneal injury while EphA2 is increased. Moreover, antago-210-treated HCECs markedly enhanced wound closure in a scratch wound assay. Antago-210 treatment resulted in increased EphA2 protein levels as well as pS897-EphA2, the pro-migratory form of EphA2. As expected, Ephrin-A1 levels were reduced, while levels of a well-known target of miR-210, Ephrin-A3, were increased by antago-210 treatment. The increase in migration with antago-210 could be inhibited by Ephrin-A1 overexpression, Ephrin-A1-Fc treatment or siRNA depletion of EphA2. However, depletion of Ephrin-A3 did not have effects on the antago-210-induced increase in migration. In addition, Ephrin-A1 overexpression and siEphA2 dampened EGFR signaling, which is increased by antago-210. Our data clearly demonstrate a link between miR-210 and EphA2/Ephrin-A1 signaling that regulates, in part, corneal epithelial migration. This interaction might potentially control the limbal-corneal epithelial boundary., (© 2021 Federation of American Societies for Experimental Biology.)