Creative Destruction: Towards a Theology of Institutions

A theology of institutions is dependent upon an imagination sparked by the cross and shaped by the hope of the resurrection. Creative destruction is the institutional process of dying so that new life might flourish for the sake of others. Relying upon the institutional imagination of James K.A. Smith, the institutional particularity of David Fitch, and L. Gregory Jones’ traditioned innovation, creative destruction becomes a means of institutional discipleship. When an institution practices creative destruction, it learns to remember, imagine, and be present so that it might cultivate habits of faithful innovation. As institutions learn to take up their cross a clearer telos comes into view and collaboration across various organizations becomes possible for a greater good. Institutions that take up the practice of creative destruction can reimagine, reset, restart or resurrect themselves through a kind of dying so that new life can emerge. Creative destruction is an apologetic for an institutional way of being-in-the-world for the sake of all beings-in-the-world.

Synergy between Piezo1 and Piezo2 channels confers high-strain mechanosensitivity to articular cartilage.

Diarthrodial joints are essential for load bearing and locomotion. Physiologically, articular cartilage sustains millions of cycles of mechanical loading. Chondrocytes, the cells in cartilage, regulate their metabolic activities in response to mechanical loading. Pathological mechanical stress can lead to maladaptive cellular responses and subsequent cartilage degeneration. We sought to deconstruct chondrocyte mechanotransduction by identifying mechanosensitive ion channels functioning at injurious levels of strain. We detected robust expression of the recently identified mechanosensitive channels, PIEZO1 and PIEZO2. Combined directed expression of Piezo1 and -2 sustained potentiated mechanically induced Ca(2+) signals and electrical currents compared with single-Piezo expression. In primary articular chondrocytes, mechanically evoked Ca(2+) transients produced by atomic force microscopy were inhibited by GsMTx4, a PIEZO-blocking peptide, and by Piezo1- or Piezo2-specific siRNA. We complemented the cellular approach with an explant-cartilage injury model. GsMTx4 reduced chondrocyte death after mechanical injury, suggesting a possible therapy for reducing cartilage injury and posttraumatic osteoarthritis by attenuating Piezo-mediated cartilage mechanotransduction of injurious strains.