The third pillar of metal homeostasis in Cupriavidus metallidurans CH34: preferences are controlled by extracytoplasmic function sigma factors.

The role of extracytoplasmic function (ECF) sigma factors in multiple metal homeostasis of the metallophilic bacterium Cupriavidus metallidurans was studied. RNA sequencing was used to predict 3084 operons in the genome of this bacterium, including 11 for ECF sigma factors, and to measure transcript abundances. Mutants carrying multiple deletions in genes for ECF sigma factors were constructed and characterized.

Platelets are relevant mediators of renal injury induced by primary endothelial lesions.

Several studies have suggested a prominent (pro)inflammatory and harmful role of platelets in renal disease, and newer work has also demonstrated platelet release of proangiogenic factors. In the present study, we investigated the role of platelets in a mouse model of selective endothelial cell injury using either platelet depletion or the pharmacological P2Y12 receptor blocker clopidogrel as an interventional strategy. The concanavalin A/anti-concanavalin A model was induced in left kidneys of C57bl/6J wild-type mice after initial platelet depletion or platelet-inhibiting therapy using clopidogrel.

FurC regulates expression of zupT for the central zinc importer ZupT of Cupriavidus metallidurans.

The zinc importer ZupT is required for the efficient allocation of zinc to zinc-dependent proteins in the metal-resistant bacterium Cupriavidus metallidurans but not for zinc import per se. The expression of zupT is upregulated under conditions of zinc starvation. C.

Histones from dying renal cells aggravate kidney injury via TLR2 and TLR4.

In AKI, dying renal cells release intracellular molecules that stimulate immune cells to secrete proinflammatory cytokines, which trigger leukocyte recruitment and renal inflammation. Whether the release of histones, specifically, from dying cells contributes to the inflammation of AKI is unknown. In this study, we found that dying tubular epithelial cells released histones into the extracellular space, which directly interacted with Toll-like receptor (TLR)-2 (TLR2) and TLR4 to induce MyD88, NF-κB, and mitogen activated protein kinase signaling.

Enhanced progenitor cell recruitment and endothelial repair after selective endothelial injury of the mouse kidney.

Primary and/or secondary injury of the renal microvascular endothelium is a common finding in various renal diseases. Besides well-known endothelial repair mechanisms, including endothelial cell (EC) proliferation and migration, homing of extrinsic cells such as endothelial progenitor cells (EPC) and hematopoietic stem cells (HSC) has been shown in various organs and may contribute to microvascular repair. However, these mechanisms have so far not been studied after selective microvascular injury in the kidney.