Functional Microendoscopy Reveals Calcium Responses of Single Cells in Tracheal Tuft Cells and Kidney Podocytes.

Microendoscopy, a crucial technology for minimally invasive investigations of organs, facilitates studies within confined cavities. However, conventional microendoscopy is often limited by probe size and the constraint of using a single excitation wavelength. In response to these constraints, a multichannel microendoscope with a slender profile of only 360 µm is engineered.

A family of NADPH/NADP biosensors reveals in vivo dynamics of central redox metabolism across eukaryotes.

The NADPH/NADP redox couple is central to metabolism and redox signalling. NADP redox state is differentially regulated by distinct enzymatic machineries at the subcellular compartment level. Nonetheless, a detailed understanding of subcellular NADP redox dynamics is limited by the availability of appropriate tools.

Glucose-stimulated insulin secretion depends on FFA1 and Gq in neonatal mouse islets.

Aims/hypothesis: After birth, the neonatal islets gradually acquire glucose-responsive insulin secretion, a process that is subjected to maternal imprinting. Although NEFA are major components of breastmilk and insulin secretagogues, their role for functional maturation of neonatal beta cells is still unclear. NEFA are the endogenous ligands of fatty acid receptor 1 (FFA1, encoded by Ffar1 in mice), a Gq-coupled receptor with stimulatory effect on insulin secretion.

The loss of pancreatic islet NADPH oxidase (NOX)2 improves islet transplantation.

Islet transplantation is a promising treatment strategy for type 1 diabetes mellitus (T1DM) patients. However, oxidative stress-induced graft failure due to an insufficient revascularization is a major problem of this therapeutic approach. NADPH oxidase (NOX)2 is an important producer of reactive oxygen species (ROS) and several studies have already reported that this enzyme plays a crucial role in the endocrine function and viability of β-cells.

Targeting Pancreatic Islet NLRP3 Improves Islet Graft Revascularization.

Hypoxia-induced islet cell death, caused by an insufficient revascularization of the grafts, is a major obstacle for successful pancreatic islet transplantation. Recently, it has been reported that the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is expressed in pancreatic islets and that its loss protects against hypoxia-induced cell death. Therefore, we hypothesized that the inhibition of NLRP3 in islets improves the survival and endocrine function of the grafts.

Evidence for NADPH oxidase activation by GPR40 in pancreatic β-cells.

Investigate the involvement of the fatty acids receptor GPR40 in the assembly and activation of NADPH oxidase and the implications on pancreatic β-cell function. BRIN-BD11 β-cells were exposed to GPR40 agonist (GW9508) or linoleic acid in different glucose concentrations. Superoxide and HO were analyzed, respectively, by DHE fluorescence and by fluorescence of the HO sensor, roGFP2-Orp1.