Therefore, using time-resolved confocal fluorescence monitoring with MitoSOX Red, we investigated various effects of mitochondria-targeted antioxidants in model pancreatic <i>β</i>-cells (insulinomaINS-1E cells) and pancreatic islets.
Here, we describe experimental protocols to knock down β-arrestins by small interference RNA, to follow subcellular localization of β-arrestins in the cytosol and nucleus of the insulinomaINS-1E rat pancreatic β-cell line, and to analyze β-arrestin protein expression by Western blot using INS-1E cells and isolated mouse or human pancreatic islets.
Glucose stimulation consistently resulted in acidification of the matrix pH in INS-1E insulinoma cells and β-cells in intact human islets or islet monolayer cultures.
Effects on cell viability and apoptosis were assessed in insulinoma cell lines INS-1E (rat) and MIN6 (mouse) <i>in vitro</i> and were confirmed <i>in vivo</i> by using a mouse model of hepatic tumor dissemination after intrasplenic xenograft.
To test the hypothesis that pro-inflammatory cytokines impair glucose-stimulated insulin secretion (GSIS) by inhibiting oxidative ATP synthesis, we probed insulin release and real-time mitochondrial respiration in rat INS-1E insulinoma cells that were exposed to a combination of 2 ng/mL interleukin-1-beta and 50 ng/mL interferon-gamma.
While insulinomas and proinsulin-secreting tumors have many physiologic parallels, these cases illustrate several key distinctions in their diagnosis and management.
The proinsulin levels and proinsulin/insulin molar ratio in patients with malignant versus benign insulinoma were 334 versus 44 pmol/L and 2.1 versus 0.9, respectively.
In insulinoma β-cells (INS-1E), Resv is previously shown to improve glucose-stimulated insulin secretion in a Sirt1-dependent mechanism and to protect against β-cell dedifferentiation in non-human primates, while inducing hypertrophy in myoblasts.
The read-through transcript INS-IGF2, composed of exons from the two genes proinsulin precursor (INS) and insulin‑like growth factor 2 (IGF2), both mapping to chromosomal subband 11p15.5, was highly expressed in the two insulinomas analyzed.
We have recently shown that palmitate-induced loss of INS-1E insulinoma cells is related to increased reactive oxygen species (ROS) production as both toxic effects are prevented by palmitoleate.
The present study provides evidence that chronically elevated concentrations of leptin and glucose induce beta-cell apoptosis through activation of the JNK pathway in human islets and in insulinoma (INS 832/13) cells.
Small interfering RNA-mediated attenuation of SOX6 expression stimulated the proliferation of insulinomaINS-1E and NIH-3T3 cells, whereas retroviral overexpression resulted in inhibition of cell growth.
Intracellular degradation of the C-peptide of proinsulin, in a human insulinoma: identification of sites of cleavage and evidence for a role for cathepsin B.
Much of the E1A-induced preproinsulin mRNA had a 5' end at the same position as the preproinsulin mRNA isolated from insulinoma cells, but a considerable fraction had 5' ends mapping heterogeneously within several hundred nucleotides of this site.
Thus, cell-free translation of human insulinoma mRNA yields an immunoreactive insulin larger than proinsulin, which is the same size as fish and rat preproinsulins recently described.