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.
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.
While insulinomas and proinsulin-secreting tumors have many physiologic parallels, these cases illustrate several key distinctions in their diagnosis and management.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.