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Florio, P., Luisi, S., Marchetti, P., Lupi, R., Cobellis, L., Falaschi, C., Sugino, H., Navalesi, R., Genazzani, A.R. and Petraglia, F. (2000) Activin A Stimulates Insulin Secretion in Cultured Human Pancreatic Islets. Journal of Endocrinological Investigation, 23, 231-234.
https://doi.org/10.1007/BF03343713

has been cited by the following article:

  • TITLE: Transcriptome Profiles and Gene Expression of Min6 Cells Are Altered by Pancreatic Stellate Cells

    AUTHORS: Ratnakar Reddy Bynigeri, Sasikala Mitnala, Ravikanth Vishnubhotla, Rupjyoti Talukdar, Surya Satyanarayana Singh, Nageshwar Reddy Duvvuru

    KEYWORDS: β-Cells, Gene Expression, Islets, Pancreatic Stellate Cells, Tran-scriptome

    JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.9 No.6, June 28, 2018

    ABSTRACT: Aim: To identify the influence of pancreatic stellate cell (PSCs) secretions on gene expression profiles of Min6 cells by whole transcriptome sequencing. Methods: Pancreatic stellate cells (PSCs) were isolated from C57BL6J mice and propagated in vitro to acquire the activated phenotype. Total RNA was isolated from monocultured (MC) and PSC cocultured (CC) Min6 cells to prepare cDNA libraries, which were subjected to whole transcriptome sequencing for identifying differential expression of β-cell transcription factors (Pdx-1, Rfx6 and NeuroD1) related to insulin gene transcription and GSIS related genes such as Glut2, Gck, Abcc8, Kcnj11 and L-type Ca2+ channels (Cacnb2, Cacna1c). qRT-PCR was used to validate the gene expression. GSIS of Min6 cells was examined by estimating insulin levels in response to high glucose challenge. Results: Transcriptome analysis of discovery set revealed that coculture of Min6 cells with PSCs caused increased expression of β-cell specific genes (Ins1, Rfx6 and NeuroD1) concomitant with decreased expression of Pdx-1, MafA and Nkx2-2. Expression of GSIS associated genes (Glut2, Gck, Abcc8, Kcnj11 and Cacnb2) was decreased in such conditions. Validation by qRT-PCR in Min6 cells cocultured with PSCs revealed increased significant expression of Ins1 (2.1 ± 0.22 folds; p ≤ 0.001), Rfx6 (1.68 ± 0.23 folds; p ≤ 0.002) and NeuroD1 (0.96 ± 0.11 folds; p ≤ 0.01), accompanied by downregulation of Cacnb2 (-0.93 ± 0.57 folds; p ≤ 0.05). PSC secretions did not restore the GSIS from glucose unresponsive higher passage Min6 cells (MC: 1.33 ± 0.42; CC: 1.55 ± 0.72 pmol/mg protein; p = ns) upon high glucose stimulation. However, glucose responsive higher passage Min6 cells cocultured with PSCs presented increased insulin secretion (MC: 7.025 ± 0.64; CC: 14.84 ± 1.01 pmol/mg protein; p ≤ 0.04) concomitant with marginal increase of insulin contents. Conclusion: PSC secretions increase Ins1, Rfx6 and NeuroD1 gene expression, GSIS from glucose responsive Min6 cells, but do not restore the GSIS from glucose unresponsive Min6 cells.