alexa Transcriptional and Functional Plasticity Induced by Chronic Insulin Exposure in a Mast Cell-Like Basophilic Leukemia Cell Model | OMICS International| Abstract
ISSN 2476-1966

Journal of Immunobiology
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  • Research Article   
  • J immuno Biol 2017, Vol 2(4): 135
  • DOI: 10.4172/2476-1966.1000135

Transcriptional and Functional Plasticity Induced by Chronic Insulin Exposure in a Mast Cell-Like Basophilic Leukemia Cell Model

Chad Jansen1#, Mark Speck1#, William E Greineisen1, Kristina Maaetoft-Udsen1, Edward Cordasco1,2, Lori MN Shimoda1, Alexander J Stokes3 and Helen Turner1*
1Laboratory of Immunology and Signal Transduction, Chaminade University, Honolulu, Hawai‘i, USA
2Undergraduate Program in Biochemistry, Chaminade University, Honolulu, Hawai‘i, USA
3Laboratory of Experimental Medicine, Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawai‘i, USA
#Contributed equally to this work
*Corresponding Author : Helen Turner, Professor of Biology, Laboratory of Immunology and Signal Transduction, Chaminade University, 3140 Waialae Ave, WSC116, Honolulu, Hawai'i, 96816, USA, Tel: 1 (808) 739 8399, Email: [email protected]

Received Date: Nov 17, 2017 / Accepted Date: Dec 06, 2017 / Published Date: Dec 11, 2017

Abstract

Objective: Secretory granules (SG) and lipid bodies (LB) are the primary organelles that mediate functional responses in mast cells. SG contains histamine and matrix-active proteases, while LB are reservoirs of arachidonic acid and its metabolites, precursors for rapid synthesis of eicosanoids such as LTC4. Both of these compartments can be dynamically or ontologically regulated, with metabolic and immunological stimuli altering lipid body content and granule numbers responding to contextual signals from tissue. We previously described that chronic in vitro or in vivo hyperinsulinemia expands the LB compartment with a concomitant loss of SG capacity, suggesting that this ratio is dynamically regulated. The objective of the current study is to determine if chronic insulin exposure initiates a transcriptional program that biases model mast cells towards a lipogenic state with accompanying loss of secretory granule biogenesis.

Methods: We used a basophilic leukemic cell line with mucosal mast cell-like features as a model system. We tested the hypothesis that chronic insulin exposure initiates a transcriptional program that biases these model mast cells towards a lipogenic state with accompanying loss of secretory granule biogenesis. Transcriptional arrays were used to map gene expression patterns. Biochemical, immunocytochemical and mediator release assays were used to evaluate organelle numbers and functional responses.

Results: In a mucosal mast cell model, the rat basophilic leukemia line RBL2H3, mast cell granularity and SG numbers are inversely correlated with LB numbers. Chronic insulin exposure appears to modulate gene networks involved in both lipid body biogenesis and secretory granule formation. Western blot analysis confirms upregulation of protein levels for LB proteins, and decreases in proteins that are markers for SG cargo.

Conclusions: The levels of insulin in the extracellular milieu may modify the phenotype of mast cell-like cells in vitro.

Keywords: Secretory granules; Lipid bodies; Mast cells; Plasticity; Hyperinsulinemia; Chronic insulin exposure; Immune system

Citation: Jansen C, Speck M, Greineisen WE, Maaetoft-Udsen K, Cordasco E, et al. (2017) Transcriptional and Functional Plasticity Induced by Chronic Insulin Exposure in a Mast Cell-Like Basophilic Leukemia Cell Model. J Immuno Biol 2: 135. Doi: 10.4172/2476-1966.1000135

Copyright: ©2017 Jansen C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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