MOJ ISSN: 2374-6912MOJCSR

Cell Science & Report
Editorial
Volume 3 Issue 4 - 2016
Unfolding the Role of PKC Isoforms in Intestinal Physiology
Patrice G Bouyer*, Natasa Petreska and Jesse Smallwood
Department of Biology, Valparaiso University, USA
Received: July 18, 2016 | Published: August 02, 2016
*Corresponding author: Patrice G Bouyer, Department of Biology, Valparaiso University, Neils Science Center, Valparaiso, USA, Tel: 219-464-5487; Fax: 219-464-5489; Email:
Citation: Bouyer PG, Petreska N, Smallwood J (2016) Unfolding the Role of PKC Isoforms in Intestinal Physiology. MOJ Cell Sci Rep 3(4): 00063. DOI: 10.15406/mojcsr.2016.03.00063

Editorial

The protein kinase C (PKC) family has twelve isoforms [1], and the number of biological events driven by PKC isoforms is expanding. Some of the pathways the PKCs are involved encompass, but not restricted to: cell division, migration, apoptosis, protein trafficking, regulation of ion transport and barrier function [1-3]. Maintenance of intestinal barrier function is critical in order to preserve normal transepithelial transport as well as to prevent pathogens and toxins from entering the body [4]. For instance, PKCα, PKCβII, PKCδ, PKCε or PKCh have been shown to modulate intestinal barrier integrity during inflammation or cell injury [3], by phosphorylating tight junction proteins or cytoskeleton proteins [3,4] . Some of the previous mentioned PKC isoforms are also involved in the regulation of ion transport in the intestine. For example, PKCα is a well known regulator of the Na/H exchanger, which participates in NaCl absorption in the intestine [5]. PKCε and PKCδ are implicated in the internalization of the Na-K-2Cl cotransporter 1, and thus decrease in fluid secretion in the colon [6]. In addition PKCδ has been also suggested to decrease Cl− secretion in the colon by blocking the K+-channel KCNQ1 [7].

As mentioned, the same isoform can be involved in very different biological processes. Thus, one important question arising from these observations: How is the same isoform driving specifically different biological events? Specificity is conveyed by the spatio-temporal distribution of the isoform, which is dependent on the association of the isoform with specific binding proteins such as receptor activated C kinase, A kinase anchoring protein or annexins [8,9]. The second mechanism being the target proteins phosphorylated by PKC isoform such as myristoylated, alanine rich C kinase substrate or adducin [9,10]. To date the proteins implicated in the specificity of the PKC isoform in intestinal biology (e.g., ion transport, barrier function) remains elusive. Much work is need if we intend to understand how barrier function and ion transport are regulated by the PKC in normal and disease states in the intestine. Defining the scaffolding and target proteins of the PKC isoform may prove very useful targets to treat diseases such intestinal inflammation or cancer [11].

References           

  1. Medina FJ, Tunez I (2013) Mechanisms and pathways underlying the therapeutic effect of transcranial magnetic stimulation. Rev Neurosci 24(5): 507-525.
  2. Abidin S, Trippe J, Funke K, Eysel UT, Benali A (2008) High- and low-frequency repetitive transcranial magnetic stimulation differentially activates c-Fos and zif268 protein expression in the rat brain. Exp Brain Res188(2): 249-261.
  3. Hellmann J, Juttner R, Roth C, Bajbouj M, Kirste I, et al. (2012) Repetitive magnetic stimulation of human-derived neuron-like cells activates cAMP-CREB pathway. Eur Arch Psychiatry Clin Neurosci 262(1): 87-91.
  4. Tasset I, Medina FJ, Jimena I, Aguera E, Gascon F, et al. (2012) Neuroprotective effects of extremely low-frequency electromagnetic fields on a Huntington's disease rat model: effects on neurotrophic factors and neuronal density. Neuroscience 209: 54-63.
  5. Ma J, Zhang Z, Su Y, Kang L, Geng D, et al. (2013) Magnetic stimulation modulates structural synaptic plasticity and regulates BDNF-TrkB signal pathway in cultured hippocampal neurons. Neurochem Int 62(1): 84-91.
  6. Cheeran B, Talelli P, Mori F, Koch G, Suppa A, et al. (2008) A common polymorphism in the brain-derived neurotrophic factor gene (BDNF) modulates human cortical plasticity and the response to rTMS. J Physiol 586(23): 5717-5725.
  7. Uhm KE, Kim YH, Yoon KJ, Hwang JM, Chang WH (2015) BDNF genotype influence the efficacy of rTMS in stroke patients. Neurosci Lett 594: 117-121.
  8. Strube W, Nitsche MA, Wobrock T, Bunse T, Rein B, et al. (2015) BDNF-Val66Met-polymorphism impact on cortical plasticity in schizophrenia patients: a proof-of-concept study. Int J Neuropsychopharmacol 18(4).
  9. Chiavetto L, Miniussi C, Zanardini R, Gazzoli A, Bignotti S, et al. (2008) 5-HTTLPR and BDNF Val66Met polymorphisms and response to rTMS treatment in drug resistant depression. Neurosci Lett 437(2): 130-134.
  10. Malaguti A, Rossini D, Lucca A, Magri L, Lorenzi C, et al. (2011) Role of COMT, 5-HT(1A), and SERT genetic polymorphisms on antidepressant response to Transcranial Magnetic Stimulation. Depress Anxiety 28(7): 568-573.
  11. Chen J, Zhou C, Wu B, Wang Y, Li Q, et al. (2013) Left versus right repetitive transcranial magnetic stimulation in treating major depression: a meta-analysis of randomised controlled trials. Psychiatry Res 210(3): 1260-1264.
  12. Fidalgo TM, Morales JL, Muzy GS, Chiavetta NM, Mendonca ME, et al. (2014) Biological markers in noninvasive brain stimulation trials in major depressive disorder: a systematic review. J ECT 30(1): 47-61.
  13. Lefaucheur JP, Andre-Obadia N, Antal A, Ayache SS, Baeken C, et al. (2014) Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS). Clin Neurophysiol 125(11): 2150-2206.
  14. Medina FJ, Tunez I (2010) Huntington's disease: the value of transcranial meganetic stimulation. Curr Med Chem 17(23): 2482-2491.
© 2014-2016 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at http://medcraveonline.com
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy