Effects of morphine preconditioning on TRPV1 sensitization and ERK1/2 phosphorylation induced by TGFβ1 in neurocytes.
Animals
Cells, Cultured
Ganglia, Spinal
/ drug effects
Ischemic Preconditioning, Myocardial
/ methods
MAP Kinase Signaling System
/ physiology
Morphine
/ pharmacology
Myocardial Reperfusion Injury
/ metabolism
Neurons
/ drug effects
Phosphorylation
Rats
Rats, Sprague-Dawley
Reperfusion Injury
/ metabolism
TRPV Cation Channels
/ metabolism
Transforming Growth Factor beta1
/ metabolism
Journal
Neuroreport
ISSN: 1473-558X
Titre abrégé: Neuroreport
Pays: England
ID NLM: 9100935
Informations de publication
Date de publication:
24 03 2021
24 03 2021
Historique:
entrez:
4
3
2021
pubmed:
5
3
2021
medline:
15
12
2021
Statut:
ppublish
Résumé
Myocardium ischemia-reperfusion injury (IRI) is the major cause of cardiac dysfunction. While intrathecal morphine preconditioning (MPC) can alleviate IRI in animal model, the molecular processes underlying IRI and MPC remain elusive. This study aims to test whether pretreatment with morphine can ameliorate the increased activity of transient receptor potential vanilloid 1 (TRPV1) induced by transforming growth beta1 (TGFβ1) in cultured dorsal root ganglion neurons as a model of the effects of cardiac ischemia on nociceptive primary afferent neurons. To simulate the effect of MPC on dorsal root ganglia (DRG) neurons during myocardial IRI in vivo, the cells were pretreated with morphine for 10 min, followed by wash-out for 30 min before TGFβ1 was added. Afterwards, DRG neurons and N2a cells in all groups were stimulated by capsaicin, and the inward current induced by capsaicin were detected by whole-cell recording on DRG neurons; the expression of TRPV1, phosphorylated (p) TRPV1, ERK1/2, and pERK1/2 were detected by western blot in N2a cells. In comparison with cells with normal culture, the inward current was enhanced of cells incubated with TGFβ1 (P < 0.05), and the relative expression of TRPV1, pTRPV1, and pERK1/2 was upregulated as well (P < 0.05); In comparison with cells incubated with TGFβ1, the inward current induced by capsaicin were decreased by pretreatment with morphine (P < 0.05), Moreover, the relative expression of TRPV1, pTRPV1, and pERK1/2 were also reduced by MPC (P < 0.05). MPC inhibits TRPV1 sensitized by TGFβ1 in DRG cells, and the mechanism might be associated with the downregulation of pERK1/2 expression.
Identifiants
pubmed: 33661801
doi: 10.1097/WNR.0000000000001603
pii: 00001756-202103020-00001
doi:
Substances chimiques
TRPV Cation Channels
0
Transforming Growth Factor beta1
0
Trpv1 protein, rat
0
Morphine
76I7G6D29C
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
339-344Informations de copyright
Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
Références
Montaigne D, Marechal X, Modine T, Coisne A, Mouton S, Fayad G, et al. Daytime variation of perioperative myocardial injury in cardiac surgery and its prevention by Rev-Erbα antagonism: a single-centre propensity-matched cohort study and a randomised study. Lancet. 2018; 391:59–69.
Ruetzler K, Khanna AK, Sessler DI. Myocardial injury after noncardiac surgery: preoperative, intraoperative, and postoperative aspects, implications, and directions. Anesth Analg. 2020; 131:173–186.
Foreman RD. Mechanisms of cardiac pain. Annu Rev Physiol. 1999; 61:143–167.
He SF, Jin SY, Yang W, Pan YL, Huang J, Zhang SJ, et al. Cardiac μ-opioid receptor contributes to opioid-induced cardioprotection in chronic heart failure. Br J Anaesth. 2018; 121:26–37.
Caterina MJ, Schumacher MA, Tominaga M, Rosen TA, Levine JD, Julius D. The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature. 1997; 389:816–824.
Xu S, Xu Y, Cheng X, Huang C, Pan Y, Jin S, et al. Inhibition of DRG-TRPV1 upregulation in myocardial ischemia contributes to exogenous cardioprotection. J Mol Cell Cardiol. 2020; 138:175–184.
Dou M, Ma Z, Cheng X, Zou G, Xu Y, Huang C, et al. Intrathecal lentivirus-mediated RNA interference targeting nerve growth factor attenuates myocardial ischaemia-reperfusion injury in rat. Br J Anaesth. 2019; 123:439–449.
Mehta JL, Attramadal H. The TGFbeta superfamily in cardiovascular biology. Cardiovasc Res. 2007; 74:181–183.
Xu Q, Zhang XM, Duan KZ, Gu XY, Han M, Liu BL, et al. Peripheral TGF-β1 signaling is a critical event in bone cancer-induced hyperalgesia in rodents. J Neurosci. 2013; 33:19099–19111.
Utreras E, Prochazkova M, Terse A, Gross J, Keller J, Iadarola MJ, Kulkarni AB. TGF-β1 sensitizes TRPV1 through Cdk5 signaling in odontoblast-like cells. Mol Pain. 2013; 9:24.
Lu YX, Gu QL, Du J, Zhao J, Liu C, Huang XL, Zou JZ. Upper airway cough syndrome in children and two inflammatory factors: TRPV1 and TGF-β2. Int J Pediatr Otorhinolaryngol. 2014; 78:445–450.
Hausenloy DJ, Yellon DM. Cardioprotective growth factors. Cardiovasc Res. 2009; 83:179–194.
Sablotzki A, Welters I, Lehmann N, Menges T, Görlach G, Dehne M, Hempelmann G. Plasma levels of immunoinhibitory cytokines interleukin-10 and transforming growth factor-beta in patients undergoing coronary artery bypass grafting. Eur J Cardiothorac Surg. 1997; 11:763–768.
Burkey TH, Hingtgen CM, Vasko MR. Isolation and culture of sensory neurons from the dorsal-root ganglia of embryonic or adult rats. Methods Mol Med. 2004; 99:189–202.
Salto R, Vílchez JD, Girón MD, Cabrera E, Campos N, Manzano M, et al. β-hydroxy-β-methylbutyrate (HMB) promotes neurite outgrowth in neuro2a cells. PLoS One. 2015; 10:e0135614.
Chen Y, Kanju P, Fang Q, Lee SH, Parekh PK, Lee W, et al. TRPV4 is necessary for trigeminal irritant pain and functions as a cellular formalin receptor. Pain. 2014; 155:2662–2672.
Owen DE, Egerton J. Culture of dissociated sensory neurons from dorsal root ganglia of postnatal and adult rats. Methods Mol Biol. 2012; 846:179–187.
Liu DL, Wang WT, Xing JL, Hu SJ. Research progress in transient receptor potential vanilloid 1 of sensory nervous system. Neurosci Bull. 2009; 25:221–227.