Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Tytuł pozycji:

Overexpression of the MSK1 Kinase in Patients With Chronic Lung Allograft Dysfunction and Its Confirmed Role in a Murine Model.

Tytuł:
Overexpression of the MSK1 Kinase in Patients With Chronic Lung Allograft Dysfunction and Its Confirmed Role in a Murine Model.
Autorzy:
Nemska S; Laboratoire d'Innovation Thérapeutique UMR 7200, LabEx Medalis, CNRS, Faculté de Pharmacie, Université de Strasbourg, Illkirch, France.; Institute of Veterinary Physiology and Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Daubeuf F; Laboratoire d'Innovation Thérapeutique UMR 7200, LabEx Medalis, CNRS, Faculté de Pharmacie, Université de Strasbourg, Illkirch, France.; Plateforme de Chimie Biologie Intégrative de Strasbourg (PCBIS) UMS 3286 CNRS, Université de Strasbourg, Labex Medalis, 300 Bld Brant, Illkirch, France.
Obrecht A; Plateforme de Chimie Biologie Intégrative de Strasbourg (PCBIS) UMS 3286 CNRS, Université de Strasbourg, Labex Medalis, 300 Bld Brant, Illkirch, France.
Israel-Biet D; Service de Pneumologie, HEGP, Paris, France.
Stern M; Hôpital Foch, Suresnes, INRAe UMR 0892, Université de Versailles Saint-Quentin Paris-Saclay, Paris, France.
Kessler R; Service de Pneumologie, CHU Strasbourg, Strasbourg, France.
Roux A; Hôpital Foch, Suresnes, INRAe UMR 0892, Université de Versailles Saint-Quentin Paris-Saclay, Paris, France.
Tavakoli R; Institute of Veterinary Physiology and Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland.
Villa P; Plateforme de Chimie Biologie Intégrative de Strasbourg (PCBIS) UMS 3286 CNRS, Université de Strasbourg, Labex Medalis, 300 Bld Brant, Illkirch, France.
Tissot A; CHU Nantes, Inserm, UMR 1064, Centre de Recherche en Transplantation et Immunologie, Nantes Université, ITUN, Nantes, France.; Service de Pneumologie, L'institut du thorax, CHU Nantes, Nantes, France.
Danger R; CHU Nantes, Inserm, UMR 1064, Centre de Recherche en Transplantation et Immunologie, Nantes Université, ITUN, Nantes, France.; Centre d'Investigation Clinique en Biothérapie, Centre de Ressources Biologiques (CRB), Labex IGO, Nantes, France.
Reber L; Laboratoire d'Innovation Thérapeutique UMR 7200, LabEx Medalis, CNRS, Faculté de Pharmacie, Université de Strasbourg, Illkirch, France.
Durand E; CHU Nantes, Inserm, UMR 1064, Centre de Recherche en Transplantation et Immunologie, Nantes Université, ITUN, Nantes, France.
Foureau A; CHU Nantes, Inserm, UMR 1064, Centre de Recherche en Transplantation et Immunologie, Nantes Université, ITUN, Nantes, France.; Service de Pneumologie, L'institut du thorax, CHU Nantes, Nantes, France.
Brouard S; CHU Nantes, Inserm, UMR 1064, Centre de Recherche en Transplantation et Immunologie, Nantes Université, ITUN, Nantes, France.; Centre d'Investigation Clinique en Biothérapie, Centre de Ressources Biologiques (CRB), Labex IGO, Nantes, France.
Magnan A; Service de Pneumologie, L'institut du thorax, CHU Nantes, Nantes, France.
Frossard N; Laboratoire d'Innovation Thérapeutique UMR 7200, LabEx Medalis, CNRS, Faculté de Pharmacie, Université de Strasbourg, Illkirch, France.
Corporate Authors:
COLT consortium
Źródło:
Transplantation [Transplantation] 2021 Jun 01; Vol. 105 (6), pp. 1212-1224.
Typ publikacji:
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: Hagerstown, MD : Lippincott Williams & Wilkins
Original Publication: Baltimore, Williams & Wilkins.
MeSH Terms:
Bronchiolitis Obliterans/*enzymology
Fibroblasts/*enzymology
Lung/*enzymology
Lung Transplantation/*adverse effects
Ribosomal Protein S6 Kinases, 90-kDa/*metabolism
Adolescent ; Adult ; Aged ; Animals ; Bronchiolitis Obliterans/drug therapy ; Bronchiolitis Obliterans/etiology ; Bronchiolitis Obliterans/pathology ; Cell Proliferation ; Cells, Cultured ; Chronic Disease ; Disease Models, Animal ; Female ; Fibroblasts/drug effects ; Fibroblasts/pathology ; France ; Humans ; Interleukin-6/metabolism ; Lung/drug effects ; Lung/pathology ; Lung/surgery ; Male ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Middle Aged ; Protein Kinase Inhibitors/pharmacology ; Re-Epithelialization ; Ribosomal Protein S6 Kinases, 90-kDa/antagonists & inhibitors ; Ribosomal Protein S6 Kinases, 90-kDa/genetics ; T-Lymphocytes/drug effects ; T-Lymphocytes/metabolism ; Up-Regulation ; Young Adult ; Mice
References:
DerHovanessian A, Wallace WD, Lynch JP III, et al. Chronic lung allograft dysfunction: evolving concepts and therapies. Semin Respir Crit Care Med. 2018;39:155–171.
Glanville AR, Verleden GM, Todd JL, et al. Chronic lung allograft dysfunction: definition and update of restrictive allograft syndrome-A consensus report from the Pulmonary Council of the ISHLT. J Heart Lung Transplant. 2019;38:483–492.
Verleden GM, Glanville AR, Lease ED, et al. Chronic lung allograft dysfunction: definition, diagnostic criteria, and approaches to treatment-A consensus report from the Pulmonary Council of the ISHLT. J Heart Lung Transplant. 2019;38:493–503.
Gauthier JM, Ruiz-Pérez D, Li W, et al. Diagnosis, pathophysiology and experimental models of chronic lung allograft rejection. Transplantation. 2018;102:1459–1466.
Royer PJ, Olivera-Botello G, Koutsokera A, et al.; SysCLAD Consortium. Chronic lung allograft dysfunction: a systematic review of mechanisms. Transplantation. 2016;100:1803–1814.
Hayes D Jr. A review of bronchiolitis obliterans syndrome and therapeutic strategies. J Cardiothorac Surg. 2011;6:92.
Yusen RD, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: thirty-second official adult lung and heart-lung transplantation report–2015; focus theme: early graft failure. J Heart Lung Transplant. 2015;34:1264–1277.
Brugière O, Roux A, Le Pavec J, et al. Role of C1q-binding anti-HLA antibodies as a predictor of lung allograft outcome. Eur Respir J. 2018;52:1701898.
Tissot A, Danger R, Claustre J, et al. Early identification of chronic lung allograft dysfunction: the need of biomarkers. Front Immunol. 2019;10:1681.
Vandermeulen E, Lammertyn E, Verleden SE, et al. Immunological diversity in phenotypes of chronic lung allograft dysfunction: a comprehensive immunohistochemical analysis. Transpl Int. 2017;30:134–143.
Aguilar PR, Michelson AP, Isakow W. Obliterative bronchiolitis. Transplantation. 2016;100:272–283.
Sarahrudi K, Estenne M, Corris P, et al. International experience with conversion from cyclosporine to tacrolimus for acute and chronic lung allograft rejection. J Thorac Cardiovasc Surg. 2004;127:1126–1132.
Jain R, Hachem RR, Morrell MR, et al. Azithromycin is associated with increased survival in lung transplant recipients with bronchiolitis obliterans syndrome. J Heart Lung Transplant. 2010;29:531–537.
Morrell MR, Despotis GJ, Lublin DM, et al. The efficacy of photopheresis for bronchiolitis obliterans syndrome after lung transplantation. J Heart Lung Transplant. 2010;29:424–431.
Benden C, Haughton M, Leonard S, et al. Therapy options for chronic lung allograft dysfunction-bronchiolitis obliterans syndrome following first-line immunosuppressive strategies: a systematic review. J Heart Lung Transplant. 2017;36:921–933.
Hachem R, Corris P. Extracorporeal photopheresis for bronchiolitis obliterans syndrome after lung transplantation. Transplantation. 2018;102:1059–1065.
Vermeulen L, De Wilde G, Van Damme P, et al. Transcriptional activation of the NF-kappaB p65 subunit by mitogen- and stress-activated protein kinase-1 (MSK1). EMBO J. 2003;22:1313–1324.
Arthur JSC. MSK activation and physiological roles. Front Biosci. 2008;13:5866–5879.
Reber L, Vermeulen L, Haegeman G, et al. Ser276 phosphorylation of NF-kB p65 by MSK1 controls SCF expression in inflammation. PLoS One. 2009;4:e4393.
Kawaguchi M, Fujita J, Kokubu F, et al. IL-17F-induced IL-11 release in bronchial epithelial cells via MSK1-CREB pathway. Am J Physiol Lung Cell Mol Physiol. 2009;296:L804–L810.
Nozato K, Fujita J, Kawaguchi M, et al. IL-17F induces CCL20 in bronchial epithelial cells. J Allergy (Cairo). 2011;2011:587204.
Reyskens KMSE, Arthur JSC. Emerging roles of the mitogen and stress activated kinases MSK1 and MSK2. Front Cell Dev Biol. 2016;4:56.
Otkjaer K, Kragballe K, Johansen C, et al. IL-20 gene expression is induced by IL-1beta through mitogen-activated protein kinase and NF-kappaB-dependent mechanisms. J Invest Dermatol. 2007;127:1326–1336.
Funding AT, Johansen C, Kragballe K, et al. Mitogen- and stress-activated protein kinase 1 is activated in lesional psoriatic epidermis and regulates the expression of pro-inflammatory cytokines. J Invest Dermatol. 2006;126:1784–1791.
Reber LL, Daubeuf F, Nemska S, et al. The AGC kinase inhibitor H89 attenuates airway inflammation in mouse models of asthma. PLoS One. 2012;7:e49512.
Yu T, Yu Q, Chen X, et al. Exclusive enteral nutrition protects against inflammatory bowel disease by inhibiting NF-κB activation through regulation of the p38/MSK1 pathway. Int J Mol Med. 2018;42:1305–1316.
Li LB, Leung DY, Goleva E. Activated p38 MAPK in peripheral blood monocytes of steroid resistant asthmatics. PLoS One. 2015;10:e0141909.
Hele DJ, Yacoub MH, Belvisi MG. The heterotopic tracheal allograft as an animal model of obliterative bronchiolitis. Respir Res. 2001;2:169–183.
Lemaître P. Study of mechanisms dependent on interleukin-17 and their modulation in development of bronchiolitis obliterans after experimental transplantation. Bull Mem Acad R Med Belg. 2010;165:367–371.
Nakagiri T, Inoue M, Minami M, et al. Immunology mini-review: the basics of T(H)17 and interleukin-6 in transplantation. Transplant Proc. 2012;44:1035–1040.
Jordan SC, Choi J, Kim I, et al. Interleukin-6, a cytokine critical to mediation of inflammation, autoimmunity and allograft rejection: therapeutic implications of IL-6 receptor blockade. Transplantation. 2017;101:32–44.
Hertz MI, Jessurun J, King MB, et al. Reproduction of the obliterative bronchiolitis lesion after heterotopic transplantation of mouse airways. Am J Pathol. 1993;142:1945–1951.
Nemska S, Daubeuf F, Frossard N. Revascularization of the graft in obliterative bronchiolitis after heterotopic tracheal transplantation. Physiol Rep. 2016;4:e12690.
Neuringer IP, Aris RM, Burns KA, et al. Epithelial kinetics in mouse heterotopic tracheal allografts. Am J Transplant. 2002;2:410–419.
Zhao Y, Steidle JF, Upchurch GR, et al. Prevention of the second stage of epithelial loss is a potential novel treatment for bronchiolitis obliterans. J Thorac Cardiovasc Surg. 2013;145:940–947.e1.
Boehler A, Chamberlain D, Kesten S, et al. Lymphocytic airway infiltration as a precursor to fibrous obliteration in a rat model of bronchiolitis obliterans. Transplantation. 1997;64:311–317.
Richards DM, Dalheimer SL, Hertz MI, et al. Trachea allograft class I molecules directly activate and retain CD8+ T cells that cause obliterative airways disease. J Immunol. 2003;171:6919–6928.
KleinJan A, Willart MA, Kuipers H, et al. Inducible costimulator blockade prolongs airway luminal patency in a mouse model of obliterative bronchiolitis. Transplantation. 2008;86:1436–1444.
Montagnoli A, Valsasina B, Croci V, et al. A Cdc7 kinase inhibitor restricts initiation of DNA replication and has antitumor activity. Nat Chem Biol. 2008;4:357–365.
Wu DJ, Xu JZ, Wu YJ, et al. Effects of fasudil on early atherosclerotic plaque formation and established lesion progression in apolipoprotein E-knockout mice. Atherosclerosis. 2009;207:68–73.
Santen S, Wang Y, Laschke MW, et al. Rho-kinase signalling regulates CXC chemokine formation and leukocyte recruitment in colonic ischemia-reperfusion. Int J Colorectal Dis. 2010;25:1063–1070.
Zhuang R, Wu J, Lin F, et al. Fasudil preserves lung endothelial function and reduces pulmonary vascular remodeling in a rat model of end-stage pulmonary hypertension with left heart disease. Int J Mol Med. 2018;42:1341–1352.
McDyer JF. Human and murine obliterative bronchiolitis in transplant. Proc Am Thorac Soc. 2007;4:37–43.
Zhao Y, LaPar DJ, Steidle J, et al. Adenosine signaling via the adenosine 2B receptor is involved in bronchiolitis obliterans development. J Heart Lung Transplant. 2010;29:1405–1414.
Fiser SM, Tribble CG, Long SM, et al. Ischemia-reperfusion injury after lung transplantation increases risk of late bronchiolitis obliterans syndrome. Ann Thorac Surg. 2002;73:1041–1047.
Wang J, Tan J, Liu Y, et al. Amelioration of lung ischemia-reperfusion injury by JNK and p38 small interfering RNAs in rat pulmonary microvascular endothelial cells in an ischemia-reperfusion injury lung transplantation model. Mol Med Rep. 2018;17:1228–1234.
Tatekawa Y, Kanehiro H, Dohi Y, et al. Intragraft expression of p38 and activated p38 MAPK (mitogen-activated protein kinase) in rat small bowel transplantation. Transpl Int. 2001;14:211–216.
Koike N, Takeyoshi I, Ohki S, et al. The comparison of mitogen-activated protein kinases that become activated within the left ventricular and right atrial tissues following heart transplantation in canine model. J Invest Surg. 2007;20:105–111.
Zhang G, Li Z, Meng C, et al. The anti-inflammatory effect of hydrogen on lung transplantation model of pulmonary microvascular endothelial cells during cold storage period. Transplantation. 2018;102:1253–1261.
Ollinger R, Thomas M, Kogler P, et al. Blockade of p38 MAPK inhibits chronic allograft vasculopathy. Transplantation. 2008;85:293–297.
Farivar AS, Mackinnon-Patterson B, Woolley S, et al. FR167653 reduces obliterative airway disease in rats. J Heart Lung Transplant. 2004;23:985–992.
Moens U, Kostenko S, Sveinbjørnsson B. The role of mitogen-activated protein kinase-activated protein kinases (MAPKAPKs) in inflammation. Genes (Basel). 2013;4:101–133.
Abécassis L, Rogier E, Vazquez A, et al. Evidence for a role of MSK1 in transforming growth factor-beta-mediated responses through p38alpha and Smad signaling pathways. J Biol Chem. 2004;279:30474–30479.
El-Gamel A, Sim E, Hasleton P, et al. Transforming growth factor beta (TGF-beta) and obliterative bronchiolitis following pulmonary transplantation. J Heart Lung Transplant. 1999;18:828–837.
El-Wakeel SA, Rahmo RM, El-Abhar HS. Anti-fibrotic impact of Carvedilol in a CCl-4 model of liver fibrosis via serum microRNA-200a/SMAD7 enhancement to bridle TGF-β1/EMT track. Sci Rep. 2018;8:14327.
Tang X, Peng R, Phillips JE, et al. Assessment of Brd4 inhibition in idiopathic pulmonary fibrosis lung fibroblasts and in vivo models of lung fibrosis. Am J Pathol. 2013;183:470–479.
Brasier AR. The nuclear factor-kappaB-interleukin-6 signalling pathway mediating vascular inflammation. Cardiovasc Res. 2010;86:211–218.
Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014;6:a016295.
Da Silva CA, Adda M, Stern M, et al. Marked stem cell factor expression in the airways of lung transplant recipients. Respir Res. 2006;7:90.
Beck IM, Clarisse D, Bougarne N, et al. Mitogen- and stress-activated protein kinase 1 MSK1 regulates glucocorticoid response element promoter activity in a glucocorticoid concentration-dependent manner. Eur J Pharmacol. 2013;715:1–9.
Davies SP, Reddy H, Caivano M, et al. Specificity and mechanism of action of some commonly used protein kinase inhibitors. Biochem J. 2000;351(Pt 1):95–105.
Anderson DR, Meyers MJ, Vernier WF, et al. Pyrrolopyridine inhibitors of mitogen-activated protein kinase-activated protein kinase 2 (MK-2). J Med Chem. 2007;50:2647–2654.
Masaoka H, Takasato Y, Nojiri T, et al. Clinical effect of Fasudil hydrochloride for cerebral vasospasm following subarachnoid hemorrhage. Acta Neurochir Suppl. 2001;77:209–211.
Boehler A, Estenne M. Post-transplant bronchiolitis obliterans. Eur Respir J. 2003;22:1007–1018.
Verleden SE, Sacreas A, Vos R, et al. Advances in understanding bronchiolitis obliterans after lung transplantation. Chest. 2016;150:219–225.
Tissot A, Foureau A, Brosseau C, et al.; consortium COLT. [COLT: Ten years of research in lung transplantation, results and perspectives]. Rev Mal Respir. 2018;35:699–705.
Golocheikine AS, Saini D, Ramachandran S, et al. Soluble CD30 levels as a diagnostic marker for bronchiolitis obliterans syndrome following human lung transplantation. Transpl Immunol. 2008;18:260–263.
Pain M, Royer PJ, Loy J, et al.; COLT Consortium. T cells promote bronchial epithelial cell secretion of matrix metalloproteinase-9 via a C-C chemokine receptor type 2 pathway: implications for chronic lung allograft dysfunction. Am J Transplant. 2017;17:1502–1514.
Scholma J, Slebos DJ, Boezen HM, et al. Eosinophilic granulocytes and interleukin-6 level in bronchoalveolar lavage fluid are associated with the development of obliterative bronchiolitis after lung transplantation. Am J Respir Crit Care Med. 2000;162:2221–2225.
Hall DJ, Baz M, Daniels MJ, et al. Immediate postoperative inflammatory response predicts long-term outcome in lung-transplant recipients. Interact Cardiovasc Thorac Surg. 2012;15:603–607.
Saito T, Takahashi H, Kaneda H, et al. Impact of cytokine expression in the pre-implanted donor lung on the development of chronic lung allograft dysfunction subtypes. Am J Transplant. 2013;13:3192–3201.
Ananieva O, Darragh J, Johansen C, et al. The kinases MSK1 and MSK2 act as negative regulators of Toll-like receptor signaling. Nat Immunol. 2008;9:1028–1036.
Darragh J, Ananieva O, Courtney A, et al. MSK1 regulates the transcription of IL-1ra in response to TLR activation in macrophages. Biochem J. 2010;425:595–602.
Elcombe SE, Naqvi S, Van Den Bosch MW, et al. Dectin-1 regulates IL-10 production via a MSK1/2 and CREB dependent pathway and promotes the induction of regulatory macrophage markers. PLoS One. 2013;8:e60086.
Fullerton JN, Gilroy DW. Resolution of inflammation: a new therapeutic frontier. Nat Rev Drug Discov. 2016;15:551–567.
Lawrence T, Fong C. The resolution of inflammation: anti-inflammatory roles for NF-kappaB. Int J Biochem Cell Biol. 2010;42:519–523.
Substance Nomenclature:
0 (IL6 protein, human)
0 (Interleukin-6)
0 (Protein Kinase Inhibitors)
EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 90-kDa)
EC 2.7.11.1 (mitogen and stress-activated protein kinase 1)
Entry Date(s):
Date Created: 20210209 Date Completed: 20210726 Latest Revision: 20240226
Update Code:
20240226
DOI:
10.1097/TP.0000000000003606
PMID:
33560725
Czasopismo naukowe
Background: Chronic lung allograft dysfunction (CLAD) and its obstructive form, the obliterative bronchiolitis (OB), are the main long-term complications related to high mortality rate postlung transplantation. CLAD treatment lacks a significant success in survival. Here, we investigated a new strategy through inhibition of the proinflammatory mitogen- and stress-activated kinase 1 (MSK1) kinase.
Methods: MSK1 expression was assessed in a mouse OB model after heterotopic tracheal allotransplantation. Pharmacological inhibition of MSK1 (H89, fasudil, PHA767491) was evaluated in the murine model and in a translational model using human lung primary fibroblasts in proinflammatory conditions. MSK1 expression was graded over time in biopsies from a cohort of CLAD patients.
Results: MSK1 mRNA progressively increased during OB (6.4-fold at D21 posttransplantation). Inhibition of MSK1 allowed to counteract the damage to the epithelium (56% restoration for H89), and abolished the recruitment of MHCII+ (94%) and T cells (100%) at the early inflammatory phase of OB. In addition, it markedly decreased the late fibroproliferative obstruction in allografts (48%). MSK1 inhibitors decreased production of IL-6 (whose transcription is under the control of MSK1) released from human lung fibroblasts (96%). Finally, we confirmed occurrence of a 2.9-fold increased MSK1 mRNA expression in lung biopsies in patients at 6 months before CLAD diagnosis as compared to recipients with stable lung function.
Conclusions: These findings suggest the overall interest of the MSK1 kinase either as a marker or as a potential therapeutic target in lung dysfunction posttransplantation.
Competing Interests: The authors declare no conflicts of interest.
(Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies