Proteomic analysis exploring the mechanism of bladder fibrosis induced by ketamine using a rat model.
Proteomic
bladder fibrosis
ketamine
Journal
Translational andrology and urology
ISSN: 2223-4691
Titre abrégé: Transl Androl Urol
Pays: China
ID NLM: 101581119
Informations de publication
Date de publication:
Aug 2021
Aug 2021
Historique:
received:
23
04
2021
accepted:
02
07
2021
entrez:
17
9
2021
pubmed:
18
9
2021
medline:
18
9
2021
Statut:
ppublish
Résumé
Long-term abuse of ketamine can cause irreversible bladder fibrosis, but the mechanism of bladder fibrosis is still under investigation. This study aims to explore the mechanism of bladder fibrosis utilizing proteomic analysis in a rat model. After building a rat model, hematoxylin and eosin (HE) staining, Masson's trichrome staining, and western blotting (WB) of collagen I were used to assess bladder pathology and fibrosis in a rat model. Next, protein expression changes in the rat bladder by proteomic technology were quantitatively detected, and reverse transcription-polymerase chain reaction (RT-PCR) and WB were used to verify the expression of proteins. Bioinformatic techniques and functional analysis were also performed. Compared to the control group, thinning of the bladder epithelium layer, infiltration of submucosal inflammatory cells, deposition of many collagen fibers, and an elevated expression of collagen I were observed in the experimental group. A total of 3,690 proteins were identified, of which 423 proteins were upregulated, and 304 proteins were down-regulated. Eight out of ten mRNA expressions and acyloxyacyl hydrolase (AOAH), mast cell (MC) protease 1 protein expressions were in line with the proteomic results. Sixty-five differential expression proteins (DEPs) were found to belong to the immune system, and 18 of them were involved in immune diseases, according to KEGG analysis. We consider that MC protease 1 and platelet activation pathways may play an important role in ketamine-induced bladder fibrosis.
Sections du résumé
BACKGROUND
BACKGROUND
Long-term abuse of ketamine can cause irreversible bladder fibrosis, but the mechanism of bladder fibrosis is still under investigation. This study aims to explore the mechanism of bladder fibrosis utilizing proteomic analysis in a rat model.
METHODS
METHODS
After building a rat model, hematoxylin and eosin (HE) staining, Masson's trichrome staining, and western blotting (WB) of collagen I were used to assess bladder pathology and fibrosis in a rat model. Next, protein expression changes in the rat bladder by proteomic technology were quantitatively detected, and reverse transcription-polymerase chain reaction (RT-PCR) and WB were used to verify the expression of proteins. Bioinformatic techniques and functional analysis were also performed.
RESULTS
RESULTS
Compared to the control group, thinning of the bladder epithelium layer, infiltration of submucosal inflammatory cells, deposition of many collagen fibers, and an elevated expression of collagen I were observed in the experimental group. A total of 3,690 proteins were identified, of which 423 proteins were upregulated, and 304 proteins were down-regulated. Eight out of ten mRNA expressions and acyloxyacyl hydrolase (AOAH), mast cell (MC) protease 1 protein expressions were in line with the proteomic results. Sixty-five differential expression proteins (DEPs) were found to belong to the immune system, and 18 of them were involved in immune diseases, according to KEGG analysis.
CONCLUSIONS
CONCLUSIONS
We consider that MC protease 1 and platelet activation pathways may play an important role in ketamine-induced bladder fibrosis.
Identifiants
pubmed: 34532254
doi: 10.21037/tau-21-351
pii: tau-10-08-3300
pmc: PMC8421841
doi:
Types de publication
Journal Article
Langues
eng
Pagination
3300-3311Informations de copyright
2021 Translational Andrology and Urology. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/tau-21-351). The authors have no conflicts of interest to declare.
Références
Neurourol Urodyn. 2018 Jun;37(5):1764-1772
pubmed: 29441609
Am J Physiol Renal Physiol. 2017 Oct 1;313(4):F961-F972
pubmed: 28331066
BJU Int. 2013 Dec;112(8):1156-62
pubmed: 23937072
Sci Rep. 2016 Aug 02;6:30881
pubmed: 27481042
Postgrad Med J. 2014 Apr;90(1062):185-90
pubmed: 24443558
Prog Lipid Res. 2000 Jan;39(1):41-82
pubmed: 10729607
BJU Int. 2018 Mar;121(3):458-465
pubmed: 29230940
Front Pharmacol. 2021 Mar 17;12:621894
pubmed: 33815106
Inflamm Res. 2021 May;70(5):543-552
pubmed: 33851234
Kidney Int. 2013 Aug;84(2):317-26
pubmed: 23515052
Cell Host Microbe. 2008 Sep 11;4(3):293-302
pubmed: 18779055
J Biol Chem. 1997 Mar 14;272(11):7127-31
pubmed: 9054407
Exp Eye Res. 2019 Aug;185:107664
pubmed: 31085182
PLoS Genet. 2011 Aug;7(8):e1002197
pubmed: 21829388
Mol Med Rep. 2015 Feb;11(2):887-95
pubmed: 25370987
J Biol Chem. 1994 Sep 23;269(38):23736-42
pubmed: 8089145
Drug Chem Toxicol. 2016;39(2):206-12
pubmed: 26324997
Blood. 2010 Jun 17;115(24):4981-90
pubmed: 20233968
Immunol Rev. 2007 Jun;217:141-54
pubmed: 17498057
Arthritis Res Ther. 2017 Nov 15;19(1):252
pubmed: 29141676
Biochem Biophys Res Commun. 1993 Mar 31;191(3):1230-6
pubmed: 8466500
Urology. 2007 May;69(5):810-2
pubmed: 17482909
Am J Physiol Renal Physiol. 2020 Apr 1;318(4):F1006-F1016
pubmed: 32003596
Respirology. 2019 Nov;24(11):1111-1114
pubmed: 31393655
Am J Physiol Regul Integr Comp Physiol. 2018 Mar 1;314(3):R353-R365
pubmed: 29118019
Biomed Pharmacother. 2017 Jan;85:611-619
pubmed: 27894668
Proteomics. 2010 Jan;10(2):343-7
pubmed: 20029838
Rheumatology (Oxford). 2019 Mar 06;:
pubmed: 30843591
Int J Urol. 2013 Oct;20(10):1024-31
pubmed: 23379290
Platelets. 2020;31(1):112-119
pubmed: 30880553