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Objective: To investigate the role of BTG2 in periodontitis and diabetic kidney disease (DKD) and its potential underlying mechanism.

Methods: Gene expression data for periodontitis and DKD were acquired from the Gene Expression Omnibus (GEO) database. Differential expression analysis identified co-expressed genes between these conditions. The Nephroseq V5 online nephropathy database validated the role of these genes in DKD. Pearson correlation analysis identified genes associated with our target gene. We employed Gene Set Enrichment Analysis (GSEA) and Protein-Protein Interaction (PPI) networks to elucidate potential mechanisms. Expression levels of BTG2 mRNA were examined using quantitative polymerase Chain Reaction (qPCR) and immunofluorescence assays. Western blotting quantified proteins involved in epithelial-to-mesenchymal transition (EMT), apoptosis, mTORC1 signaling, and autophagy. Additionally, wound healing and flow cytometric apoptosis assays evaluated podocyte migration and apoptosis, respectively.

Results: Analysis of GEO database data revealed BTG2 as a commonly differentially expressed gene in both DKD and periodontitis. BTG2 expression was reduced in DKD compared to normal conditions and correlated with proteinuria. GSEA indicated enrichment of BTG2 in the EMT and mTORC1 signaling pathways. The PPI network highlighted BTG2's relevance to S100A9, S100A12, and FPR1. Immunofluorescence assays demonstrated significantly lower BTG2 expression in podocytes under high glucose (HG) conditions. Reduced BTG2 expression in HG-treated podocytes led to increased levels of EMT markers (α-SMA, vimentin) and the apoptotic protein Bim, alongside a decrease in nephrin. Lower BTG2 levels were associated with increased podocyte mobility and apoptosis, as well as elevated RPS6KB1 and mTOR levels, but reduced autophagy marker LC3.

Conclusion: Our findings suggest that BTG2 is a crucial intermediary gene linking DKD and periodontitis. Modulating autophagy via inhibition of the mTORC1 signaling pathway, and consequently suppressing EMT, may be pivotal in the interplay between periodontitis and DKD.

Titel:	Deciphering the molecular nexus of BTG2 in periodontitis and diabetic kidney disease.
Autor/in / Beteiligte Person:	Pan, B ; Teng, Y ; Wang, R ; Chen, D ; Chen, H
Link:	Full Text Finder (Volltext)
Zeitschrift:	BMC medical genomics, Jg. 17 (2024-06-03), Heft 1, S. 152
Veröffentlichung:	London : BioMed Central, 2024
Medientyp:	academicJournal
ISSN:	1755-8794 (electronic)
DOI:	10.1186/s12920-024-01915-6
Schlagwort:	Humans Immediate-Early Proteins metabolism Immediate-Early Proteins genetics Podocytes metabolism Podocytes pathology Signal Transduction Autophagy Protein Interaction Maps Mechanistic Target of Rapamycin Complex 1 metabolism Cell Movement Periodontitis genetics Periodontitis metabolism Periodontitis pathology Diabetic Nephropathies metabolism Diabetic Nephropathies genetics Diabetic Nephropathies pathology Tumor Suppressor Proteins metabolism Tumor Suppressor Proteins genetics Epithelial-Mesenchymal Transition Apoptosis
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [BMC Med Genomics] 2024 Jun 03; Vol. 17 (1), pp. 152. <i>Date of Electronic Publication: </i>2024 Jun 03. MeSH Terms: Periodontitis* / genetics ; Periodontitis* / metabolism ; Periodontitis* / pathology ; Diabetic Nephropathies* / metabolism ; Diabetic Nephropathies* / genetics ; Diabetic Nephropathies* / pathology ; Tumor Suppressor Proteins* / metabolism ; Tumor Suppressor Proteins* / genetics ; Epithelial-Mesenchymal Transition* ; Apoptosis* ; Humans ; Immediate-Early Proteins / metabolism ; Immediate-Early Proteins / genetics ; Podocytes / metabolism ; Podocytes / pathology ; Signal Transduction ; Autophagy ; Protein Interaction Maps ; Mechanistic Target of Rapamycin Complex 1 / metabolism ; Cell Movement References: Pathol Res Pract. 2023 Jul;247:154577. (PMID: 37257243) ; BMC Nephrol. 2021 Jan 6;22(1):3. (PMID: 33407253) ; Curr Mol Med. 2013 Jan;13(1):24-57. (PMID: 22834835) ; Cancers (Basel). 2023 Mar 13;15(6):. (PMID: 36980622) ; Acta Pharm Sin B. 2021 Sep;11(9):2749-2767. (PMID: 34589395) ; Microvasc Res. 2022 May;141:104315. (PMID: 35007537) ; Nat Rev Mol Cell Biol. 2019 Feb;20(2):69-84. (PMID: 30459476) ; Trends Endocrinol Metab. 2016 Oct;27(10):681-695. (PMID: 27372267) ; Diabetes Care. 2007 Feb;30(2):306-11. (PMID: 17259499) ; Front Immunol. 2023 Mar 17;14:1098700. (PMID: 37006240) ; Genesis. 2024 Feb;62(1):e23529. (PMID: 37345818) ; J Ethnopharmacol. 2012 May 7;141(1):111-8. (PMID: 22353431) ; J Inflamm Res. 2022 Mar 10;15:1757-1769. (PMID: 35300216) ; Physiol Genomics. 2022 Jul 1;54(7):231-241. (PMID: 35503009) ; Cureus. 2022 Jul 29;14(7):e27440. (PMID: 36051741) ; Front Oncol. 2022 Dec 14;12:1049928. (PMID: 36591524) ; J Cell Sci. 2012 Mar 1;125(Pt 5):1259-73. (PMID: 22399812) ; Carcinogenesis. 2013 Jun;34(6):1343-51. (PMID: 23430956) ; Kidney Int. 2023 Feb;103(2):282-296. (PMID: 36470394) ; Kidney Int. 2017 Nov;92(5):1071-1083. (PMID: 28890325) ; Front Immunol. 2022 Aug 25;13:980805. (PMID: 36091038) ; Acta Anat (Basel). 1995;154(1):8-20. (PMID: 8714286) ; J Clin Invest. 2011 Feb;121(2):468-74. (PMID: 21370523) ; Clin J Am Soc Nephrol. 2017 Dec 7;12(12):2032-2045. (PMID: 28522654) ; Sleep Breath. 2023 Oct;27(5):1655-1666. (PMID: 36547852) ; Adv Sci (Weinh). 2022 Apr;9(12):e2103675. (PMID: 35112806) ; Am J Nephrol. 1995;15(5):411-7. (PMID: 7503141) ; Br Dent J. 2022 Sep;233(6):494. (PMID: 36151179) ; J Am Soc Nephrol. 2010 Feb;21(2):212-22. (PMID: 20019167) ; J Cell Biol. 2007 Jul 30;178(3):437-51. (PMID: 17646396) ; Nat Rev Rheumatol. 2018 Sep;14(9):528-541. (PMID: 30076385) ; Nephrol Dial Transplant. 2015 Jan;30(1):84-91. (PMID: 25074436) ; PLoS One. 2014 May 16;9(5):e97165. (PMID: 24835775) ; Lancet. 2020 Feb 29;395(10225):709-733. (PMID: 32061315) ; Br Dent J. 2020 Jul;229(2):125. (PMID: 32710061) ; Evid Based Complement Alternat Med. 2014;2014:123497. (PMID: 24864150) ; Kidney Int. 2016 Apr;89(4):779-91. (PMID: 26924060) ; Am J Pathol. 2000 Dec;157(6):1905-16. (PMID: 11106563) ; J Cell Sci. 2010 Oct 15;123(Pt 20):3467-77. (PMID: 20930141) ; Int J Ophthalmol. 2021 Jan 18;14(1):141-147. (PMID: 33469496) ; Kidney Int. 2008 Sep;74(5):631-40. (PMID: 18509315) ; BMC Oral Health. 2022 Jan 16;22(1):12. (PMID: 35034610) ; Int J Mol Sci. 2012;13(3):2893-2917. (PMID: 22489132) ; J Mol Cell Cardiol. 2023 Jun;179:30-41. (PMID: 37062247) ; Biochem Biophys Res Commun. 2015 Jul 3;462(3):208-14. (PMID: 25951976) ; Am J Physiol Renal Physiol. 2006 May;290(5):F1202-12. (PMID: 16368739) ; Genet Mol Res. 2014 Sep 01;13(3):7149-56. (PMID: 25222220) Grant Information: Y2023365 Wenzhou Municipal Science and Technology Bureau Contributed Indexing: Keywords: Autophagy; Bioinformatics analysis; Diabetic kidney disease; EMT; Periodontitis Substance Nomenclature: 0 (Tumor Suppressor Proteins) ; 141490-22-4 (BTG2 protein, human) ; 0 (Immediate-Early Proteins) ; EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1) Entry Date(s): Date Created: 20240603 Date Completed: 20240604 Latest Revision: 20240612 Update Code: 20240612 PubMed Central ID: PMC11149328

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Deciphering the molecular nexus of BTG2 in periodontitis and diabetic kidney disease.