Deletion of platelet-derived growth factor receptor β suppresses tumorigenesis in metabolic dysfunction-associated steatohepatitis (MASH) mice with diabetes.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
11 Oct 2024
Historique:
received: 28 05 2024
accepted: 08 10 2024
medline: 12 10 2024
pubmed: 12 10 2024
entrez: 11 10 2024
Statut: epublish

Résumé

The platelet-derived growth factor (PDGF) family contributes to the progression of steatohepatitis; however, changes in and the characteristics of isoform-specific expression remain unclear. Since diabetes is a major driver of metabolic dysfunction-associated steatohepatitis (MASH), we characterized the mouse model of diabetic MASH (dMASH) by focusing on PDGF signaling. Pdgfa-d expression was markedly higher in hepatic stellate cells among flow-sorted cells in control mice and also increased in dMASH. In contrast, a reanalysis of human single-cell RNA-Seq data showed the distinct distribution of each PDGF isoform with disease progression. Furthermore, inflammation and fibrosis in the liver were less severe in diabetic MASH using tamoxifen-induced PDGF receptor β (PDGFRβ)-deficient mice (KO) than in control dMASH using floxed mice (FL) at 12 weeks old. Despite the absence of tumors, the expression of tumor-related genes was lower in KO than in FL. Tumorigenesis was significantly lower in 20-week-old KO. An Ingenuity Pathway Analysis of differentially expressed miRNA between FL and KO identified functional networks associated with hepatotoxicity and cancer. Therefore, PDGFRβ signals play important roles in the progression of steatohepatitis and tumorigenesis in MASH, with the modulation of miRNA expression posited as a potential underlying mechanism.

Identifiants

pubmed: 39394459
doi: 10.1038/s41598-024-75713-6
pii: 10.1038/s41598-024-75713-6
doi:

Substances chimiques

Receptor, Platelet-Derived Growth Factor beta EC 2.7.10.1
MicroRNAs 0
Platelet-Derived Growth Factor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

23829

Subventions

Organisme : Japan Society for the Promotion of Science
ID : JP21K08549
Organisme : Japan Society for the Promotion of Science
ID : JP24K02855
Organisme : Japan Society for the Promotion of Science
ID : 23H02957
Organisme : Moonshot Research and Development Program
ID : JPMJMS2021

Informations de copyright

© 2024. The Author(s).

Références

Villanueva, A. Hepatocellular carcinoma. N Engl. J. Med. 380, 1450–1462 (2019).
pubmed: 30970190 doi: 10.1056/NEJMra1713263
Anstee, Q. M., Reeves, H. L., Kotsiliti, E., Govaere, O. & Heikenwalder, M. From NASH to HCC: current concepts and future challenges. Nat. Rev. Gastroenterol. Hepatol. 16, 411–428 (2019).
pubmed: 31028350 doi: 10.1038/s41575-019-0145-7
Gastaldelli, A. & Cusi, K. From NASH to diabetes and from diabetes to NASH: mechanisms and treatment options. JHEP Rep. 1, 312–328 (2019).
pubmed: 32039382 pmcid: 7001557 doi: 10.1016/j.jhepr.2019.07.002
Takakura, K. et al. Mouse models for investigating the underlying mechanisms of nonalcoholic steatohepatitis-derived hepatocellular carcinoma. World J. Gastroenterol. 24, 1989–1994 (2018).
pubmed: 29760542 pmcid: 5949712 doi: 10.3748/wjg.v24.i18.1989
Fujii, M. et al. A murine model for non-alcoholic steatohepatitis showing evidence of association between diabetes and hepatocellular carcinoma. Med. Mol. Morphol. 46, 141–152 (2013).
pubmed: 23430399 doi: 10.1007/s00795-013-0016-1
Zou, X. et al. Targeting the PDGF/PDGFR signaling pathway for cancer therapy: a review. Int. J. Biol. Macromol. 202, 539–557 (2022).
pubmed: 35074329 doi: 10.1016/j.ijbiomac.2022.01.113
Onogi, Y. et al. PDGFRβ regulates adipose tissue expansion and glucose metabolism via vascular remodeling in diet-induced obesity. Diabetes. 66, 1008–1021 (2017).
pubmed: 28122789 doi: 10.2337/db16-0881
Kikuchi, A. & Monga, S. P. PDGFRα in liver pathophysiology: emerging roles in development, regeneration, fibrosis, and cancer. Gene Expr. 16, 109–127 (2015).
pubmed: 25700367 pmcid: 4410163 doi: 10.3727/105221615X14181438356210
Gao, Z. et al. Deletion of the PDGFR-β gene affects key fibroblast functions important for wound healing. J. Biol. Chem. 280, 9375–9389 (2005).
pubmed: 15590688 doi: 10.1074/jbc.M413081200
Czochra, P. et al. Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice. J. Hepatol. 45, 419–428 (2006).
pubmed: 16842882 doi: 10.1016/j.jhep.2006.04.010
Kocabayoglu, P. et al. β-PDGF receptor expressed by hepatic stellate cells regulates fibrosis in murine liver injury, but not carcinogenesis. J. Hepatol. 63, 141–147 (2015).
pubmed: 25678385 pmcid: 4475471 doi: 10.1016/j.jhep.2015.01.036
Wei, T. et al. Overexpression of platelet-derived growth factor receptor alpha promotes tumor progression and indicates poor prognosis in hepatocellular carcinoma. Oncotarget. 5, 10307–10317 (2014).
pubmed: 25333264 pmcid: 4279374 doi: 10.18632/oncotarget.2537
Ramachandran, P. et al. Resolving the fibrotic niche of human liver cirrhosis at single-cell level. Nature. 575, 512–518 (2019).
pubmed: 31597160 pmcid: 6876711 doi: 10.1038/s41586-019-1631-3
Ramachandran, P., Matchett, K. P., Dobie, R., Wilson-Kanamori, J. R. & Henderson, N. C. Single-cell technologies in hepatology: new insights into liver biology and disease pathogenesis. Nat. Rev. Gastroenterol. Hepatol. 17, 457–472 (2020).
pubmed: 32483353 doi: 10.1038/s41575-020-0304-x
Loft, A. et al. Liver-fibrosis-activated transcriptional networks govern hepatocyte reprogramming and intra-hepatic communication. Cell. Metab. 33, 1685–1700e9 (2021).
pubmed: 34237252 doi: 10.1016/j.cmet.2021.06.005
Wang, Z. Y. et al. Single-cell and bulk transcriptomics of the liver reveals potential targets of NASH with fibrosis. Sci. Rep. 11, 19396 (2021).
pubmed: 34588551 pmcid: 8481490 doi: 10.1038/s41598-021-98806-y
Xiong, X. et al. Landscape of intercellular crosstalk in healthy and NASH liver revealed by single-cell secretome gene analysis. Mol. Cell. 75, 644–660e5 (2019).
pubmed: 31398325 pmcid: 7262680 doi: 10.1016/j.molcel.2019.07.028
Wang, X., He, Y., MacKowiak, B. & Gao, B. MicroRNAs as regulators, biomarkers and therapeutic targets in liver diseases. Gut. 70, 784–795 (2021).
pubmed: 33127832 doi: 10.1136/gutjnl-2020-322526
Oura, K., Morishita, A. & Masaki, T. Molecular and functional roles of microRNAs in the progression of hepatocellular carcinoma—A review. Int. J. Mol. Sci. 21, 8362 (2020).
pubmed: 33171811 pmcid: 7664704 doi: 10.3390/ijms21218362
López-Pastor, A. R., Infante-Menéndez, J., Escribano, Ó. & Gómez-Hernández, A. miRNA dysregulation in the development of non-alcoholic fatty liver disease and the related disorders type 2 diabetes mellitus and cardiovascular disease. Front. Med. (Lausanne). 7, 527059 (2020).
pubmed: 33102495 doi: 10.3389/fmed.2020.527059
Kleiner, D. E. et al. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology. 41, 1313–1321 (2005).
pubmed: 15915461 doi: 10.1002/hep.20701
Guilliams, M. & Scott, C. L. Liver macrophages in health and disease. Immunity. 55, 1515–1529 (2022).
pubmed: 36103850 doi: 10.1016/j.immuni.2022.08.002
Hamaguchi, E. et al. Histological course of nonalcoholic fatty liver disease in Japanese patients: tight glycemic control, rather than weight reduction, ameliorates liver fibrosis. Diabetes Care. 33, 284–286 (2010).
pubmed: 19880582 doi: 10.2337/dc09-0148
Soto-Heredero, G., Gómez de las Heras, M. M., Gabandé-Rodríguez, E., Oller, J. & Mittelbrunn, M. Glycolysis – a key player in the inflammatory response. FEBS J. 287, 3350–3369 (2020).
pubmed: 32255251 pmcid: 7496292 doi: 10.1111/febs.15327
Onogi, Y. et al. Pro-inflammatory macrophages coupled with glycolysis remodel adipose vasculature by producing platelet-derived growth factor-B in obesity. Sci. Rep. 10, 670 (2020).
pubmed: 31959796 pmcid: 6970998 doi: 10.1038/s41598-019-57368-w
Okekawa, A. et al. Platelet-derived growth factor signaling in pericytes promotes hypothalamic inflammation and obesity. Mol. Med. 30, 21 (2024).
pubmed: 38317079 pmcid: 10845801 doi: 10.1186/s10020-024-00793-z
Abuduyimiti, T. et al. Diabetes accelerates steatohepatitis in mice: liver pathology and single-cell gene expression signatures. Am. J. Pathol. 194, 693–707 (2024).
pubmed: 38309428 doi: 10.1016/j.ajpath.2024.01.007
Su, T. et al. Single-cell transcriptomics reveals zone-specific alterations of liver sinusoidal endothelial cells in cirrhosis. Cell. Mol. Gastroenterol. Hepatol. 11, 1139–1161 (2021).
pubmed: 33340713 doi: 10.1016/j.jcmgh.2020.12.007
Kikuchi, A. et al. Hepatic stellate cell–specific platelet-derived growth factor receptor-α loss reduces fibrosis and promotes repair after hepatocellular injury. Am. J. Pathol. 190, 2080–2094 (2020).
pubmed: 32615075 pmcid: 7527859 doi: 10.1016/j.ajpath.2020.06.006
Lim, B. J. et al. Selective deletion of hepatocyte platelet-derived growth factor receptor α and development of liver fibrosis in mice. Cell. Commun. Signal. 16, 93 (2018).
pubmed: 30509307 pmcid: 6276164 doi: 10.1186/s12964-018-0306-2
Stock, P. et al. Platelet-derived growth factor receptor-α: a novel therapeutic target in human hepatocellular cancer. Mol. Cancer Ther. 6, 1932–1941 (2007).
pubmed: 17604334 doi: 10.1158/1535-7163.MCT-06-0720
Campbell, J. S. et al. Platelet-derived growth factor C induces liver fibrosis, steatosis, and hepatocellular carcinoma. Proc. Natl. Acad. Sci. U S A. 102, 3389–3394 (2005).
pubmed: 15728360 pmcid: 552940 doi: 10.1073/pnas.0409722102
Lau, E. Y. T. et al. Cancer-associated fibroblasts regulate tumor-initiating cell plasticity in hepatocellular carcinoma through c-Met/FRA1/HEY1 signaling. Cell. Rep. 15, 1175–1189 (2016).
pubmed: 27134167 doi: 10.1016/j.celrep.2016.04.019
Qu, K. et al. MCM7 promotes cancer progression through cyclin D1-dependent signaling and serves as a prognostic marker for patients with hepatocellular carcinoma. Cell. Death Dis. 8, e2603 (2017).
pubmed: 28182015 pmcid: 5386449 doi: 10.1038/cddis.2016.352
de Conti, A. et al. MicroRNA deregulation in nonalcoholic steatohepatitisassociated liver carcinogenesis. Oncotarget. 8, 88517–88528 (2017).
pubmed: 29179453 pmcid: 5687623 doi: 10.18632/oncotarget.19774
Ren, X. et al. PDGFBB regulates the transformation of fibroblasts into cancerassociated fibroblasts via the lncRNA LURAP1LAS1/LURAP1L/IKK/IκB/NFκB signaling pathway. Oncol. Lett. 22, 537 (2021).
pubmed: 34079593 pmcid: 8157341 doi: 10.3892/ol.2021.12798
Chiariello, M., Marinissen, M. J. & Gutkind, J. S. Regulation of c-myc expression by PDGF through rho GTPases. Nat. Cell. Biol. 3, 580–586 (2001).
pubmed: 11389443 doi: 10.1038/35078555
Kim, T. H. et al. Circulating miRNA is a useful diagnostic biomarker for nonalcoholic steatohepatitis in nonalcoholic fatty liver disease. Sci. Rep. 11, 14639 (2021).
pubmed: 34282172 pmcid: 8289842 doi: 10.1038/s41598-021-94115-6
Hochreuter, M. Y., Dall, M., Treebak, J. T. & Barrès, R. MicroRNAs in non-alcoholic fatty liver disease: progress and perspectives. Mol. Metab. 65, 101581 (2022).
pubmed: 36028120 pmcid: 9464960 doi: 10.1016/j.molmet.2022.101581
Chen, Y. et al. A novel miR-1291-ERRα-CPT1C axis modulates tumor cell proliferation, metabolism and tumorigenesis. Theranostics. 10, 7193–7210 (2020).
pubmed: 32641987 pmcid: 7330864 doi: 10.7150/thno.44877
Fondevila, M. F. et al. The L-α-lysophosphatidylinositol/G protein–coupled receptor 55 system induces the development of nonalcoholic steatosis and steatohepatitis. Hepatology. 73, 606–624 (2021).
pubmed: 32329085 doi: 10.1002/hep.31290
Watanabe, E. et al. Stromal cell-derived factor 1 (SDF1) attenuates platelet-derived growth factor-B (PDGF-B)-induced vascular remodeling for adipose tissue expansion in obesity. Angiogenesis. 23, 667–684 (2020).
pubmed: 32699964 doi: 10.1007/s10456-020-09738-6
Kilkenny, C., Browne, W. J., Cuthill, I. C., Emerson, M. & Altman, D. G. Improving Bioscience Research Reporting: the ARRIVE guidelines for Reporting Animal Research. PLoS Biol. 8, e1000412 (2010).
pubmed: 20613859 pmcid: 2893951 doi: 10.1371/journal.pbio.1000412
Schulz, C. et al. A lineage of myeloid cells independent of myb and hematopoietic stem cells. Science. 336, 86–90 (2012).
pubmed: 22442384 doi: 10.1126/science.1219179
Tanaka, T. et al. Oestrogen receptor α in T cells controls the T cell immune profile and glucose metabolism in mouse models of gestational diabetes mellitus. Diabetologia. 64, 1660–1673 (2021).
pubmed: 33796910 doi: 10.1007/s00125-021-05447-x
Wada, T. et al. Eplerenone prevented obesity-induced inflammasome activation and glucose intolerance. J. Endocrinol. 235, 179–191 (2017).
pubmed: 28855315 doi: 10.1530/JOE-17-0351
Wada, T. et al. A transdermal treatment with MC903 ameliorates diet-induced obesity by reducing visceral fat and increasing myofiber thickness and energy consumption in mice. Nutr. Metab. (Lond). 20, 10 (2023).
pubmed: 36774476 doi: 10.1186/s12986-023-00732-5
Ishikawa, A. et al. Estrogen regulates sex-specific localization of regulatory T cells in adipose tissue of obese female mice. PLoS One. 15, e0230885 (2020).
pubmed: 32240221 pmcid: 7117686 doi: 10.1371/journal.pone.0230885

Auteurs

Tsutomu Wada (T)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. twada@pha.u-toyama.ac.jp.

Yuki Takeda (Y)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Akira Okekawa (A)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Go Komatsu (G)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Yuichi Iwasa (Y)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Yasuhiro Onogi (Y)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Research Center for Pre-Disease Science, University of Toyama, 2630 Sugitani, Toyama, Japan.

Ichiro Takasaki (I)

Department of Pharmacology, Graduate School of Science and Engineering, University of Toyama, 3190, Gofuku, Toyama, Japan.

Takeru Hamashima (T)

Department of Pathology, University of Toyama, 2630 Sugitani, Toyama, Japan.

Masakiyo Sasahara (M)

Department of Pathology, University of Toyama, 2630 Sugitani, Toyama, Japan.

Hiroshi Tsuneki (H)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Department of Integrative Pharmacology, University of Toyama, 2630 Sugitani, Toyama, Japan.

Toshiyasu Sasaoka (T)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. tsasaoka@pha.u-toyama.ac.jp.

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