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. 2023 Jul 19;20:29. doi: 10.1186/s12989-023-00543-9

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Glycosylation level affectsGpnmb function. A. Structural domain of GPNMB protein. B. Molecular weight of GPNMB changed from 95 kD to 65 kD following treatment with 5 μg/ml of tunicamycin. C. Representative western blot results showing an action time of 16 h following treatment with 5 μg/ml of tunicamycin. D. Representative western blot results showing that the Gpnmb-OE group causes a reversal of the tunicamycin-induced elevation in α-SMA, COL1, and FN1 proteins compared to the Gpnmb-NC group. E. *P < 0.05 indicates that the α-SMA protein levels were higher in the Gpnmb-OE group than in the control group; #P < 0.05 indicates that the COL1 expression levels were lower in the Gpnmb-OE group than in the control group after tunicamycin treatment; and &P < 0.05 indicates that FN1 expression levels were lower in the Gpnmb-OE group than in the control group after tunicamycin treatment