A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling

Bromodomains are epigenetic readers that modulate gene expression linked to inflammation and cartilage degeneration. Emerging evidence suggests their dysregulation plays a pivotal role in osteoarthritis (OA) pathogenesis, making them promising therapeutic targets. We evaluated the therapeutic effica...

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Main Authors: Hyemi Lee, Seong Jae Han, Subin Ok, Kwang Min Lee, Seungseok Choi, Injoo Yoon, Somang Choi, Jina Kim, Serim Ryu, Min-Hee Son, In-Hyun Lee, Chanmi Cho, Siyoung Yang
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Language:English
Published: Frontiers Media S.A. 2025-07-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1633334/full
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author Hyemi Lee
Seong Jae Han
Subin Ok
Kwang Min Lee
Seungseok Choi
Injoo Yoon
Somang Choi
Jina Kim
Serim Ryu
Min-Hee Son
In-Hyun Lee
Chanmi Cho
Siyoung Yang
author_facet Hyemi Lee
Seong Jae Han
Subin Ok
Kwang Min Lee
Seungseok Choi
Injoo Yoon
Somang Choi
Jina Kim
Serim Ryu
Min-Hee Son
In-Hyun Lee
Chanmi Cho
Siyoung Yang
author_sort Hyemi Lee
collection DOAJ
description Bromodomains are epigenetic readers that modulate gene expression linked to inflammation and cartilage degeneration. Emerging evidence suggests their dysregulation plays a pivotal role in osteoarthritis (OA) pathogenesis, making them promising therapeutic targets. We evaluated the therapeutic efficacy of a novel carboxamide derivative bromodomain inhibitor (NCD) as a potentially safer alternative for preventing OA progression. The inhibitory effects of NCD were assessed through both in vitro and in vivo models. In vitro, mouse primary chondrocytes were stimulated with IL-1β, and the effects of NCD treatment were analyzed using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. In vivo, destabilization of the medial meniscus (DMM) surgery was performed in 12-week-old male C57BL/6 mice, followed by either oral administration or intra-articular (IA) NCD injection. Cartilage integrity was assessed by histology. We analyzed changes in the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways to elucidate the mechanism of NCD. NCD treatment significantly suppressed IL-1β-induced expression of matrix metalloproteinases (Mmp3 and Mmp13) and cyclooxygenase-2 (Cox2) in mouse chondrocytes. In the DMM mouse model, both oral IA administration of NCD alleviated OA-related cartilage destruction. Mechanistically, NCD inhibited IκB degradation and reduced Erk and Jnk phosphorylation, indicating suppression of the NF-κB and MAPK signaling pathways. This study demonstrates that targeting bromodomains with a novel carboxamide-based inhibitor effectively attenuates OA cartilage destruction by suppressing these signaling pathways. These findings support the therapeutic potential of epigenetic modulation in mitigating OA pathogenesis.
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spelling doaj-art-c44de972c1bf47aabccf634deef7375e2025-08-20T03:58:36ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-07-011610.3389/fimmu.2025.16333341633334A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signalingHyemi Lee0Seong Jae Han1Subin Ok2Kwang Min Lee3Seungseok Choi4Injoo Yoon5Somang Choi6Jina Kim7Serim Ryu8Min-Hee Son9In-Hyun Lee10Chanmi Cho11Siyoung Yang12Department of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaCentralBio Co., Ltd., Incheon, Republic of KoreaDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaDepartment of Life Science and Environmental Biochemistry, and Life and Industry Convergence Research Institute, Pusan National University, Miryang, Republic of KoreaDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaNew Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation, Daegu, Republic of KoreaBenobio Co., Ltd, Seongnam, Republic of KoreaBenobio Co., Ltd, Seongnam, Republic of KoreaBenobio Co., Ltd, Seongnam, Republic of KoreaDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of KoreaBromodomains are epigenetic readers that modulate gene expression linked to inflammation and cartilage degeneration. Emerging evidence suggests their dysregulation plays a pivotal role in osteoarthritis (OA) pathogenesis, making them promising therapeutic targets. We evaluated the therapeutic efficacy of a novel carboxamide derivative bromodomain inhibitor (NCD) as a potentially safer alternative for preventing OA progression. The inhibitory effects of NCD were assessed through both in vitro and in vivo models. In vitro, mouse primary chondrocytes were stimulated with IL-1β, and the effects of NCD treatment were analyzed using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. In vivo, destabilization of the medial meniscus (DMM) surgery was performed in 12-week-old male C57BL/6 mice, followed by either oral administration or intra-articular (IA) NCD injection. Cartilage integrity was assessed by histology. We analyzed changes in the NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways to elucidate the mechanism of NCD. NCD treatment significantly suppressed IL-1β-induced expression of matrix metalloproteinases (Mmp3 and Mmp13) and cyclooxygenase-2 (Cox2) in mouse chondrocytes. In the DMM mouse model, both oral IA administration of NCD alleviated OA-related cartilage destruction. Mechanistically, NCD inhibited IκB degradation and reduced Erk and Jnk phosphorylation, indicating suppression of the NF-κB and MAPK signaling pathways. This study demonstrates that targeting bromodomains with a novel carboxamide-based inhibitor effectively attenuates OA cartilage destruction by suppressing these signaling pathways. These findings support the therapeutic potential of epigenetic modulation in mitigating OA pathogenesis.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1633334/fullbromodomainarthritiscarboxamide derivativemitogen-activated protein kinaseNF-κB
spellingShingle Hyemi Lee
Seong Jae Han
Subin Ok
Kwang Min Lee
Seungseok Choi
Injoo Yoon
Somang Choi
Jina Kim
Serim Ryu
Min-Hee Son
In-Hyun Lee
Chanmi Cho
Siyoung Yang
A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling
Frontiers in Immunology
bromodomain
arthritis
carboxamide derivative
mitogen-activated protein kinase
NF-κB
title A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling
title_full A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling
title_fullStr A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling
title_full_unstemmed A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling
title_short A novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of NF-κB and MAPK signaling
title_sort novel carboxamide bromodomain inhibitor attenuates osteoarthritis via epigenetic repression of nf κb and mapk signaling
topic bromodomain
arthritis
carboxamide derivative
mitogen-activated protein kinase
NF-κB
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1633334/full
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