IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis

Mohammad Amjad Hossain,1 Aravinthan Adithan,1 Md Jahangir Alam,1 Spandana Rajendra Kopalli,2 Bumseok Kim,1 Chang-Won Kang,1 Ki-Chul Hwang,3 Jong-Hoon Kim1 1College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, Iksan-city, Jeollabuk-Do, Republic of Korea; 2Departm...

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Autores principales:	Hossain MA, Adithan A, Alam MJ, Kopalli SR, Kim B, Kang CW, Hwang KC, Kim JH
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2021
Materias:	insulin-like growth factor-1 chondrocyte cartilage development osteoarthritis rabbit Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/bb74bdc24e0344e88abdeb98e7eebc7e
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spelling	oai:doaj.org-article:bb74bdc24e0344e88abdeb98e7eebc7e2021-12-02T16:17:55ZIGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis1178-7031https://doaj.org/article/bb74bdc24e0344e88abdeb98e7eebc7e2021-07-01T00:00:00Zhttps://www.dovepress.com/igf-1-facilitates-cartilage-reconstruction-by-regulating-pi3kakt-mapk--peer-reviewed-fulltext-article-JIRhttps://doaj.org/toc/1178-7031Mohammad Amjad Hossain,1 Aravinthan Adithan,1 Md Jahangir Alam,1 Spandana Rajendra Kopalli,2 Bumseok Kim,1 Chang-Won Kang,1 Ki-Chul Hwang,3 Jong-Hoon Kim1 1College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, Iksan-city, Jeollabuk-Do, Republic of Korea; 2Department of Integrative Bioscience and Biotechnology, Sejong University, Gwangjin-gu, Seoul, 05006, Republic of Korea; 3Institute for Bio-Medical Convergence, College of Medicine, Catholic Kwandong University, Gangneung-si, Gangwon-do, Republic of KoreaCorrespondence: Jong-Hoon KimCollege of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, 79 Gobong-ro, Iksan-city, Jeollabuk-Do, 54596, Republic of KoreaEmail jhkim1@jbnu.ac.krPurpose: The pathogenesis of osteoarthritis (OA) is characterized by joint degeneration. The pro-inflammatory cytokine interleukin (IL)-1β plays a vital role in the pathogenesis of OA by stimulation of specific signaling pathways like NF-κB, PI3K/Akt, and MAPKs pathways. The catabolic role of growth factors in the OA may be inhibited cytokine-activated pathogen. The purpose of this study was to investigate the potential effects of insulin-like growth factor-1 (IGF-1) on IL-1β-induced apoptosis in rabbit chondrocytes in vitro and in an in vivo rabbit knee OA model.Methods: In the present study, the OA developed in chondrocyte with the treatment of IL-1β and articular cartilage ruptures by removal of cartilage from the rabbit knee femoral condyle. After IGF-1 treatment, immunohistochemistry and qRT-PCR were identified OA expression with changes in MMPs (matrix metalloproteinases). The production of ROS (intracellular reactive oxygen species) in the OA was detected by flow cytometry. Further, the disease progression was microscopically investigated and pathophysiological changes were analyzed using histology. The NF-κB, PI3K/Akt and P38 (MAPK) specific pathways that are associated with disease progression were also checked using the Western blot technique.Results: The expression of MMPs and various apoptotic markers are down-regulated following administration of IGF-1 in a dose-dependent fashion while significantly up-regulation of TIMP-1. The results showed that higher levels of ROS were observed upon treatment of chondrocytes and chondral OA with IL-1β. Collectively, our results indicated that IGF-1 protected NF-κB pathway by suppression of PI3K/Akt and MAPKs specific pathways. Furthermore, the macroscopic and pathological investigation showed that it has a chondroprotective effect by the formation of hyaline cartilage.Conclusion: Our results indicate a protective effect of IGF-1 against OA pathogenesis by inhibition of NF-κB signaling via regulation of the MAPK and PI3K/Akt signaling pathways and prevention of apoptosis by suppression of ROS production.Keywords: insulin-like growth factor-1, chondrocyte, cartilage development, osteoarthritis, rabbitHossain MAAdithan AAlam MJKopalli SRKim BKang CWHwang KCKim JHDove Medical Pressarticleinsulin-like growth factor-1chondrocytecartilage developmentosteoarthritisrabbitPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 14, Pp 3555-3568 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	insulin-like growth factor-1 chondrocyte cartilage development osteoarthritis rabbit Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	insulin-like growth factor-1 chondrocyte cartilage development osteoarthritis rabbit Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Hossain MA Adithan A Alam MJ Kopalli SR Kim B Kang CW Hwang KC Kim JH IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis
description	Mohammad Amjad Hossain,1 Aravinthan Adithan,1 Md Jahangir Alam,1 Spandana Rajendra Kopalli,2 Bumseok Kim,1 Chang-Won Kang,1 Ki-Chul Hwang,3 Jong-Hoon Kim1 1College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, Iksan-city, Jeollabuk-Do, Republic of Korea; 2Department of Integrative Bioscience and Biotechnology, Sejong University, Gwangjin-gu, Seoul, 05006, Republic of Korea; 3Institute for Bio-Medical Convergence, College of Medicine, Catholic Kwandong University, Gangneung-si, Gangwon-do, Republic of KoreaCorrespondence: Jong-Hoon KimCollege of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, 79 Gobong-ro, Iksan-city, Jeollabuk-Do, 54596, Republic of KoreaEmail jhkim1@jbnu.ac.krPurpose: The pathogenesis of osteoarthritis (OA) is characterized by joint degeneration. The pro-inflammatory cytokine interleukin (IL)-1β plays a vital role in the pathogenesis of OA by stimulation of specific signaling pathways like NF-κB, PI3K/Akt, and MAPKs pathways. The catabolic role of growth factors in the OA may be inhibited cytokine-activated pathogen. The purpose of this study was to investigate the potential effects of insulin-like growth factor-1 (IGF-1) on IL-1β-induced apoptosis in rabbit chondrocytes in vitro and in an in vivo rabbit knee OA model.Methods: In the present study, the OA developed in chondrocyte with the treatment of IL-1β and articular cartilage ruptures by removal of cartilage from the rabbit knee femoral condyle. After IGF-1 treatment, immunohistochemistry and qRT-PCR were identified OA expression with changes in MMPs (matrix metalloproteinases). The production of ROS (intracellular reactive oxygen species) in the OA was detected by flow cytometry. Further, the disease progression was microscopically investigated and pathophysiological changes were analyzed using histology. The NF-κB, PI3K/Akt and P38 (MAPK) specific pathways that are associated with disease progression were also checked using the Western blot technique.Results: The expression of MMPs and various apoptotic markers are down-regulated following administration of IGF-1 in a dose-dependent fashion while significantly up-regulation of TIMP-1. The results showed that higher levels of ROS were observed upon treatment of chondrocytes and chondral OA with IL-1β. Collectively, our results indicated that IGF-1 protected NF-κB pathway by suppression of PI3K/Akt and MAPKs specific pathways. Furthermore, the macroscopic and pathological investigation showed that it has a chondroprotective effect by the formation of hyaline cartilage.Conclusion: Our results indicate a protective effect of IGF-1 against OA pathogenesis by inhibition of NF-κB signaling via regulation of the MAPK and PI3K/Akt signaling pathways and prevention of apoptosis by suppression of ROS production.Keywords: insulin-like growth factor-1, chondrocyte, cartilage development, osteoarthritis, rabbit
format	article
author	Hossain MA Adithan A Alam MJ Kopalli SR Kim B Kang CW Hwang KC Kim JH
author_facet	Hossain MA Adithan A Alam MJ Kopalli SR Kim B Kang CW Hwang KC Kim JH
author_sort	Hossain MA
title	IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis
title_short	IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis
title_full	IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis
title_fullStr	IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis
title_full_unstemmed	IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis
title_sort	igf-1 facilitates cartilage reconstruction by regulating pi3k/akt, mapk, and nf-kb signaling in rabbit osteoarthritis
publisher	Dove Medical Press
publishDate	2021
url	https://doaj.org/article/bb74bdc24e0344e88abdeb98e7eebc7e
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_version_	1718384253153050624

IGF-1 Facilitates Cartilage Reconstruction by Regulating PI3K/AKT, MAPK, and NF-kB Signaling in Rabbit Osteoarthritis

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