Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats
Background: Post-traumatic joint contracture (PTJC) mainly manifests as excessive inflammation leading to joint capsule fibrosis. Transforming growth factor (TGF)-β1, a key regulator of inflammation and fibrosis, can promote fibroblast activation, proliferation, migration, and differentiation into m...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-01-01
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| Series: | Frontiers in Bioengineering and Biotechnology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fbioe.2022.1078527/full |
| _version_ | 1797962118206586880 |
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| author | Yuxin Zhang Yuxin Zhang Yuxin Zhang Zengguang Wang Chenyu Zong Xiaoding Gu Shuai Fan Lili Xu Bin Cai Shenji Lu Shenji Lu |
| author_facet | Yuxin Zhang Yuxin Zhang Yuxin Zhang Zengguang Wang Chenyu Zong Xiaoding Gu Shuai Fan Lili Xu Bin Cai Shenji Lu Shenji Lu |
| author_sort | Yuxin Zhang |
| collection | DOAJ |
| description | Background: Post-traumatic joint contracture (PTJC) mainly manifests as excessive inflammation leading to joint capsule fibrosis. Transforming growth factor (TGF)-β1, a key regulator of inflammation and fibrosis, can promote fibroblast activation, proliferation, migration, and differentiation into myofibroblasts. Platelet-rich plasma (PRP) is considered to have strong potential for improving tissue healing and regeneration, the ability to treat joint capsule fibrosis remains largely unknown.Methods: In this study, we aimed to determine the antifibrotic potential of PRP in vivo or in vitro and its possible molecular mechanisms. The TGF-β1-induced primary joint capsule fibroblast model and rat PTJC model were used to observe several fibrotic markers (TGF-β1, α-SMA, COL-Ⅰ, MMP-9) and signaling transduction pathway (Smad2/3) using histological staining, qRT-PCR and western blot.Results: Fibroblasts transformed to myofibroblasts after TGF-β1 stimulation with an increase of TGF-β1, α-SMA, COL-Ⅰ, MMP-9 and the activation of Smad2/3 in vitro. However, TGF-β1-induced upregulation or activation of these fibrotic markers or signaling could be effectively suppressed by the introduction of PRP. Fibrotic markers’ similar changes were observed in the rat PTJC model and PRP effectively reduced inflammatory cell infiltration and collagen fiber deposition in the posterior joint capsule. Interestingly, HE staining showed that articular cartilage was degraded after rat PTJC, and PRP injection also have the potential to protect articular cartilage.Conclusion: PRP can attenuate pathological changes of joint capsule fibrosis during PTJC, which may be implemented by inhibiting TGF-β1/Smad2/3 signaling and downstream fibrotic marker expression in joint capsule fibroblasts. |
| first_indexed | 2024-04-11T01:08:16Z |
| format | Article |
| id | doaj.art-21be63659216488195709aee1a953e60 |
| institution | Directory Open Access Journal |
| issn | 2296-4185 |
| language | English |
| last_indexed | 2024-04-11T01:08:16Z |
| publishDate | 2023-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Bioengineering and Biotechnology |
| spelling | doaj.art-21be63659216488195709aee1a953e602023-01-04T10:26:22ZengFrontiers Media S.A.Frontiers in Bioengineering and Biotechnology2296-41852023-01-011010.3389/fbioe.2022.10785271078527Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in ratsYuxin Zhang0Yuxin Zhang1Yuxin Zhang2Zengguang Wang3Chenyu Zong4Xiaoding Gu5Shuai Fan6Lili Xu7Bin Cai8Shenji Lu9Shenji Lu10Department of Rehabilitation Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Oral Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai, ChinaDepartment of Rehabilitation Medicine, Huangpu Branch, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Key Laboratory of Orthopedic Implants, Department of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Orthopedics, Affiliated Hospital of Nantong University, Nantong, ChinaDepartment of Rehabilitation Medicine, Huangpu Branch, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Rehabilitation Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Rehabilitation Medicine, Huangpu Branch, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaBackground: Post-traumatic joint contracture (PTJC) mainly manifests as excessive inflammation leading to joint capsule fibrosis. Transforming growth factor (TGF)-β1, a key regulator of inflammation and fibrosis, can promote fibroblast activation, proliferation, migration, and differentiation into myofibroblasts. Platelet-rich plasma (PRP) is considered to have strong potential for improving tissue healing and regeneration, the ability to treat joint capsule fibrosis remains largely unknown.Methods: In this study, we aimed to determine the antifibrotic potential of PRP in vivo or in vitro and its possible molecular mechanisms. The TGF-β1-induced primary joint capsule fibroblast model and rat PTJC model were used to observe several fibrotic markers (TGF-β1, α-SMA, COL-Ⅰ, MMP-9) and signaling transduction pathway (Smad2/3) using histological staining, qRT-PCR and western blot.Results: Fibroblasts transformed to myofibroblasts after TGF-β1 stimulation with an increase of TGF-β1, α-SMA, COL-Ⅰ, MMP-9 and the activation of Smad2/3 in vitro. However, TGF-β1-induced upregulation or activation of these fibrotic markers or signaling could be effectively suppressed by the introduction of PRP. Fibrotic markers’ similar changes were observed in the rat PTJC model and PRP effectively reduced inflammatory cell infiltration and collagen fiber deposition in the posterior joint capsule. Interestingly, HE staining showed that articular cartilage was degraded after rat PTJC, and PRP injection also have the potential to protect articular cartilage.Conclusion: PRP can attenuate pathological changes of joint capsule fibrosis during PTJC, which may be implemented by inhibiting TGF-β1/Smad2/3 signaling and downstream fibrotic marker expression in joint capsule fibroblasts.https://www.frontiersin.org/articles/10.3389/fbioe.2022.1078527/fullplatelet-rich plasmapost-traumatic joint contracturejoint capsule fibrosistransforming growth factor-β1fibroblasts |
| spellingShingle | Yuxin Zhang Yuxin Zhang Yuxin Zhang Zengguang Wang Chenyu Zong Xiaoding Gu Shuai Fan Lili Xu Bin Cai Shenji Lu Shenji Lu Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats Frontiers in Bioengineering and Biotechnology platelet-rich plasma post-traumatic joint contracture joint capsule fibrosis transforming growth factor-β1 fibroblasts |
| title | Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats |
| title_full | Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats |
| title_fullStr | Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats |
| title_full_unstemmed | Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats |
| title_short | Platelet-rich plasma attenuates the severity of joint capsule fibrosis following post-traumatic joint contracture in rats |
| title_sort | platelet rich plasma attenuates the severity of joint capsule fibrosis following post traumatic joint contracture in rats |
| topic | platelet-rich plasma post-traumatic joint contracture joint capsule fibrosis transforming growth factor-β1 fibroblasts |
| url | https://www.frontiersin.org/articles/10.3389/fbioe.2022.1078527/full |
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