Enhanced BMP signalling causes growth plate cartilage dysrepair in rats
Growth plate cartilage injuries often result in bony repair at the injury site and premature mineralisation at the uninjured region causing bone growth defects, for which underlying mechanisms are unclear. With the prior microarray study showing upregulated bone morphogenetic protein (BMP) signallin...
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Published in | Bone (New York, N.Y.) Vol. 145; p. 115874 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
01.04.2021
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Abstract | Growth plate cartilage injuries often result in bony repair at the injury site and premature mineralisation at the uninjured region causing bone growth defects, for which underlying mechanisms are unclear. With the prior microarray study showing upregulated bone morphogenetic protein (BMP) signalling during the injury site bony repair and with the known roles of BMP signalling in bone healing and growth plate endochondral ossification, this study used a rat tibial growth plate drill-hole injury model with or without systemic infusion of BMP antagonist noggin to investigate roles of BMP signalling in injury repair responses within the injury site and in the adjacent “uninjured” cartilage. At days 8, 14 and 35 post-injury, increased expression of BMP members and receptors and enhanced BMP signalling (increased levels of phosphorylated (p)-Smad1/5/8) were found during injury site bony repair. After noggin treatment, injury site bony repair at days 8 and 14 was reduced as shown by micro-CT and histological analyses and lower mRNA expression of osteogenesis-related genes Runx2 and osteocalcin (by RT-PCR). At the adjacent uninjured cartilage, the injury caused increases in the hypertrophic zone/proliferative zone height ratio and in mRNA expression of hypertrophy marker collagen-10, but a decrease in chondrogenesis marker Sox9 at days 14 and/or 35, which were accompanied by increased BMP signalling (increased levels of pSmad1/5/8 protein and BMP7, BMPR1a and target gene Dlx5 mRNA). Noggin treatment reduced the hypertrophic zone/proliferative zone height ratio and collagen-10 mRNA expression, but increased collagen-2 mRNA levels at the adjacent growth plate. This study has identified critical roles of BMP signalling in the injury site bony repair and in the hypertrophic degeneration of the adjacent growth plate in a growth plate drill-hole repair model. Moreover, suppressing BMP signalling can potentially attenuate the undesirable bony repair at injury site and suppress the premature hypertrophy but potentially rescue chondrogenesis at the adjacent growth plate.
•Trauma injury often leads to dysrepair at the injured growth plate cartilage, for which molecular mechanisms are unclear.•BMP signalling was shown upregulated in a prior microarray study, but its function in growth plate repair is unclear.•Systemic treatment with BMP inhibitor noggin suppressed the bony repair at the growth plate injury site in rats.•Systemic BMP inhibitor noggin treatment attenuated premature hypertrophy at the adjacent uninjured growth plate cartilage.•Enhanced BMP signalling promotes injury site bony repair and premature hypertrophy at the uninjured growth plate cartilage. |
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AbstractList | Growth plate cartilage injuries often result in bony repair at the injury site and premature mineralisation at the uninjured region causing bone growth defects, for which underlying mechanisms are unclear. With the prior microarray study showing upregulated bone morphogenetic protein (BMP) signalling during the injury site bony repair and with the known roles of BMP signalling in bone healing and growth plate endochondral ossification, this study used a rat tibial growth plate drill-hole injury model with or without systemic infusion of BMP antagonist noggin to investigate roles of BMP signalling in injury repair responses within the injury site and in the adjacent "uninjured" cartilage. At days 8, 14 and 35 post-injury, increased expression of BMP members and receptors and enhanced BMP signalling (increased levels of phosphorylated (p)-Smad1/5/8) were found during injury site bony repair. After noggin treatment, injury site bony repair at days 8 and 14 was reduced as shown by micro-CT and histological analyses and lower mRNA expression of osteogenesis-related genes Runx2 and osteocalcin (by RT-PCR). At the adjacent uninjured cartilage, the injury caused increases in the hypertrophic zone/proliferative zone height ratio and in mRNA expression of hypertrophy marker collagen-10, but a decrease in chondrogenesis marker Sox9 at days 14 and/or 35, which were accompanied by increased BMP signalling (increased levels of pSmad1/5/8 protein and BMP7, BMPR1a and target gene Dlx5 mRNA). Noggin treatment reduced the hypertrophic zone/proliferative zone height ratio and collagen-10 mRNA expression, but increased collagen-2 mRNA levels at the adjacent growth plate. This study has identified critical roles of BMP signalling in the injury site bony repair and in the hypertrophic degeneration of the adjacent growth plate in a growth plate drill-hole repair model. Moreover, suppressing BMP signalling can potentially attenuate the undesirable bony repair at injury site and suppress the premature hypertrophy but potentially rescue chondrogenesis at the adjacent growth plate. Growth plate cartilage injuries often result in bony repair at the injury site and premature mineralisation at the uninjured region causing bone growth defects, for which underlying mechanisms are unclear. With the prior microarray study showing upregulated bone morphogenetic protein (BMP) signalling during the injury site bony repair and with the known roles of BMP signalling in bone healing and growth plate endochondral ossification, this study used a rat tibial growth plate drill-hole injury model with or without systemic infusion of BMP antagonist noggin to investigate roles of BMP signalling in injury repair responses within the injury site and in the adjacent “uninjured” cartilage. At days 8, 14 and 35 post-injury, increased expression of BMP members and receptors and enhanced BMP signalling (increased levels of phosphorylated (p)-Smad1/5/8) were found during injury site bony repair. After noggin treatment, injury site bony repair at days 8 and 14 was reduced as shown by micro-CT and histological analyses and lower mRNA expression of osteogenesis-related genes Runx2 and osteocalcin (by RT-PCR). At the adjacent uninjured cartilage, the injury caused increases in the hypertrophic zone/proliferative zone height ratio and in mRNA expression of hypertrophy marker collagen-10, but a decrease in chondrogenesis marker Sox9 at days 14 and/or 35, which were accompanied by increased BMP signalling (increased levels of pSmad1/5/8 protein and BMP7, BMPR1a and target gene Dlx5 mRNA). Noggin treatment reduced the hypertrophic zone/proliferative zone height ratio and collagen-10 mRNA expression, but increased collagen-2 mRNA levels at the adjacent growth plate. This study has identified critical roles of BMP signalling in the injury site bony repair and in the hypertrophic degeneration of the adjacent growth plate in a growth plate drill-hole repair model. Moreover, suppressing BMP signalling can potentially attenuate the undesirable bony repair at injury site and suppress the premature hypertrophy but potentially rescue chondrogenesis at the adjacent growth plate. •Trauma injury often leads to dysrepair at the injured growth plate cartilage, for which molecular mechanisms are unclear.•BMP signalling was shown upregulated in a prior microarray study, but its function in growth plate repair is unclear.•Systemic treatment with BMP inhibitor noggin suppressed the bony repair at the growth plate injury site in rats.•Systemic BMP inhibitor noggin treatment attenuated premature hypertrophy at the adjacent uninjured growth plate cartilage.•Enhanced BMP signalling promotes injury site bony repair and premature hypertrophy at the uninjured growth plate cartilage. |
ArticleNumber | 115874 |
Author | Xian, Cory J. Chung, Rosa Xian, Claire H. Su, Yu-Wen Fan, Jian Chen, Yuhui Yao, Lufeng Wang, Liping Wong, Derick S.K. Foster, Bruce K. Xu, Jiake Wang, Liang |
Author_xml | – sequence: 1 givenname: Yu-Wen surname: Su fullname: Su, Yu-Wen organization: University of South Australia, UniSA Clinical and Health Sciences, Adelaide, SA 5001, Australia – sequence: 2 givenname: Derick S.K. surname: Wong fullname: Wong, Derick S.K. organization: University of South Australia, UniSA Clinical and Health Sciences, Adelaide, SA 5001, Australia – sequence: 3 givenname: Jian surname: Fan fullname: Fan, Jian organization: Department of Orthopedics, Tongji Hospital, Tongji University, Shanghai 200065, China – sequence: 4 givenname: Rosa surname: Chung fullname: Chung, Rosa organization: University of South Australia, UniSA Clinical and Health Sciences, Adelaide, SA 5001, Australia – sequence: 5 givenname: Liping surname: Wang fullname: Wang, Liping organization: University of South Australia, UniSA Clinical and Health Sciences, Adelaide, SA 5001, Australia – sequence: 6 givenname: Yuhui surname: Chen fullname: Chen, Yuhui organization: Department of Orthopedics, Orthopaedic Hospital of Guangdong Province, the Third Affiliated Hospital of Southern Medical University, Academy of Orthopaedics of Guangdong Province, Guangzhou 510630, Guangdong, China – sequence: 7 givenname: Claire H. surname: Xian fullname: Xian, Claire H. organization: Discipline of Physiology, Adelaide Medical School, The University of Adelaide, Adelaide, SA 5005, Australia – sequence: 8 givenname: Lufeng surname: Yao fullname: Yao, Lufeng organization: Ningbo No. 6 Hospital, Ningbo University, Ningbo 315040, China – sequence: 9 givenname: Liang surname: Wang fullname: Wang, Liang organization: Department of Orthopedics, Orthopaedic Hospital of Guangdong Province, the Third Affiliated Hospital of Southern Medical University, Academy of Orthopaedics of Guangdong Province, Guangzhou 510630, Guangdong, China – sequence: 10 givenname: Bruce K. surname: Foster fullname: Foster, Bruce K. organization: Department of Orthopaedic Surgery, Flinders Medical Centre, Bedford Park, SA 5042, Australia – sequence: 11 givenname: Jiake surname: Xu fullname: Xu, Jiake organization: School of Pathology and Laboratory Medicine, University of Western Australia, Nedlands, WA 6009, Australia – sequence: 12 givenname: Cory J. surname: Xian fullname: Xian, Cory J. email: cory.xian@unisa.edu.au organization: University of South Australia, UniSA Clinical and Health Sciences, Adelaide, SA 5001, Australia |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33548573$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_bioactmat_2021_10_002 crossref_primary_10_1016_j_cej_2024_152463 crossref_primary_10_7717_peerj_14603 crossref_primary_10_1016_j_cdev_2024_203927 crossref_primary_10_1016_j_toxlet_2024_06_010 crossref_primary_10_3390_cancers15174367 crossref_primary_10_1177_20417314231187956 |
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Keywords | BMP signalling Growth plate BMPs Injury repair Cartilage degeneration Bone growth defects |
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SubjectTerms | BMP signalling BMPs Bone growth defects Cartilage degeneration Growth plate Injury repair |
Title | Enhanced BMP signalling causes growth plate cartilage dysrepair in rats |
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