{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T17:09:18Z","timestamp":1790356158845,"version":"4.1.0"},"reference-count":0,"publisher":"S. Karger AG","issue":"1","license":[{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2017,1,1]],"date-time":"2017-01-01T00:00:00Z","timestamp":1483228800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Physiol Biochem"],"published-print":{"date-parts":[[2017]]},"abstract":"<jats:p>Background\/Aims: This study aimed to explore the role of TGF-\u03b2 in tendon-to-bone healing after anterior cruciate ligament (ACL) reconstruction using bone marrow-derived mesenchymal stem cells (BMSCs) through the TGF-\u03b2\/MAPK signaling pathway in a New Zealand white rabbit model. Methods: A total of 72 healthy male New Zealand white rabbits were selected for these experiments. Flow cytometry and immunofluorescence were used to detect the expression of BMSC surface markers, and qRT-PCR was performed to detect TGF-\u03b2 mRNA expression. The ACL reconstruction model was established with autografts. The rabbits were randomly divided into the following groups: inhibition of TGF-\u03b2 (inhibition), over-expression of TGF-\u03b2 (over-expression), empty vector and untreated (n = 18 per group). Hematoxylineosin (HE) staining, toluidine blue staining and Masson trichrome staining were conducted to observe any chondrocyte-like cell growth, and biomechanical tests were used to calculate the maximum load and rigidity. Three-dimensional CT imaging and Western blotting were applied to detect changes in bone tunnel size and bone density and the expression levels of TGF-\u03b2\/MAPK signaling pathway-related proteins, respectively. Results: CD90 and CD44 were positively expressed, while CD11b was not detected. Compared with the empty vector and untreated groups, TGF-\u03b2 mRNA expression was significantly decreased in the inhibition group but increased in the over-expression group; the latter group had a larger number of fibroblasts, a tighter tendon-bone interface, an increased number of chondrocyte-like cells and fibrochondrocytes, and more collagen fibers than the inhibition, empty vector and untreated groups. Compared with the empty vector and untreated groups, the maximum load and rigidity; the CT values of bone tunnel and bone tunnel margin; and the protein expression levels of TGF-\u03b2, p-ERK1\/2, p-p38, p-JNK, c-jun and c-myc were significantly down-regulated in the inhibition group but up-regulated in the over-expression group. Conclusion: Our study indicated that up-regulating TGF-\u03b2 expression in BMSCs from New Zealand white rabbits could promote tendon-to-bone healing after ACL reconstruction by regulating the TGF-\u03b2\/MAPK signaling pathway.<\/jats:p>","DOI":"10.1159\/000456046","type":"journal-article","created":{"date-parts":[[2017,1,26]],"date-time":"2017-01-26T17:14:39Z","timestamp":1485450879000},"page":"213-226","source":"Crossref","is-referenced-by-count":56,"title":["Up-Regulation of TGF-\u03b2 Promotes Tendon-to-Bone Healing after Anterior Cruciate Ligament Reconstruction using Bone Marrow-Derived Mesenchymal Stem Cells through the TGF-\u03b2\/MAPK Signaling Pathway in a New Zealand White Rabbit Model"],"prefix":"10.1159","volume":"41","author":[{"given":"Rui","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong-Gang","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2017,1,20]]},"container-title":["Cellular Physiology and Biochemistry"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/456046","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/456046","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/456046","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T13:13:23Z","timestamp":1745414003000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000456046"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2017]]},"references-count":0,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2017,5,4]]}},"URL":"https:\/\/doi.org\/10.1159\/000456046","archive":["Portico"],"relation":{},"ISSN":["1015-8987","1421-9778"],"issn-type":[{"value":"1015-8987","type":"print"},{"value":"1421-9778","type":"electronic"}],"subject":[],"published":{"date-parts":[[2017]]}}}