ArticleMolecular and cellular biochemistry2014
The role of TGFβ1 stimulating ROCK I signal pathway to reorganize actin in a rat experimental model of developmental dysplasia of the hip.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- Interleukin-1β and tumor necrosis factor-α increase stiffness and impair contractile function of articular chondrocytes.Acta biochimica et biophysica Sinica · 2015Article
Corrections and comments
- Retraction · 2015-08-17Ethical Violations by Author · Compromised Peer Review · Investigation by Journal/Publisher · · The retraction notice specifies that the 'Publisher and Editor retract this article in accordance with the recommendations of the Committee on Publication Ethics (COPE).';
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Importance of actin organization in control of chondrocyte phenotype is well established, but little is known about the role of transforming growth factor-β1 (TFGβ1) in regulating of ROCK I signal pathway. Here, we investigated the role of the TGFβ1, a well-studied member of the TGF-β superfamily, in chondrogenesis. Newborn Rats were randomly assigned to developmental dysplasia of the hip (DDH) group and control group. The isolated hips were performed with HE staining and immunohistochemistry. The chondrocytes was isolated and stained by immunofluorescence. The relative quantification of TGFβ1 on mRNA level was determined using real-time RT-PCR, and its secretion in culture supernatant in each well was detected by means of ELISA. The expression of ROCK I and ROCK II was detected by means of Western Blot. The relative amounts of actin in detergent-soluble and insoluble fractions were determined. Furthermore, TGFβ1 were employed to stimulate normal primary culture chondrocytes in vitro. We found TFGβ1 significantly changed in acetabulum chondrocytes after mechanical overloading. Over expression of TFGβ1 was observed by means of RT-PCR and ELISA assay. The expression of ROCK I was significantly increased in DDH acetabulum chondrocytes compared with normal cells. The detergent-soluble actin was confirmed reorganization in DDH chondrocytes. Furthermore, TFGβ1 can stimulate the ROCK I signaling to modulate actin location in vitro. In conclusion, our data suggested that TFGβ1 expression suppresses chondrogenesis through the control of ROCK signaling and actin organization.
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Registered trials
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