ArticleBiochemical and biophysical research communications2011
Deletion of Smad4 in fibroblasts leads to defective chondrocyte maturation and cartilage production in a TGFβ type II receptor independent manner.
Article in Biochemical and biophysical research communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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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.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- The role of fibroblast growth factor 8 in cartilage development and disease.Journal of cellular and molecular medicine · 2022Review
- Whole-exome sequencing analysis in 10 families of sporadic microtia with thoracic deformities.Molecular genetics & genomic medicine · 2021Article
- Generation of an Fsp1 (fibroblast-specific protein 1)-Flpo transgenic mouse strain.Genesis (New York, N.Y. : 2000) · 2020Article
- BMP7 Signaling inMolecular cancer research : MCR · 2018Article
- Notch1 Pathway Activity Determines the Regulatory Role of Cancer-Associated Fibroblasts in Melanoma Growth and Invasion.PloS one · 2015Article
- Utilizing past and present mouse systems to engineer more relevant pancreatic cancer models.Frontiers in physiology · 2014Review
- Cdc42 promotes host defenses against fatal infection.Infection and immunity · 2013Article
- Immunohistological localization of BMP-2, BMP-7, and their receptors in knee joints with focal cartilage lesions.TheScientificWorldJournal · 2012Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The transforming growth factor β (TGFβ) superfamily growth factors play vital roles during the development, homeostasis, and pathogenesis of multi-cellular organisms. Smad4 serves as an exclusive co-activating smad that elicits most of the transcription responses invoked by the TGFβ superfamily members. We used Cre recombinase driven by the Fsp1/S100A4 promoter to delete the Smad4 gene in fibroblasts. We show that Fsp1/S100A4 is expressed in the elastic and fibrocartilage, and demonstrate that the fsp1-Cre; Smad4 flox/flox mutants have normal body size, but exhibit a short ear phenotype due to the deletion of the Smad4 gene in the ear chondrocytes. In contrast, TGFβ type II receptor deletion using Fsp1-cre does not lead to this phenotype, supporting the notion that non-TGFβ mediated signaling via Smad4 is essential for proper formation of ear cartilage during development. Smad4 deficiency in Fsp1(+) fibroblasts leads to defective chondrocyte maturation and cartilage production, likely due to a deficiency in bone morphogenic protein 5 (BMP-5) mediated signaling via Smad4. Our results emphasize the importance of BMP signaling pathways in the maturation and function of certain lineages of chondrocytes and offer an insight into the heterogeneity of the chondrocyte population in the body.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.