2017
DOI: 10.1242/bio.021436
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Smad4 regulates growth plate matrix production and chondrocyte polarity

Abstract: Smad4 is an intracellular effector of the TGFβ family that has been implicated in Myhre syndrome, a skeletal dysplasia characterized by short stature, brachydactyly and stiff joints. The TGFβ pathway also plays a critical role in the development, organization and proliferation of the growth plate, although the exact mechanisms remain unclear. Skeletal phenotypes in Myhre syndrome overlap with processes regulated by the TGFβ pathway, including organization and proliferation of the growth plate and polarity of t… Show more

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Cited by 11 publications
(8 citation statements)
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“…30 In fact, these pathways involved in cell polarity are highly conserved whereby cells regulate the cytoskeletal organization above and beyond the subcellular organelle localization to facilitate cell proliferation and migration. SMAD4 regulates cell polarity in chondrocytes 31 that is a process changing theshape, size, migration and orientation of the chondrocytes. SMAD4 also plays in 'stem cell maintenance'.…”
Section: S Mad 4 Modul Ate S S Tem Cell Fe Atu R E Smentioning
confidence: 99%
“…30 In fact, these pathways involved in cell polarity are highly conserved whereby cells regulate the cytoskeletal organization above and beyond the subcellular organelle localization to facilitate cell proliferation and migration. SMAD4 regulates cell polarity in chondrocytes 31 that is a process changing theshape, size, migration and orientation of the chondrocytes. SMAD4 also plays in 'stem cell maintenance'.…”
Section: S Mad 4 Modul Ate S S Tem Cell Fe Atu R E Smentioning
confidence: 99%
“…The pattern of malformations and minor anomalies observed in patients with Myhre syndrome including ToF, Hirschsprung disease, schwannoma, nerve sheath tumors, and iris abnormalities suggests that Myhre syndrome may also be viewed as a neurocristopathy (Brazel, 1992; Lewis et al, 2017; Mort et al, 2015; Ritter & Martin, 2019). At least at present, other manifestations of Myhre syndrome, such as short stature and progressive fibrotic changes, might be linked to the specific role of SMAD4 in organization and proliferation of extracellular matrix (Whitaker et al, 2017).…”
Section: Discussionmentioning
confidence: 99%
“…[55][56][57] For example, Smad4 depletion in chondrocytes using either Tbx18-Cre or Col2a-Cre resulted in chondrodysplasia and subsequent shortening of the limbs. [58][59][60] Multiple defects in the growth plate were observed, including an imbalance in ECM synthesis and degradation, altered chondrocyte polarity, and altered chondrocyte hypertrophy. Postnatal disruption of Smad4 in osteoblasts using Bglap-Cre-mediated recombination affected bone formation, and the mice had a reduced bone mass and bone mineral density.…”
Section: Ltbp3 (Ad and Gd)mentioning
confidence: 99%
“…Since the systemic knockout of Smad4 is lethal during early embryonic development, many of these mouse models focus on phenotypes of Smad4 ablation in specific tissues or cell types using the Cre/Lox system 55–57 . For example, Smad4 depletion in chondrocytes using either Tbx18 ‐Cre or Col2a ‐Cre resulted in chondrodysplasia and subsequent shortening of the limbs 58–60 . Multiple defects in the growth plate were observed, including an imbalance in ECM synthesis and degradation, altered chondrocyte polarity, and altered chondrocyte hypertrophy.…”
Section: Mouse Models For Acromelic Dysplasiasmentioning
confidence: 99%