Cross-talk between Wnt and Bone Morphogenetic Protein 2 (BMP-2) Signaling in Differentiation Pathway of C2C12 Myoblasts

Nakashima, Aiko; Katagiri, Takenobu; Tamura, Masato

doi:10.1074/jbc.m504612200

Cited by 137 publications

(138 citation statements)

References 57 publications

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“…Indeed modulation of canonical Wnt signaling by BMP2 has been reported previously [36]. To confirm the co-expression of the red reporter and SP7, Wnt1TR positive and negative cells isolated by FACS were deposited onto glass microscope slides by cytocentrifugation, fixed and then subsequently immunostained for SP7.…”

Section: Discussionmentioning

confidence: 89%

Progenitors in Peripheral Nerves Launch Heterotopic Ossification

Olmsted-Davis

Salisbury²,

Hoang³

et al. 2017

Stem Cells Translational Medicine

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Studies presented here, using a murine model of bone morphogenetic protein type 2 (BMP2)-induced HO show that the protein initiates HO by signaling through progenitors in the endoneurium of peripheral nerves. In the mouse, these cells were identified in the endoneurium one day after BMP2 induction using antibody against phosphoSMAD (PS) 1, 5, and 8. Studies conducted in a tracking mouse that contains a tamoxifen-regulated Wnt1-Cre recombinase crossed with a td Tomato red (TR) reporter (Wnt1CreErt:Ai9Tm) confirmed their neural origin. In this model both BMP2 induction and tamoxifen are absolutely required to induce TR. SP7+(osterix+)TR+ cells were found in the endoneurium on day 1 and associated with bone on day 7. Quantification of TR+ and TR− cells isolated by FACS showed that all SP7+ cells were found in the TR+ population, whereas only about 80 percent of the TR+ cells expressed SP7. Pre-chondrocytes (Sox 9+) and transient brown fat (tBAT, UCP1+) also co-expressed TR, suggesting that the progenitor in nerves is multi-potential. The endoneurium of human nerves near the site of HO contained many PS+ cells, and SP7+ cells were found in nerves and on bone in tissue from patients with HO. Control tissues and nerves did not contain these PS+ and SP7+ cells. Some osteoblasts on bone from patients with HO were positive for PS, suggesting the continued presence of BMP during bone formation. The data suggests that the progenitors for HO are derived from the endoneurium in both the mouse model of HO and in humans with HO.

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Section: Discussionmentioning

confidence: 89%

Progenitors in Peripheral Nerves Launch Heterotopic Ossification

Olmsted-Davis

Salisbury²,

Hoang³

et al. 2017

Stem Cells Translational Medicine

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“…The myoblast cell line C2C12 and the osteoblast cell line MC3T3-E1 were obtained and cultured as described previously [18]. For osteoblastic differentiation, MC3T3-E1 cells were cultured for 3 weeks in α-MEM containing both 5 mM β-glycerophosphate and 100 g/mL of ascorbic acid, with medium changes every 3 days.…”

Section: Cell Culturesmentioning

confidence: 99%

“…The plasmid DNA was transfected into cells using Lipofectamine 2000 (Invitrogen) as described previously [18].…”

Section: Expression Plasmids and Transfectionmentioning

confidence: 99%

“…Total RNA was extracted from the cells using Isogen (Nippongene, Toyama, Japan) as described previously [18].…”

Section: Reverse Transcription-polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

“…RT-PCR was performed as previously described [18] Quantitative RT-PCR (qRT-PCR) was performed using assay-on-demand TaqMan probes (Applied Biosystems) and the StepOne ® real time PCR system [21,22]. The relative level of gene expression was quantified using the comparative C T method with GAPDH as the endogenous control.…”

Section: Reverse Transcription-polymerase Chain Reaction (Rt-pcr)mentioning

confidence: 99%

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Regulation of neuropeptide Y Y1 receptor expression by bone morphogenetic protein 2 in C2C12 myoblasts

Kurebayashi

Sato

Fujisawa

et al. 2013

Biochemical and Biophysical Research Communications

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The neuropeptide Y (NPY) system is known as one of the major neural signaling pathways. NPY, produced by peripheral tissues including osteoblasts, is known to bind to the Y1 receptor. Recently, osteoblast-specific Y1 receptor knockout mice were developed and were found to have a high bone mass phenotype, indicating a role for the NPY-Y1 receptor axis as a regulator of bone homeostasis. However, regulation of Y1 receptor expression during osteoblastic differentiation remains unexplored. In the present study, we examined the role of bone morphogenetic protein

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Cenani–Lenz syndrome and other related syndactyly disorders due to variants in LRP4, GREM1/FMN1, and APC: Insight into the pathogenesis and the relationship to polyposis through the WNT and BMP antagonistic pathways

Al‐Qattan

Alkuraya

2018

American J of Med Genetics Pt A

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Cenani–Lenz (C–L) syndrome is characterized by oligosyndactyly, metacarpal synostosis, phalangeal disorganization, and other variable facial and systemic features. Most cases are caused by homozygous and compound heterozygous missense and splice mutations of the LRP4 gene. Currently, the syndrome carries one OMIM number (212780). However, C–L syndrome‐like phenotypes as well as other syndactyly disorders with or without metacarpal synostosis/phalangeal disorganization are also known to be associated with specific LRP4 mutations, adenomatous polyposis coli (APC) truncating mutations, genomic rearrangements of the GREM1‐FMN1 locus, as well as FMN1 mutations. Surprisingly, patients with C–L syndrome‐like phenotype caused by APC truncating mutations have no polyposis despite the increased levels of β catenin. The LRP4 and APC proteins act on the WNT (wingless‐type integration site family) canonical pathway, whereas the GREM‐1 and FMN1 proteins act on the bone morphogenetic protein (BMP) pathway. In this review, we discuss the different mutations associated with C–L syndrome, classify its clinical features, review familial adenomatous polyposis caused by truncating APC mutations and compare these mutations to the splicing APC mutation associated with syndactyly, and finally, explore the pathophysiology through a review of the cross talks between the WNT canonical and the BMP antagonistic pathways.

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Cross-talk between Wnt and Bone Morphogenetic Protein 2 (BMP-2) Signaling in Differentiation Pathway of C2C12 Myoblasts

Cited by 137 publications

References 57 publications

Progenitors in Peripheral Nerves Launch Heterotopic Ossification

Progenitors in Peripheral Nerves Launch Heterotopic Ossification

Regulation of neuropeptide Y Y1 receptor expression by bone morphogenetic protein 2 in C2C12 myoblasts

Cenani–Lenz syndrome and other related syndactyly disorders due to variants in LRP4, GREM1/FMN1, and APC: Insight into the pathogenesis and the relationship to polyposis through the WNT and BMP antagonistic pathways

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