Noggin Combined With Human Dental Pulp Stem Cells to Promote Skeletal Muscle Regeneration

A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in...

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Published inStem cells international Vol. 2024; no. 1; p. 2812390
Main Authors Zhang, Meng-Han, Yu, Li-Ming, Zhang, Wei-Hua, Deng, Jia-Jia, Sun, Bing-Jing, Chen, Mei-Hua, Huang, Wei, Li, Jiao, He, Hua, Han, Xin-Xin, Liu, Yue-Hua
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Published United States John Wiley & Sons, Inc 01.01.2024
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Abstract A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7 + satellite‐like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p‐Smad1/5/9, while Noggin eliminated BMP4‐induced p‐Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p‐Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin‐pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin‐treated DPSCs can benefit the Pax7 + SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite‐like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite‐like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.
AbstractList A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7 + satellite-like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p-Smad1/5/9, while Noggin eliminated BMP4-induced p-Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p-Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin-pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin-treated DPSCs can benefit the Pax7 + SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite-like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite-like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.
A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7+ satellite-like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p-Smad1/5/9, while Noggin eliminated BMP4-induced p-Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p-Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin-pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin-treated DPSCs can benefit the Pax7+ SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite-like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite-like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.
A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7[sup.+] satellite-like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p-Smad1/5/9, while Noggin eliminated BMP4-induced p-Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p-Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin-pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin-treated DPSCs can benefit the Pax7[sup.+] SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite-like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite-like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.
A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7 satellite-like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p-Smad1/5/9, while Noggin eliminated BMP4-induced p-Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p-Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin-pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin-treated DPSCs can benefit the Pax7 SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite-like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite-like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.
A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7+ satellite-like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p-Smad1/5/9, while Noggin eliminated BMP4-induced p-Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p-Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin-pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin-treated DPSCs can benefit the Pax7+ SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite-like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite-like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to their high proliferative and differentiation capacities. However, the current myogenic induction efficiency of human DPSCs hinders their use in muscle regeneration due to the unknown induction mechanism. In this study, we treated human DPSCs with Noggin, a secreted antagonist of bone morphogenetic protein (BMP), and discovered that Noggin can effectively promote myotube formation. We also found that Noggin can accelerate the skeletal myogenic differentiation (MyoD) of DPSCs and promote the generation of Pax7+ satellite-like cells. Noggin increased the expression of myogenic markers and the transcriptional and translational abundance of satellite cell (SC) markers in DPSCs. Moreover, BMP4 inhibited Pax7 expression and activated p-Smad1/5/9, while Noggin eliminated BMP4-induced p-Smad1/5/9 in DPSCs. This finding suggests that Noggin antagonizes BMP by downregulating p-Smad and facilitates the MyoD of DPSCs. Then, we implanted Noggin-pretreated DPSCs combined with Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML) and observed a 73% reduction in the size of the defect and a 69% decrease in scar tissue. Noggin-treated DPSCs can benefit the Pax7+ SC pool and promote muscle regeneration. This work reveals that Noggin can enhance the production of satellite-like cells from the MyoD of DPSCs by regulating BMP/Smad signaling, and these satellite-like cell bioconstructs might possess a relatively fast capacity for muscle regeneration.
Audience Academic
Author Zhang, Wei-Hua
Yu, Li-Ming
He, Hua
Zhang, Meng-Han
Huang, Wei
Chen, Mei-Hua
Deng, Jia-Jia
Li, Jiao
Han, Xin-Xin
Liu, Yue-Hua
Sun, Bing-Jing
AuthorAffiliation 3 Department of Neurosurgery, Third Affiliated Hospital of Second Military Medical University, Shanghai, China
1 Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China
2 School of Stomatology Affiliated to Medical College, Zhejiang University, Hangzhou, China
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Snippet A proper source of stem cells is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an ideal source for the treatment of muscle injuries due to...
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StartPage 2812390
SubjectTerms Antibodies
Biomarkers
Bone growth
Bone morphogenetic proteins
Cell cycle
Cell differentiation
Dental pulp
Muscles
Musculoskeletal system
MyoD protein
Myogenesis
Myotubes
Neuromuscular diseases
Noggin protein
Regeneration
Satellite cells
Skeletal muscle
Smad protein
Stem cell transplantation
Stem cells
Tibialis anterior muscle
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Title Noggin Combined With Human Dental Pulp Stem Cells to Promote Skeletal Muscle Regeneration
URI https://www.ncbi.nlm.nih.gov/pubmed/39758702
https://www.proquest.com/docview/3151687949
https://www.proquest.com/docview/3151879393
https://pubmed.ncbi.nlm.nih.gov/PMC11699990
https://doaj.org/article/7e80171f4dcc4c9aaa68b52f502e8e27
Volume 2024
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