p38a MAPK is involved in BMP‐2‐induced odontoblastic differentiation of human dental pulp cells

Qin, Wei; Zhao, Lin; Deng, Rong; Li, D. D.; Song, Zhenyuan; Tian, Yaguang; Wang, R. F.; Ling, Junqi; Zhu, Xiaofeng

doi:10.1111/j.1365-2591.2011.01965.x

Cited by 29 publications

(22 citation statements)

References 45 publications

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“…BMP2-activated p38 was found to participate in BMP2-induced commitment of C3H10T1/2 MPCs to the adipocyte lineage [28]. BMP2 increased ALP activity and matrix mineralization through phosphorylation of p38α in human dental pulp cells (HDPCs) [29]. Moreover, BMPs-induced activation of MAPKs was also found to be essential for other physiological and pathological process, such as chondrogenesis, retina regeneration, tumor angiogenesis and cancer cells metastasis [30], [31], [32], [33].…”

Section: Discussionmentioning

confidence: 98%

“…Several growth factors have shown to trigger MAPKs in different cell models [27], [28], [29], [30], [37], [71], [72], [73], [74]. IGF-1 promoted phosphorylation of p38, ERK1/2 and JNKs, through which to induce expression of osterix in human mesenchymal stem cells [37].…”

Section: Discussionmentioning

confidence: 99%

“…HGF promoted activation of ERK1/2 and p38, and subsequently induced proliferation of lung adenocarcinoma cell line H441 [73]. In addition, MAPKs can also be activated by BMPs stimulation [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], [41], [42], which represents an important mechanism for non-Smads pathway(s) of BMPs signaling. The activation of MAPKs by BMPs could lead to various effects depending on the cell context.…”

Section: Discussionmentioning

confidence: 99%

“…These activated receptors transmit signals by phosphorylating the transcription factors Smads (Smad1, 5, and/or 8) [9], [10], [22], [23], [24], [25], [26], which in turn form a heterodimeric complex with Smad4 in the nucleus and modulate context-dependent gene expression in collaboration with other co-activators. However, growing evidences have implied that BMPs also utilize diverse intracellular signaling molecules in addition to Smads to regulate a wide array of cellular functions [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], [41], [42], [43], [44], [45]. These are collectively called the non-Smads (non-canonical) pathway of BMPs signaling.…”

Section: Introductionmentioning

confidence: 99%

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P38 and ERK1/2 MAPKs Act in Opposition to Regulate BMP9-Induced Osteogenic Differentiation of Mesenchymal Progenitor Cells

et al. 2012

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Although previous studies have demonstrated that BMP9 is highly capable of inducing osteogenic differentiation and bone formation, the precise molecular mechanism involved remains to be fully elucidated. In this current study, we explore the possible involvement and detail effects of p38 and ERK1/2 MAPKs on BMP9-indcued osteogenic differentiation of mesenchymal progenitor cell (MPCs). We find that BMP9 simultaneously stimulates the activation of p38 and ERK1/2 in MPCs. BMP9-induced early osteogenic marker, such as alkaline phosphatase (ALP), and late osteogenic markers, such as matrix mineralization and osteocalcin (OC) are inhibited by p38 inhibitor SB203580, whereas enhanced by ERK1/2 inhibitor PD98059. BMP9-induced activation of Runx2 and Smads signaling are reduced by SB203580, and yet increased by PD98059 in MPCs. The in vitro effects of inhibitors are reproduced with adenoviruses expressing siRNA targeted p38 and ERK1/2, respectively. Using mouse calvarial organ culture and subcutaneous MPCs implantation, we find that inhibition of p38 activity leads to significant decrease in BMP9-induced osteogenic differentiation and bone formation, however, blockage of ERK1/2 results in effective increase in BMP9-indcued osteogenic differentiation in vivo. Together, our results reveal that p38 and ERK1/2 MAPKs are activated in BMP9-induced osteogenic differentiation of MPCs. What is most noteworthy, however, is that p38 and ERK1/2 act in opposition to regulate BMP9-induced osteogenic differentiation of MPCs.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

P38 and ERK1/2 MAPKs Act in Opposition to Regulate BMP9-Induced Osteogenic Differentiation of Mesenchymal Progenitor Cells

et al. 2012

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“…NM_004621.5), and shRNA constructs were generated as described previously (13). Target sequences (Thermo Fisher Scientific, Inc., Waltham, MA, USA) were selected through software provided on the manufacturer's website.…”

Section: Methodsmentioning

confidence: 99%

Role of transient receptor potential channel 6 in the odontogenic differentiation of human dental pulp cells

Yang

Song

Wang

et al. 2017

Experimental and Therapeutic Medicine

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Pulp capping is a restorative technique employed in an attempt to maintain pulpal vitality and generate reparative dentin. Ca2+ released from capping materials is suggested to promote reparative dentin formation. Transient receptor potential channel 6 (TRPC6) is a receptor-operated Ca2+ channel that serves an important role in Ca2+ influx in the majority of non-excitable cells, and influences the calcium signaling and cell respond. Therefore, the purpose of the present study was to gain an insight into the role of TRPC6 in the odontoblastic differentiation of human dental pulp cells (HDPCs). Human dental pulp tissues and HDPCs were obtained from healthy third molars. By immunohistochemical staining, TRPC6 was observed to be highly expressed in the dental pulp tissue, particularly in the odontoblast layer. In addition, the protein level of TRPC6 was increased in a time-dependent manner during odontogenic differentiation of HDPCs. Downregulation of TRPC6 by a lentivirus vector containing TRPC6 shRNA inhibited the process of odontogenic differentiation in HDPCs. In conclusion, the current data demonstrated that TRPC6 served a significant role in the odontogenic differentiation of HDPCs, suggesting it may be a promising therapeutic target in regenerative endodontics.

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Retracted: Downregulated microRNA‐488 enhances odontoblast differentiation of human dental pulp stem cells via activation of the p38 MAPK signaling pathway

Zhao

Cheng

et al. 2018

Journal Cellular Physiology

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Human dental pulp stem cells (hDPSCs) are primarily derived from the pulp tissues of permanent third molar teeth. They were widely used in human bone tissue engineering. It was previously indicated that microRNA (miR) expressions are closely associated with hDPSCs development. However, the specific effect of miR-488 on hDPSCs still remains unclear. In this study, we aimed to investigate effects of miR-488 on the differentiation of hDPSCs into odontoblast cells through the p38 mitogen-activated protein kinases (MAPK) signaling pathway by binding to MAPK1. The hDPSCs were isolated and cultured in vitro. Dual-luciferase reporter gene assay was performed to test the relationship between MAPK1 (p38) and miR-488. Reverse transcription quantitative polymerase chain reaction and western blot analysis were used to detect the mRNA and protein expressions of p38 MAPK signaling pathway-related genes (MAPK1, Ras, and Mitogen-activated protein kinase kinase 3/6 [MKK3/6]), along with expressions of dentin Sialophosphoprotein (DSPP), alkaline phosphatase (ALP), and osteonectin (OCN). ALP staining and alizarin red staining were conducted to detect ALP activity and degree of mineralization. Initially, we found that MAPK1 was the target gene of miR-488. Besides, downregulation of miR-488 was observed to stimulate the p38 MAPK signaling pathway and to increase the messenger RNA and protein expressions of DSPP, ALP, and OCN. Furthermore, ALP activity and formation of a mineralized nodule in hDPSCs were enhanced upon downregulation of miR-488. The aforementioned findings provided evidence supporting that downregulation of miR-488 promotes odontoblastic differentiation of hDPSCs through the p38 MAPK signaling pathway by targeting MAPK1, paving the basis for further study about hDPSCs.

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p38a MAPK is involved in BMP‐2‐induced odontoblastic differentiation of human dental pulp cells

Abstract: p38α MAPK is involved in BMP-2-induced odontoblastic differentiation of HDPCs.

Cited by 29 publications

References 45 publications

P38 and ERK1/2 MAPKs Act in Opposition to Regulate BMP9-Induced Osteogenic Differentiation of Mesenchymal Progenitor Cells

P38 and ERK1/2 MAPKs Act in Opposition to Regulate BMP9-Induced Osteogenic Differentiation of Mesenchymal Progenitor Cells

Role of transient receptor potential channel 6 in the odontogenic differentiation of human dental pulp cells

Retracted: Downregulated microRNA‐488 enhances odontoblast differentiation of human dental pulp stem cells via activation of the p38 MAPK signaling pathway

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