20-hydroxyecdysone-induced bone morphogenetic protein-2-dependent osteogenic differentiation through the ERK pathway in human periodontal ligament stem cells
“…Hence, it was concluded that β-ecdysone induced proliferation of osteoblasts in vitro on MG-63 and primary osteoblasts at low doses. The observed results are in agreement with the earlier studies which demonstrated that β-ecdysone exhibited osteoprotective effects [36] , [37] induced the osteogenic differentiation in mouse mesenchymal stem cells [38] and in human periodontal ligament stem cells [39] . Fig.…”
BackgroundIndian ethnomedicine acclaims Tinosporacordifolia as a bone strengthening agent and prescribes it for the treatment of bone fractures, gout and other inflammatory diseases of the bone.Objective(a) To understand the potential of T. cordifolia to act as a Selective Estrogen Receptor Modulator (SERM) on in vitro models. (b) To understand the toxic effects (if any) of T. cordifolia in vivo. (c) To understand the effects of β-ecdysone (proposed osteoprotective principle of T. cordifolia) on the growth of human osteoblast-like cells MG-63 and rat primary culture of osteoblasts. (d) To conduct phytochemical analysis on T. cordifolia extract to confirm the presence of β-ecdysone.Materials and MethodsThe role of T. cordifolia as SERM was analyzed by investigating the effect of the extract on the growth of MCF-7 and HeLa cells. The effects of T. cordifolia in vivo was studied by biochemical (Liver function and renal function tests) and histopathological (Hematoxylin/Eosin staining) analysis. Phytochemical analysis of T.cordifolia was carried out by performing FT-IR and LC-ESI-MS analysis.Results(a) T. cordifolia extract exerted non-estrogenic effects on MCF-7 and HeLa cells implicating its role as SERM. (b) High doses of T. cordifolia extract (750 and 1000 mg/kg body wt.) showed impairment of hepatic and renal function, induced pathological alterations in hepatic and renal architecture in albino rats. (c) β-ecdysone an ecdysteroid proposed as the osteoprotective principle of T. cordifolia exhibited significant prostimulatory effects on osteoblast cells and rat primary osteoblasts. (d) Phytochemical analysis confirmed the presence of β-ecdysone in alcoholic extract of T. cordifolia extract substantiating its role as the osteoprotective principle of T. cordifolia.Conclusion(a) T. cordifolia could function as SERM and can have applications in the therapy of osteoporosis. (b) β-ecdysone is the osteoprotective principle of T. cordifolia.
“…Hence, it was concluded that β-ecdysone induced proliferation of osteoblasts in vitro on MG-63 and primary osteoblasts at low doses. The observed results are in agreement with the earlier studies which demonstrated that β-ecdysone exhibited osteoprotective effects [36] , [37] induced the osteogenic differentiation in mouse mesenchymal stem cells [38] and in human periodontal ligament stem cells [39] . Fig.…”
BackgroundIndian ethnomedicine acclaims Tinosporacordifolia as a bone strengthening agent and prescribes it for the treatment of bone fractures, gout and other inflammatory diseases of the bone.Objective(a) To understand the potential of T. cordifolia to act as a Selective Estrogen Receptor Modulator (SERM) on in vitro models. (b) To understand the toxic effects (if any) of T. cordifolia in vivo. (c) To understand the effects of β-ecdysone (proposed osteoprotective principle of T. cordifolia) on the growth of human osteoblast-like cells MG-63 and rat primary culture of osteoblasts. (d) To conduct phytochemical analysis on T. cordifolia extract to confirm the presence of β-ecdysone.Materials and MethodsThe role of T. cordifolia as SERM was analyzed by investigating the effect of the extract on the growth of MCF-7 and HeLa cells. The effects of T. cordifolia in vivo was studied by biochemical (Liver function and renal function tests) and histopathological (Hematoxylin/Eosin staining) analysis. Phytochemical analysis of T.cordifolia was carried out by performing FT-IR and LC-ESI-MS analysis.Results(a) T. cordifolia extract exerted non-estrogenic effects on MCF-7 and HeLa cells implicating its role as SERM. (b) High doses of T. cordifolia extract (750 and 1000 mg/kg body wt.) showed impairment of hepatic and renal function, induced pathological alterations in hepatic and renal architecture in albino rats. (c) β-ecdysone an ecdysteroid proposed as the osteoprotective principle of T. cordifolia exhibited significant prostimulatory effects on osteoblast cells and rat primary osteoblasts. (d) Phytochemical analysis confirmed the presence of β-ecdysone in alcoholic extract of T. cordifolia extract substantiating its role as the osteoprotective principle of T. cordifolia.Conclusion(a) T. cordifolia could function as SERM and can have applications in the therapy of osteoporosis. (b) β-ecdysone is the osteoprotective principle of T. cordifolia.
“…Thus, bivalves could be very likely self-biosynthesize of ecdysone derived from cholesterol using CYPs, but the effect of CYP should be carefully considered. In human, ecdysone stimulates the expression of BMP2 mediated by ERK in human periodontal ligament stem cells [51]. Thus, we proposed that bivalve species possessed the relative elements in hormone signal pathway that could play vital roles in the neuroendocrine-biomineralization crosstalk during metamorphosis.…”
BackgroundMarine bivalves undergo complex development processes, such as shell morphology conversion and changes of anatomy and life habits. In this study, the transcriptomes of pearl oyster Pinctada fucata martensii and Pacific oyster Crassostrea gigas at different development stages were analyzed to determine the key molecular events related to shell formation, settlement and metamorphosis.ResultAccording to the shell matrix proteome, biomineralization-related genes exhibited a consensus expression model with the critical stages of shell formation. Differential expression analysis of P. f. martensii, revealed the negative regulation and feedback of extracellular matrixs as well as growth factor pathways involved in shell formation of larvae, similar to that in C. gigas. Furthermore, neuroendocrine pathways in hormone receptors, neurotransmitters and neuropeptide receptors were involved in shell formation, settlement and metamorphosis.ConclusionOur research demonstrated the main clusters of regulation elements related to shell formation, settlement and metamorphosis. The regulation of shell formation and metamorphosis could be coupled forming the neuroendocrine-biomineralization crosstalk in metamorphosis. These findings could provide new insights into the regulation in bivalve development.Electronic supplementary materialThe online version of this article (10.1186/s12864-019-5505-8) contains supplementary material, which is available to authorized users.
“…The intracellular signal transduction pathway associated with ERK is thought to be a classical MAPKs signal transduction pathway. The MAPK/ERK signalling pathway plays an important role in osteogenesis and has become a hotspot for recent research 17 – 20 . As an important receptor, tyrosine kinase, EGFR could combine with EGF on the membrane, activate the phosphorylation cascade (EGF/EGFR → Ras → Raf → MAPK/ERK), and cause the changes to transcription factors and proteins in the nucleus, eventually having a variety of biological functions 21 .…”
Coptidis Rhizoma binds to the membrane receptors on hPDLSC/CMC, and the active ingredient Berberine (BER) that can be extracted from it may promote the proliferation and osteogenesis of periodontal ligament stem cells (hPDLSC). The membrane receptor that binds with BER on the cell surface of hPDLSC, the mechanism of direct interaction between BER and hPDLSC, and the related signal pathway are not yet clear. In this research, EGFR was screened as the affinity membrane receptor between BER and hPDLSC, through retention on CMC, competition with BER and by using a molecular docking simulation score. At the same time, the MAPK PCR Array was selected to screen the target genes that changed when hPDLSC was simulated by BER. In conclusion, BER may bind to EGFR on the cell membrane of hPDLSC so the intracellular ERK signalling pathways activate, and nuclear-related genes of FOS change, resulting in the effect of osteogenesis on PDLSC.
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