A Tryptamine Derivative, SST-VEDI-1, Inhibits Apoptosis and Stimulates Mineralization in Osteoblasts

Mikami, Yohei; Somei, Masanori; Takagi, Minoru

doi:10.1507/endocrj.k08e-340

Cited by 6 publications

(3 citation statements)

References 38 publications

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“…For example, parathyroid hormone (PTH) regulates the osterix expression predominantly through cAMP-dependent protein kinase A (PKA) signaling in osteoblast-like cells (27) and the overexpression of PKA inhibitor γ (PKIγ) suppressed the OSX expression in C2C12 cells (34). In addition, SST-VEDI-1, which is also a tryptamine derivative and has a similar chemical structure to that of SSH-BM-I, regulates cAMP level (28). Based on the findings of these reports, it is therefore possible that the cAMPdependent signaling pathway via TAAR1 may act on the SSH-BM-I-mediated osteoblast differentiation.…”

Section: Discussionmentioning

confidence: 96%

SSH-BM-I, a Tryptamine Derivative, Stimulates Mineralization in Terminal Osteoblast Differentiation but Inhibits Osteogenesis of Pre-committed Progenitor Cells

2011

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Abstract. SSH-BM-I was synthesized from tryptamine by using a newly developed synthetic method, and it has structural similarity to bromomelatonin. Recently, it had been reported that SSH-BM-I increases osteoblasts in scales of gold fish. However, the effect of SSH-BM-I on osteoblast differentiation in mammalian cells has not yet been examined. Therefore, this study examined the effect of SSH-BM-I on osteoblast differentiation in mesenchymal progenitor-like cells and mature osteoblast-like cells. SSH-BM-I enhanced terminal osteoblast differentiation, as indicated by mineralization, which was accompanied by upregulation of the osteogenic marker genes bone sialoprotein (BSP) and osteocalcin (OC). However, in mesenchymal progenitor ROB-C26 cultures, no mineralized nodules were observed regardless of SSH-BM-I treatment, although BMP-2 was able to induce nodule formation in these cells. Furthermore, BMP-2-induced nodule formation was suppressed by SSH-BM-I treatment in ROB-C26 cultures. We further investigated the impact of the timing and duration of SSH-BM-I treatment on osteoblast differentiation. The effect of SSH-BM-I treatment on osteoblast differentiation of ROB-C26 in the presence of BMP-2 switches from negative to positive sometime between day 6 and 9, because SSH-BM-I treatment enhanced the formation of mineralized nodules when it was started on day 9, but suppressed nodule formation when it was started at day 6 or earlier. These results suggest that the stimulatory effects of SSH-BM-I on the formation of mineralized nodules depend on the degree of cell differentiation.

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Section: Discussionmentioning

confidence: 96%

SSH-BM-I, a Tryptamine Derivative, Stimulates Mineralization in Terminal Osteoblast Differentiation but Inhibits Osteogenesis of Pre-committed Progenitor Cells

2011

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“…Previously, we newly synthesized several compounds containing MS-IPA1 from tryptamine (3). Some of these compounds exhibited an inhibitory effect on apoptosis of osteoblasts (8). In addition, it has been reported that SSH-BM-I, which is also synthesized from tryptamine and has a similar chemical structure to MS-IPA1, increases osteoblast number in the scales of gold fish (9).…”

Section: Discussionmentioning

confidence: 99%

“…A previous report has proposed the hypothesis that a tryptamine compound is metabolized in our body to the corresponding tryptamine derivatives such as SST-VED-I-1, and its biological activity can be modified to become stronger than or different from the original tryptamine compound (7). In fact, recently, we demonstrated that SST-VED-I-1 inhibits starvation-induced apoptosis in osteoblasts, although the original tryptamine compound does not have such an effect (8).…”

Section: Introductionmentioning

confidence: 89%

Inhibitory Effects of a Tryptamine Derivative on Ultraviolet Radiation–Induced Apoptosis in MC3T3-E1 Mouse Osteoblasts

Mikami¹,

Senoo²,

Lee³

et al. 2011

J Pharmacol Sci

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Abstract. MS-IPA1 is a new synthetic compound that is synthesized from tryptamine. Recently, our group demonstrated that SST-VED-I-1, which has a similar chemical structure to MS-IPA1, inhibits starvation-induced apoptosis in osteoblasts. However, the effects of MS-IPA1 on apoptosis in osteoblasts have not yet been examined. Therefore, this study examined the effects of this compound on apoptosis in osteoblasts. In this study, MC3T3-E1 mouse osteoblasts were used and apoptosis was induced by ultraviolet radiation (UV). We investigated the effect of MS-IPA1 on apoptosis by analyzing caspase3/7 activity, translocation of phosphatidylserine (PS), and mRNA expression levels of Bcl-2 and Bax. In addition, it was investigated whether MS-IPA1 affects cell proliferation and cell cycle progression. We found that MS-IPA1 had no effect on cell proliferation or cell cycle progression. However, MS-IPA1 suppressed UV-induced cell death in a dose-dependent manner, which was accompanied with the inhibition of caspase activation and translocation of PS. Furthermore, after UV exposure, Bcl-2 expression was increased in the MS-IPA1-treated cells as compared to that in the vehicle-treated cells. In contrast, Bax expression was decreased in the MS-IPA1-treated cell as compared to that in the vehicle-treated cells. These results suggest that MS-IPA1 has an inhibitory effect on apoptosis in osteoblasts through a Bcl-2 family-dependent signaling pathway.

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Current status of drug therapies for osteoporosis and the search for stem cells adapted for bone regenerative medicine

et al. 2013

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A number of factors can lead to bone disorders such as osteoporosis, in which the balance of bone resorption vs. bone formation is upset (i.e., more bone is resorbed than is formed). The result is a loss of bone mass, with a concomitant decrease in bone density. Drugs for osteoporosis can be broadly classified as "bone resorption inhibitors", which impede bone resorption by osteoclasts, and "bone formation accelerators", which augment bone formation by osteoblasts. Here, we describe representative drugs in each class, i.e., the bisphosphonates and the parathyroid hormone. In addition, we introduce two novel bone formation accelerators, SST-VEDI and SSH-BMI, which are currently under investigation by our research group. On the other hand, regenerative therapy, characterized by (ideally) the use of a patient's own cells to regenerate lost tissue, is now a matter of global interest. At present, candidate cell sources for regenerative therapy include embryonic stem cells (created from embryos based on the fertilization of oocytes), induced pluripotent stem cells (created artificially by using somatic cells as the starting material), and somatic stem cells (found in the tissues of the adult body). This review summarizes the identifying features and the therapeutic potential of each of these stem cell types for bone regenerative medicine. Although a number of different kinds of somatic stem cells have been reported, we turn our attention toward two that are of particular interest for prospective applications in bone repair: the dedifferentiated fat cell, and the deciduous dental pulp-derived stem cell.

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A Tryptamine Derivative, SST-VEDI-1, Inhibits Apoptosis and Stimulates Mineralization in Osteoblasts

Cited by 6 publications

References 38 publications

SSH-BM-I, a Tryptamine Derivative, Stimulates Mineralization in Terminal Osteoblast Differentiation but Inhibits Osteogenesis of Pre-committed Progenitor Cells

SSH-BM-I, a Tryptamine Derivative, Stimulates Mineralization in Terminal Osteoblast Differentiation but Inhibits Osteogenesis of Pre-committed Progenitor Cells

Inhibitory Effects of a Tryptamine Derivative on Ultraviolet Radiation–Induced Apoptosis in MC3T3-E1 Mouse Osteoblasts

Current status of drug therapies for osteoporosis and the search for stem cells adapted for bone regenerative medicine

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