Establishment of a clonal osteogenic cell line from newborn mouse calvaria

Kodama, Hiroaki; Amagai, Yuji; Sudo, Hiroko; Kasai, S; Yamamoto, S.

doi:10.2330/joralbiosci1965.23.899

Cited by 483 publications

(202 citation statements)

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“…29) We further investigated the effects of benidipine on osteoblastic functions using osteoblastic cell line MC3T3-E1, 30) which is widely used in studies on various aspects of osteoblast differentiation since it expresses osteoblast markers and forms a mineralized extracellular matrix. 31,32) There we showed that benidipine stimulated not only ALP activity but also mineral deposition. In an attempt to elucidate its target of action, we first demonstrated that blocking L-type calcium channel promotes osteoblast differentiation from the following observations: 1) The effect of benidipine was completely abolished by an excess amount of Bay K 8644, a calcium channel agonist; 2) Verapamil and diltiazem, which belong to a structurally different class of calcium channel blockers from benidipine, also enhanced ALP activity.…”

mentioning

confidence: 92%

Effects of Various Antihypertensive Drugs on the Function of Osteoblast.

Nishiya

Sugimoto

2001

Biological & Pharmaceutical Bulletin

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Several studies have suggested that high blood pressure is associated with abnormalities in calcium metabolism, leading to increased calcium loss, secondary activation of the parathyroid gland, and increased removal of calcium from bone. [1][2][3][4][5][6][7] Consistently, studies in hypertensive rats have shown that hypercalciuria and ensuing hyperparathyroidism lead to reduced growth and detectable decrease in total bonemineral content later in life. 8,9) Recently, it was also shown that higher blood pressure in elderly white women is statistically associated with increased bone loss at the femoral neck, which may contribute to bone fracture. 10) Drugs used as primary choice for the treatment of hypertension include calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor type1 (AT1) antagonists, diuretics, b-blockers, and a-blockers. 11) The first three drugs are especially widely used in Japan. The mechanism by which each drug lowers blood pressure differs. Calcium channel blockers primarily inhibit calcium influx through the L-type voltage-dependent calcium channel at the level of vascular smooth muscle, thereby disrupting the excitation contraction process. 12,13) Both ACE inhibitors and AT1 antagonists interfere with the renin-angiotensin system (RAS). The former inactivates the conversion of angiotensin I into angiotensin II (Ang II), which is a vasoconstrictive peptide, while the latter blocks the binding of Ang II to its receptor. 14,15) Osteoblasts are derived from mesenchymal stem cells and play a pivotal role in bone formation. During differentiation, they first express type I collagen, then alkaline phosphatase (ALP), and other bone matrix proteins and finally form mineralized bone. Osteoblasts express voltage-dependent calcium channels. 16) Various bone regulatory factors such as vitamin D 3 , [17][18][19] parathyroid hormone, 17,20,21) and prostaglandin E 2 17,22) cause a rise in intracellular calcium concentration ([Ca 2ϩ ] i ), at least part of which is decreased by dihydropyridine-type calcium channel blockers. These factors also promote or inhibit osteoblast differentiation. [23][24][25][26] Thus, it is suggested that signaling through the L-type calcium channel may be important for osteoblast functions. However, the fact that these factors give rise to multiple signals independent of calcium influx (i.e., transcription of specific genes, 27) cAMP production, 20,28) release of calcium ion from intracellular store 17) ) obscures the role of L-type calcium channel. Recently, Kosaka and Uchii found that a calcium channel blocker benidipine, but not amlodipine or nifedipine, increased ALP activity of osteoblastic cells isolated from neonatal mouse calvaria. 29) We further investigated the effects of benidipine on osteoblastic functions using osteoblastic cell line MC3T3-E1, 30) which is widely used in studies on various aspects of osteoblast differentiation since it expresses osteoblast markers and forms a mineralized extracellular matrix. 31,32) There we ...

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confidence: 92%

Effects of Various Antihypertensive Drugs on the Function of Osteoblast.

Nishiya

Sugimoto

2001

Biological & Pharmaceutical Bulletin

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“…MC3T3-E1 cells retain many osteoblast-like features such as high ALP activity, type I collagen synthesis and mineralization in vitro [5,6]. The ALP of this cell is known to be activated by PTH [9[.…”

Section: Discussionmentioning

confidence: 99%

“…However, the involvement of protein kinase C in signal transduction system remains unclear. Therefore, we studied the effects of TPA and OAG, potent activators of protein kinase C [1], on DNA synthesis and ALP activity in osteoblast-like MC3T3-E1 cells cloned from newborn mouse calvaria [5,6]. We also studied the interaction of these protein kinase C activators with other osteoblast modulators, IGF-I [7,8] and PTH [9].…”

Section: Introductionmentioning

confidence: 99%

Possible involvement of protein kinase C in proliferation and differentiation of osteoblast‐like cells

et al. 1989

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In cloned osteoblast-like cells, MC3T3-E1, 12-O-tetradeeanoylphorbol-13-acetate (TPA), a protein kinase C activating phorbol ester, and I-oleoyl-2-acetylglycerol (OAG), a specific activator for protein kinase C, stimulated DNA synthesis in a dose-dependent manner. Both TPA and OAG acted synergistically with insulin-like growth factor I to stimulate DNA synthesis. TPA as well as OAG suppressed the increase in alkaline phosphatase activity of MC3T3-E 1 cells induced by parathyroid hormone. These results suggest that protein kinase C is involved in the process which directs osteoblastlike cells toward proliferation.Protein kinase C; Osteoblast

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“…In chronic inflammatory diseases such as rheumatoid arthritis and periodontitis, characterized by the destruction of mineralized tissue, it has been recognized that bradykinin is involved in the process of bone resorption [2,3]. In in vitro studies, it has recently been reported that bradykinin stimulates the production of prostaglandins in osteoblasts [4,5], including osteoblast-like MC3T3-E1 cells derived from newborn mouse calvaria [6,7]. As for the signal transduction mechanism of bradykinin in osteoblasts, it has been reported that bradykinin induces phosphoinositide (PI) hydrolysis and causes an increase in intracellular Ca2+ [5,8] [9,10].…”

Section: Bradykininmentioning

confidence: 99%