Angiotensin II suppresses osteoblastic differentiation and mineralized nodule formation via AT1 receptor in ROS17/2.8 cells

Nakai, Kumiko; Kawato, Takayuki; Morita, Toyoko; Yamazaki, Yoji; Tanaka, Hideki; Tonogi, Morio; Oki, Hidero; Maeno, Masao

doi:10.5114/aoms.2015.52369

Cited by 28 publications

(35 citation statements)

References 46 publications

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“…However, AT1 selective antagonist of losartan is used for treatment of hypertension and cardiac hypertrophy. Losartan also rescued bone formation reduced by Ang II in osteoblasts (Nakai et al, ). In contrast, Losartan decreased bone volume/tissue volume (%) whereas rescued blood pressure in hypertension mouse model (Asaba et al, ).…”

Section: Discussionmentioning

confidence: 97%

LIPUS suppressed LPS‐induced IL‐1α through the inhibition of NF‐κB nuclear translocation via AT1‐PLCβ pathway in MC3T3‐E1 cells

Nagao

Tanabe

Manaka

et al. 2017

Journal Cellular Physiology

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Inflammatory cytokines, interleukin (IL)-1, IL-6, and TNF-α, are involved in inflammatory bone diseases such as rheumatoid osteoarthritis and periodontal disease. Particularly, periodontal disease, which destroys alveolar bone, is stimulated by lipopolysaccharide (LPS). Low-intensity pulsed ultrasound (LIPUS) is used for bone healing in orthopedics and dental treatments. However, the mechanism underlying effects of LIPUS on LPS-induced inflammatory cytokine are not well understood. We therefore aimed to investigate the role of LIPUS on LPS-induced IL-1α production. Mouse calvaria osteoblast-like cells MC3T3-E1 were incubated in the presence or absence of LPS (Porphyromonas gingivalis), and then stimulated with LIPUS for 30 min/day. To investigate the role of LIPUS, we determined the expression of IL-1α stimulated with LIPUS and treated with an angiotensin II receptor type 1 (AT1) antagonist, Losartan. We also investigate to clarify the pathway of LIPUS, we transfected siRNA silencing AT1 (siAT1) in MC3T3-E1. LIPUS inhibited mRNA and protein expression of LPS-induced IL-1α. LIPUS also reduced the nuclear translocation of NF-κB by LPS-induced IL-1α. Losartan and siAT1 blocked all the stimulatory effects of LIPUS on IL-1α production and IL-1α-mediated NF-κB translocation induced by LPS. Furthermore, PLCβ inhibitor U73122 recovered NF-κB translocation. These results suggest that LIPUS inhibits LPS-induced IL-1α via AT1-PLCβ in osteoblasts. We exhibit that these findings are in part of the signaling pathway of LIPUS on the anti-inflammatory effects of IL-1α expression.

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Section: Discussionmentioning

confidence: 97%

LIPUS suppressed LPS‐induced IL‐1α through the inhibition of NF‐κB nuclear translocation via AT1‐PLCβ pathway in MC3T3‐E1 cells

Nagao

Tanabe

Manaka

et al. 2017

Journal Cellular Physiology

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“…25(OH)D levels inversely correlate with renin activity in plasma as well as with elevated circulating levels of angiotensin II [18][19][20]. Some data suggest that angiotensin II may have an effect on osteoblastic differentiation and expression of osteogenesis-related transcription factors [21]. There are also studies about the effect of spironolactone on improving vitamin D metabolism (changes in kidney gene expression) [22].…”

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confidence: 99%

Vitamin D serum levels in women using contraception containing drospirenone – a preliminary study

Ciebiera

Włodarczyk²,

Słabuszewska-Jóźwiak

et al. 2019

aoms

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Vitamin D is a group of steroid compounds soluble in fats. Vitamin D has powerful, pleiotropic effects all over the human body. It is synthesized in human skin, but can also be found in dietary supplements and fortified foods. Vitamin D receptors (VDR) can be found in many tissues, as well as in the female reproductive tract [1,2]. According to recent reports, it is believed that vitamin D has a beneficial effect on lowering the risk of various diseases, e.g. multiple forms of cancer, diabetes, cardiovascular diseases, metabolic syndrome, multiple sclerosis, inflammatory bowel diseases and uterine fibroids [1][2][3][4][5][6]. Vitamin D regulates cell proliferation and differentiation, inhibits angiogenesis and stimulates apoptosis [1,2,4,5]. Vitamin D levels are mostly measured using serum 25-hydroxyvitamin D (25(OH)D) concentration, which is considered to be the best known marker of vitamin D obtained through both diet and body synthesis. According to Holick, the vitamin D level should be higher than 30 ng/ml [1].Ethinylestradiol (EE2) is a derivative of 17β-estradiol (E2), the major endogenous human estrogen. EE2 is used in many forms of combined oral contraception (COC) and is one of the most commonly used medications for this purpose. Ethinylestradiol is hormonally effective by activating the estrogen receptor and thus exerts its estrogenic effects [7].Drospirenone is a steroidal progestin (of the spironolactone group) used in contraception and hormonal replacement therapy. It is also an aldosterone antagonist with potassium-sparing properties. It is an agonist of the progesterone receptor and an antagonist of the mineralocorticoid and androgen receptors, and hence a progestagen, antimineralocorticoid and antiandrogen. Drospirenone does not present any estrogenic or glucocorticoid or antiglucocorticoid activity. It has a potent antigonadotropic effect at sufficient dosages as a result of progesterone receptor activation. It has been stated that drospirenone has a pharmacological profile that is closely related to that of natural progesterone [8]. Drospirenone is about ten times more potent as an antimineralocorticoid in comparison to spironolactone [8][9][10]. The drospirenone antimineralocorticoid activity promotes sodium excretion and prevents water retention [10].It is believed that contraceptives containing estrogens or estrogens combined with progestins may affect 25(OH)D serum concentrations.

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“…In these osteoblastic cells, Ang II also promoted decrease in Runt‐related transcription factor 2 (RUNX2) and bone formation marker osteocalcin (OCN), while Osterix (Osx) and osteopontin (OPN) expression was unaffected. Mineralized nodule formation and calcium content in mineralized nodules decreased during the differentiation of ROS17/2.8 cells with Ang II stimulus . In cardiac fibroblasts, Ang II bound to AT1 receptors promoted increase in integrins α and β (ITGA5 and ITGB5) …”

Section: Introductionmentioning

confidence: 99%

“…Araújo et al., in addition to showing lower RANKL production in telmisartan‐treated rats with EP, reported increased OPG in these same animals, a finding that disfavors bone resorption during disease progression. Some osteoblast markers such as alkaline phosphatase (ALP) may be increased in patients with periodontitis; however, in osteoblastic ROS17/2.8 cells, Ang II suppressed ALP activity . In these osteoblastic cells, Ang II also promoted decrease in Runt‐related transcription factor 2 (RUNX2) and bone formation marker osteocalcin (OCN), while Osterix (Osx) and osteopontin (OPN) expression was unaffected.…”

Section: Introductionmentioning

confidence: 99%

AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers

Dionísio

Souza

Ishikiriama

et al. 2019

Journal of Periodontology

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Background:The initiation and progression of periodontitis might involve a local renin-angiotensin system in periodontal tissue. This study hypothesized that Losartan treatment could promote protection to rats submitted to experimental periodontitis (EP) by attenuating alveolar bone loss due to reduction in inflammatory cytokines, better reactive oxidant species regulation and maintenance of the balance between bone formation and resorption factors. Methods:One hundred and thirty rats were submitted to EP with a silk suture thread (4.0) placed around the lower right first molar for 1, 3, 7, and 14 consecutive days. The study comprised four groups: G1-control without EP; G2-animals with EP treated with water; G3-Losartan-treated animals (treatment started at the same day of EP induction), and G4-animals previously treated with Losartan for 30 days followed by induction of EP and continuity of treatment.Results: G2 rats had greater bone loss volume, increased number, and thickness and decreased separation of trabeculae. On the other hand, G4 animals showed significant improvements in these parameters. Histological analysis revealed that EP favors inflammatory cell infiltration and junctional epithelium, cementum with alveolar bone crest destruction, but animals pretreated with Losartan (G4) did not show these features. Although the G3 animals did not demonstrate the improvements detected in G4, mRNA expression results were similar. In mandibular tissue, EP promoted mRNA increases for ACE, AT1 receptor, and inflammatory mediators as well as decreases for antioxidant enzymes. However, Losartan treatments attenuated these responses in addition to promoting an increase in bone formation markers and transcription factors.Conclusion: AT1 receptor modulates EP progression. K E Y W O R D Santi-inflammatory agents, antioxidant(s), bone biology, connective tissue biology, cytokine(s), experimental periodontitis, gene expression J Periodontol. 2020;91:533-544.

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Angiotensin II suppresses osteoblastic differentiation and mineralized nodule formation via AT1 receptor in ROS17/2.8 cells

Cited by 28 publications

References 46 publications

LIPUS suppressed LPS‐induced IL‐1α through the inhibition of NF‐κB nuclear translocation via AT1‐PLCβ pathway in MC3T3‐E1 cells

LIPUS suppressed LPS‐induced IL‐1α through the inhibition of NF‐κB nuclear translocation via AT1‐PLCβ pathway in MC3T3‐E1 cells

Vitamin D serum levels in women using contraception containing drospirenone – a preliminary study

AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers

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