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The antimicrobial peptide, human β-defensin-1, potentiates in vitro osteoclastogenesis via activation of the p44/42 mitogen-activated protein kinases

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ชื่อเรื่อง : The antimicrobial peptide, human β-defensin-1, potentiates in vitro osteoclastogenesis via activation of the p44/42 mitogen-activated protein kinases
นักวิจัย : Makeudom A. , Supanchart C. , Montreekachon P. , Khongkhunthian S. , Sastraruji T. , Krisanaprakornkit J. , Krisanaprakornkit S.
คำค้น : -
หน่วยงาน : มหาวิทยาลัยเชียงใหม่
ผู้ร่วมงาน : -
ปีพิมพ์ : 2560
อ้างอิง : 01969781 , 2-s2.0-85024853295 , 10.1016/j.peptides.2017.07.004 , https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85024853295&origin=inward , http://cmuir.cmu.ac.th/jspui/handle/6653943832/40125
ที่มา : -
ความเชี่ยวชาญ : -
ความสัมพันธ์ : -
ขอบเขตของเนื้อหา : -
บทคัดย่อ/คำอธิบาย :

© 2017 Elsevier Inc. Previous studies have demonstrated increased expression and raised levels of human β-defensin (hBD)-1 in gingival tissue and crevicular fluid of patients with chronic periodontitis and peri-implantitis, oral bone-resorbing diseases caused by enhanced osteoclastogenesis. Therefore, we aimed to investigate the effect of hBD-1 on osteoclast formation and function and to elucidate the involved signaling pathway in vitro. Human peripheral blood mononuclear cells (PBMCs) were first incubated with various doses of hBD-1 and cell viability was assayed by MTT. PBMCs were treated with macrophage-colony stimulating factor and receptor activator of nuclear factor kappa-B ligand (RANKL) in the presence or absence of non-toxic doses of hBD-1. In vitro osteoclastogenesis was analyzed by tartrate-resistant acid phosphatase (TRAP) staining, osteoclast-specific gene expression, and a resorption pit assay. Involvement of mitogen-activated protein kinases (MAPKs) was studied by immunoblotting and specific MAPK inhibitors. HBD-1 potentiated induction of in vitro osteoclastogenesis by RANKL, as shown by significantly increased number of TRAP-positive multinuclear cells and resorption areas on the dentin slices, and further up-regulated expressions of osteoclast-specific genes compared to those by RANKL treatment (p <  0.05). However, hBD-1 treatment without RANKL failed to induce formation of osteoclast-like cells. A significant and further increase in transient phosp horylation of the p44/42 MAPKs was demonstrated by hBD-1 co-treatment (p  <  0.05), consistent with the inhibitory effect by pretreatment with U0126 or PD98059 on hBD-1-enhanced osteoclastogenesis. Collectively, hBD-1 potentiates the induction of in vitro osteoclastogenesis by RANKL via enhanced phosphorylation of the p44/42 MAPKs.

บรรณานุกรม :
Makeudom A. , Supanchart C. , Montreekachon P. , Khongkhunthian S. , Sastraruji T. , Krisanaprakornkit J. , Krisanaprakornkit S. . (2560). The antimicrobial peptide, human β-defensin-1, potentiates in vitro osteoclastogenesis via activation of the p44/42 mitogen-activated protein kinases.
    เชียงใหม่ : มหาวิทยาลัยเชียงใหม่ .
Makeudom A. , Supanchart C. , Montreekachon P. , Khongkhunthian S. , Sastraruji T. , Krisanaprakornkit J. , Krisanaprakornkit S. . 2560. "The antimicrobial peptide, human β-defensin-1, potentiates in vitro osteoclastogenesis via activation of the p44/42 mitogen-activated protein kinases".
    เชียงใหม่ : มหาวิทยาลัยเชียงใหม่ .
Makeudom A. , Supanchart C. , Montreekachon P. , Khongkhunthian S. , Sastraruji T. , Krisanaprakornkit J. , Krisanaprakornkit S. . "The antimicrobial peptide, human β-defensin-1, potentiates in vitro osteoclastogenesis via activation of the p44/42 mitogen-activated protein kinases."
    เชียงใหม่ : มหาวิทยาลัยเชียงใหม่ , 2560. Print.
Makeudom A. , Supanchart C. , Montreekachon P. , Khongkhunthian S. , Sastraruji T. , Krisanaprakornkit J. , Krisanaprakornkit S. . The antimicrobial peptide, human β-defensin-1, potentiates in vitro osteoclastogenesis via activation of the p44/42 mitogen-activated protein kinases. เชียงใหม่ : มหาวิทยาลัยเชียงใหม่ ; 2560.