Humanin suppresses receptor activator of nuclear factor-B ligand-induced osteoclast differentiation via AMP-activated protein kinase activation

• 발행기관: 대한생리학회-대한약리학회
• 저자명: Namju Kang Ki Woo Kim Dong Min Shin
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제23권 제5호, 411~417쪽, 전체 7쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2019.09.30

영문 초록

Humanin (HN) is a mitochondrial peptide that exhibits cytoprotective actions against various stresses and diseases. HN has been shown to induce the phosphorylation of AMP-activated protein kinase (AMPK), which is a negative regulator of receptor activator of nuclear factor-B ligand (RANKL). However, the role of HN in osteoclastogenesis or other skeletal disorders remains unknown. Here, we examined whether HN regulates osteoclastogenesis via AMPK activation using bone marrowderived macrophage (BMM) cultures. Our results show that HN inhibited RANKL-induced osteoclast formation and reduced the expression of genes involved in osteoclastogenesis, including nuclear factor of activated T-cells cytoplasmic 1, osteoclastassociated receptor, cathepsin K, and tartrate-resistant acid phosphatase. Moreover, HN increased the levels of phosphorylated AMPK protein; compound C, an AMPK inhibitor, recovered HN-induced osteoclast differentiation. In addition, we found that HN significantly decreased the levels of RANKL-induced reactive oxygen species in BMMs. Therefore, these results indicate that HN plays an important role in osteoclastogenesis and may function as an inhibitor of bone disorders via AMPK activation.

목차

INTRODUCTION

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RESULTS

DISCUSSION

키워드

AMP-activated protein kinase Humanin Osteoclastogenesis Receptor activator of nuclear factor-kB ligand