Abstract
Vitamin K2 (VK2, menaquinone) is a drug for osteoporosis. VK2 acts as a cofactor for γ-glutamyl carboxylase, which catalyzes the carboxylation of specific glutamic acid residues (γ-carboxylation) of substrate proteins. Here we demonstrate that VK2 also regulate osteoblastgenic marker gene expression. Using VK2-immobilzed nanobeads new target proteins were purified and identified from osteoblastic cell line. They are prohibitin 1 and 2 (PHB1 & 2), respectively. To confirm the PHBs function on VK2-dependent transcription, PHB1 & 2 were knock-down and osteocalcin gene 2 transcriptions were analyzed, indicating that PHBs regulate VK2-dependent transcription. Taken together PHBs are VK2 target proteins for osteoblastgenic transcription.
Highlights
Vitamin K (VK) is a fat-soluble vitamin that was discovered in 1929 [1]
VK2 was administrated to the osteoblastic cell line MC3T3-E1, and its osteoblast differentiation markers were analyzed
Alkaline phosphatase (ALP) activity was analyzed in several doses (~1 μM) of VK2
Summary
Vitamin K (VK) is a fat-soluble vitamin that was discovered in 1929 [1]. The most common form of VK in animals is MK-4, which is produced by intestinal bacteria or is metabolically converted from other VKs [3]. VK was originally discovered as an essential factor for blood coagulation [4]. VK-dependent γ-carboxylation plays an important role in bone homeostasis. Osteocalcin, a critical regulator of calcium uptake and bone mineralization in osteoblasts, is activated by γ-carboxylation [5]. Undercarboxylation of osteocalcin due to vitamin K deficiency is thought to result in osteoporosis [7]. MK-4, one of the most potent VKs, has been widely used as a therapeutic drug for the above-mentioned diseases [8]
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