Author
Keke Luo
Bio: Keke Luo is an academic researcher from Chinese Ministry of Education. The author has contributed to research in topics: Osteoblast & Skeletal fluorosis. The author has an hindex of 2, co-authored 3 publications receiving 7 citations.
Papers
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TL;DR: In this paper, the authors investigated the function of the miRNA let-7c-5p to regulate CyclinD1 in fluoride-induced osteoblast proliferation and activation.
8 citations
TL;DR: In this article, the role and specific molecular mechanism of miR-486-3p in fluoride-induced osteoblast proliferation and activation via CyclinD1 was investigated.
Abstract: Fluoride is a persistent environmental pollutant, and its excessive intake contributes to skeletal and dental fluorosis The mechanisms underlying fluoride-induced abnormal osteoblast proliferation and activation, which are related to skeletal fluorosis, have not yet been fully clarified As important epigenetic regulators, microRNAs (miRNAs) participate in bone metabolism On the basis of our previous miRNA-seq results and bioinformatics analysis, this study investigated the role and specific molecular mechanism of miR-486-3p in fluoride-induced osteoblast proliferation and activation via CyclinD1 Herein, in the fluoride-challenged population, we observed that miR-486-3p expression decreased while CyclinD1 and transforming growth factor (TGF)-β1 increased, and miR-486-3p level correlated negatively with the expression of CyclinD1 and TGF-β1 genes Further, we verified that sodium fluoride (NaF) decreases miR-486-3p expression in human osteoblasts and overexpression of miR-486-3p reduces fluoride-induced osteoblast proliferation and activation Meanwhile, we demonstrated that miR-486-3p regulates NaF-induced upregulation of CyclinD1 by directly targeting its 3'-untranslated region (3'-UTR) In addition, we observed that NaF activates the TGF-β1/Smad2/3/CyclinD1 axis and miR-486-3p mediates transcriptional regulation of CyclinD1 by TGF-β1/Smad2/3 signaling pathway via targeting TGF-β1 3'-UTR in vitro This study, thus, contributes significantly in revealing the mechanism of miR-486-3p-mediated CyclinD1 upregulation in skeletal fluorosis and sheds new light on endemic fluorosis treatment
8 citations
TL;DR: It is demonstrated that fluoride exposure induced the downregulation of miR-4755-5p and downregulation promoted fluoride-induced osteoblast activation by increasing Cyclin D1 protein expression.
6 citations
TL;DR: In this article , a series of scutellarin and scutellarein-N,N-bis-substituted carbamate-l-amino acid derivatives were designed, synthesized and evaluated as multifunctional therapeutic agents for the treatment of Alzheimer's disease.
5 citations
TL;DR: Wang et al. as discussed by the authors designed and evaluated scutellarein hybrids for the treatment of Alzheimer's disease (AD) using a 2-hydroxymethyl-3,5,6-trimethylpyrazine fragment.
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01 Jan 2009
TL;DR: In this article, a review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.
Abstract: MicroRNAs (miRNAs) are endogenous ∼23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.
646 citations
TL;DR: In this paper, a comprehensive review of the pathogenesis of skeletal fluorosis is presented, which summarizes and analyzes relevant findings to provide a basis for comprehensive understandings of the disease and propose more effective prevention and therapeutic strategies.
Abstract: Fluorine is widely dispersed in nature and has multiple physiological functions. Although it is usually regarded as an essential trace element for humans, this view is not held universally. Moreover, chronic fluorosis, mainly characterized by skeletal fluorosis, can be induced by long-term excessive fluoride consumption. High concentrations of fluoride in the environment and drinking water are major causes, and patients with skeletal fluorosis mainly present with symptoms of osteosclerosis, osteochondrosis, osteoporosis, and degenerative changes in joint cartilage. Etiologies for skeletal fluorosis have been established, but the specific pathogenesis is inconclusive. Currently, active osteogenesis and accelerated bone turnover are considered critical processes in the progression of skeletal fluorosis. In recent years, researchers have conducted extensive studies in fields of signaling pathways (Wnt/β-catenin, Notch, PI3K/Akt/mTOR, Hedgehog, parathyroid hormone, and insulin signaling pathways), stress pathways (oxidative stress and endoplasmic reticulum stress pathways), epigenetics (DNA methylation and non-coding RNAs), and their inter-regulation involved in the pathogenesis of skeletal fluorosis. In this review, we summarised and analyzed relevant findings to provide a basis for comprehensive understandings of the pathogenesis of skeletal fluorosis and hopefully propose more effective prevention and therapeutic strategies.
19 citations
TL;DR: Based on the recent research focus on the novel cholinesterase inhibitors with multiple bio-functions, a review aims at summarizing and discussing the most recent studies excavating the potential carbamate-based MTDLs with choline inhibition efficacy, to accelerate the pace of pleiotropic choline-based inhibitors for coping Alzheimer's disease as discussed by the authors .
Abstract: Alzheimer's disease (AD), as the fourth leading cause of death among the elderly worldwide, has brought enormous challenge to the society. Due to its extremely complex pathogeneses, the development of multi-target directed ligands (MTDLs) becomes the major strategy for combating AD. Carbamate moiety, as an essential building block in the development of MTDLs, exhibits structural similarity to neurotransmitter acetylcholine (ACh) and has piqued extensive attention in discovering multifunctional cholinesterase inhibitors. To date, numerous preclinical studies demonstrate that carbamate-based cholinesterase inhibitors can prominently increase the level of ACh and improve cognition impairments and behavioral deficits, providing a privileged strategy for the treatment of AD. Based on the recent research focus on the novel cholinesterase inhibitors with multiple biofunctions, this review aims at summarizing and discussing the most recent studies excavating the potential carbamate-based MTDLs with cholinesterase inhibition efficacy, to accelerate the pace of pleiotropic cholinesterase inhibitors for coping AD.
16 citations
TL;DR: In this paper, the authors investigated the function of the miRNA let-7c-5p to regulate CyclinD1 in fluoride-induced osteoblast proliferation and activation.
8 citations
TL;DR: In this article, the role and specific molecular mechanism of miR-486-3p in fluoride-induced osteoblast proliferation and activation via CyclinD1 was investigated.
Abstract: Fluoride is a persistent environmental pollutant, and its excessive intake contributes to skeletal and dental fluorosis The mechanisms underlying fluoride-induced abnormal osteoblast proliferation and activation, which are related to skeletal fluorosis, have not yet been fully clarified As important epigenetic regulators, microRNAs (miRNAs) participate in bone metabolism On the basis of our previous miRNA-seq results and bioinformatics analysis, this study investigated the role and specific molecular mechanism of miR-486-3p in fluoride-induced osteoblast proliferation and activation via CyclinD1 Herein, in the fluoride-challenged population, we observed that miR-486-3p expression decreased while CyclinD1 and transforming growth factor (TGF)-β1 increased, and miR-486-3p level correlated negatively with the expression of CyclinD1 and TGF-β1 genes Further, we verified that sodium fluoride (NaF) decreases miR-486-3p expression in human osteoblasts and overexpression of miR-486-3p reduces fluoride-induced osteoblast proliferation and activation Meanwhile, we demonstrated that miR-486-3p regulates NaF-induced upregulation of CyclinD1 by directly targeting its 3'-untranslated region (3'-UTR) In addition, we observed that NaF activates the TGF-β1/Smad2/3/CyclinD1 axis and miR-486-3p mediates transcriptional regulation of CyclinD1 by TGF-β1/Smad2/3 signaling pathway via targeting TGF-β1 3'-UTR in vitro This study, thus, contributes significantly in revealing the mechanism of miR-486-3p-mediated CyclinD1 upregulation in skeletal fluorosis and sheds new light on endemic fluorosis treatment
8 citations