{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2022,3,30]],"date-time":"2022-03-30T15:29:54Z","timestamp":1648654194452},"reference-count":21,"publisher":"American Scientific Publishers","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["j biomed nanotechnol"],"published-print":{"date-parts":[[2021,7,1]]},"abstract":"<jats:p>Achondroplasia is a kind of congenital dysplasia due to the defect of endochondral ossification. Achondroplasia is considered to be a protein folding disease leading to endoplasmic reticulum stress. Endoplasmic reticulum stress may lead to disease by affecting the function and survival\n state of chondrocytes, but the specific mechanism requires further study. In this study, bioinformatics methods, online database mining, screening of differentially expressed genes for pathway enrichment, and interaction analysis were conducted to detect the Wnt family member 5a (Wnt5a) gene.\n Additionally, we designed a novel DNAzymes-based nanocomposite that can simultaneously silence Wnt5a genes in chondrocytes. The nanocomposite was composed of amino-functionalized cobalt oxyhydroxide nanoflakes modified by DNAzymes that target the Wnt5a gene. Further, we conducted <jats:italic>in vitro<\/jats:italic>\n experiments to verify that Wnt5a can mediate the mitogen-activated protein kinase signaling pathway through the endoplasmic reticulum stress pathway to affect the proliferation of chondrocytes.<\/jats:p>","DOI":"10.1166\/jbn.2021.3119","type":"journal-article","created":{"date-parts":[[2021,8,27]],"date-time":"2021-08-27T04:34:25Z","timestamp":1630038865000},"page":"1426-1434","source":"Crossref","is-referenced-by-count":0,"title":["The Effect of Wnt Family Member 5a Gene Silencing on the Proliferation of Achondroplasia Using a DNAzymes-CoOOH Nanocomposite"],"prefix":"10.1166","volume":"17","author":[{"given":"Hairui","family":"Xie","sequence":"first","affiliation":[{"name":"Department of Pediatrics Center, Zhujiang Hospital of Southern Medical University, Guangzhou 510280, Guangdong, PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lili","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Center, Zhujiang Hospital of Southern Medical University, Guangzhou 510280, Guangdong, PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhijiang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Center, Zhujiang Hospital of Southern Medical University, Guangzhou 510280, Guangdong, PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hong","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Center, Zhujiang Hospital of Southern Medical University, Guangzhou 510280, Guangdong, PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"17","reference":[{"issue":"(4)","key":"r1","doi-asserted-by":"crossref","first-page":"pp.291","DOI":"10.1002\/dvdy.24479","article-title":"Achondroplasia: Development, pathogenesis, and therapy.","volume":"246","author":"Ornitz","year":"2017","journal-title":"Developmental Dynamics"},{"issue":"(3)","key":"r2","first-page":"pp.185","article-title":"Bone dysplasia series. achondroplasia, hypochondroplasia and thanatophoric dysplasia: Review and update.","volume":"50","author":"Lemyre","year":"1999","journal-title":"Canadian Association of Radiologists Journal"},{"issue":"(R1)","key":"r3","doi-asserted-by":"crossref","first-page":"pp.R2","DOI":"10.1093\/hmg\/ddv419","article-title":"Advances in treatment of achon-droplasia and osteoarthritis.","volume":"25","author":"Klag","year":"2016","journal-title":"Human Molecular Genetics"},{"issue":"(5-6)","key":"r4","doi-asserted-by":"crossref","first-page":"pp.104","DOI":"10.1007\/s10354-020-00741-6","article-title":"New developments in the management of achondroplasia.","volume":"170","author":"H\u00d4gler","year":"2020","journal-title":"Wiener Medizinische Wochenschrift"},{"key":"r5","doi-asserted-by":"crossref","first-page":"p.1.","DOI":"10.1186\/s13023-018-0972-6","article-title":"Achondroplasia: A comprehensive clinical review.","volume":"14","author":"Pauli","year":"2019","journal-title":"Orphanet Journal of Rare Diseases"},{"issue":"(8)","key":"r6","doi-asserted-by":"crossref","first-page":"pp.399","DOI":"10.1007\/s10038-004-0165-0","article-title":"Rapid detection of FGFR3 gene mutation in achondroplasia by DHPLC system-coupling heteroduplex and fluorescence-enhanced primer-extension analysis.","volume":"49","author":"Su","year":"2004","journal-title":"Journal of Human Genetics"},{"issue":"(1)","key":"r7","doi-asserted-by":"crossref","first-page":"pp.11","DOI":"10.3109\/10837459709022605","article-title":"Evaluation of in vitro release rate and in vivo absorption characteristics of four metoprolol tartrate immediate-release tablet formulations.","volume":"2","author":"Rekhi","year":"1997","journal-title":"Pharmaceutical Development and Technology"},{"issue":"(3)","key":"r8","doi-asserted-by":"crossref","first-page":"p.156.","DOI":"10.1007\/s00604-019-3279-y","article-title":"A hybrid material composed of guanine-rich single stranded DNA and cobalt(III) oxyhydroxide (CoOOH) nanosheets as a fluorescentprobe for ascorbic acid via formation of a complex between G-quadruplex and thioflavin T.","volume":"186","author":"Liu","year":"2019","journal-title":"Microchimica Acta"},{"issue":"(11)","key":"r9","doi-asserted-by":"crossref","first-page":"pp.2503","DOI":"10.1093\/hmg\/dds065","article-title":"An activating fgfr3 mutation affects trabecular bone formation via a paracrine mechanism during growth.","volume":"21","author":"Mugniery","year":"2012","journal-title":"Human Molecular Genetics"},{"issue":"(3)","key":"r10","doi-asserted-by":"crossref","first-page":"p.665.","DOI":"10.3390\/ijms18030665","article-title":"Endoplasmic reticulum stress and unfolded protein response in cartilage pathophysiology; 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