{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T04:34:57Z","timestamp":1791434097995,"version":"4.3.3"},"reference-count":54,"publisher":"Springer Science and Business Media LLC","issue":"1","content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Biomed Sci"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Dysmorphogenesis and multiple organ defects are well known in zebrafish (<jats:italic>Danio rerio<\/jats:italic>) embryos with T-box transcription factor 5 (<jats:italic>tbx5<\/jats:italic>) deficiencies, mimicking human Holt-Oram syndrome.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Using an oligonucleotide-based microarray analysis to study the expression of special genes in <jats:italic>tbx5<\/jats:italic> morphants, we demonstrated that GH and some GH-related genes were markedly downregulated. Zebrafish embryos microinjected with <jats:italic>tbx5<\/jats:italic>-morpholino (MO) antisense RNA and mismatched antisense RNA in the 1-cell stage served as controls, while zebrafish embryos co-injected with exogenous growth hormone (GH) concomitant with <jats:italic>tbx5<\/jats:italic>-MO comprised the treatment group.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>The attenuating effects of GH in <jats:italic>tbx5<\/jats:italic>-MO knockdown embryos were quantified and observed at 24, 30, 48, 72, and 96\u2009h post-fertilization. Though the understanding of mechanisms involving GH in the <jats:italic>tbx5<\/jats:italic> functioning complex is limited, exogenous GH supplied to <jats:italic>tbx5<\/jats:italic> knockdown zebrafish embryos is able to enhance the expression of downstream mediators in the GH and insulin-like growth factor (IGF)-1 pathway, including <jats:italic>igf1<\/jats:italic>, <jats:italic>ghra<\/jats:italic>, and <jats:italic>ghrb<\/jats:italic>, and signal transductors (<jats:italic>erk1<\/jats:italic>, <jats:italic>akt2<\/jats:italic>), and eventually to correct dysmorphogenesis in various organs including the heart and pectoral fins. Supplementary GH also reduced apoptosis as determined by a TUNEL assay and decreased the expression of apoptosis-related genes and proteins (<jats:italic>bcl2<\/jats:italic> and <jats:italic>bad<\/jats:italic>) according to semiquantitative reverse-transcription polymerase chain reaction and immunohistochemical analysis, respectively, as well as improving cell cycle-related genes (<jats:italic>p27<\/jats:italic> and <jats:italic>cdk2<\/jats:italic>) and cardiomyogenetic genes (<jats:italic>amhc<\/jats:italic>, <jats:italic>vmhc<\/jats:italic>, and <jats:italic>cmlc2<\/jats:italic>).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Based on our results, <jats:italic>tbx5<\/jats:italic> knockdown causes a pseudo GH deficiency in zebrafish during early embryonic stages, and supplementation of exogenous GH can partially restore dysmorphogenesis, apoptosis, cell growth inhibition, and abnormal cardiomyogenesis in <jats:italic>tbx5<\/jats:italic> knockdown zebrafish in a paracrine manner.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1423-0127-19-63","type":"journal-article","created":{"date-parts":[[2012,7,9]],"date-time":"2012-07-09T14:13:42Z","timestamp":1341843222000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The paracrine effect of exogenous growth hormone alleviates dysmorphogenesis caused by tbx5 deficiency in zebrafish (Danio rerio) embryos"],"prefix":"10.1186","volume":"19","author":[{"given":"Tzu-Chun","family":"Tsai","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jen-Kann","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sie-Lin","family":"Choo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu-Yu","family":"Yeh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ren-Bing","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsin-Yu","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jen-Her","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2012,7,9]]},"reference":[{"key":"402_CR1","doi-asserted-by":"publisher","first-page":"30","DOI":"10.1038\/ng0197-30","volume":"15","author":"CT Basson","year":"1997","unstructured":"Basson CT, Bachinsky DR, Lin RC, Levi T, Elkins JA, Soults J, Grayzel D, Kroumpouzou E, Traill TA, Leblanc-Straceski J, Renault B, Kucherlapati R, Seidman JG, Seidman CE: Mutations in human TBX5 cause limb and cardiac malformation in Holt-Oram syndrome. 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