{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T14:28:50Z","timestamp":1761488930875},"reference-count":40,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2012,9,18]],"date-time":"2012-09-18T00:00:00Z","timestamp":1347926400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2012,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Tissue\u2010specific patterns of gene expression play an important role in the distinctive features of each organ. Small CTD phosphatases (SCPs) 1\u20133 are recruited by repressor element 1 (RE\u20101)\u2010silencing transcription factor\/neuron\u2010restrictive silencer factor (REST\/NRSF) to neuronal genes that contain RE\u20101 elements, leading to neuronal gene silencing in non\u2010neuronal cells. SCPs are highly expressed in the heart and contain microRNAs (miR)\u201026b, 26a\u20102, and 26a\u20101 with the same seed sequence in their introns. Therefore, we tried to investigate the roles of miR\u201026b and its host gene in neonatal rat cardiomyocytes. Overexpression of miR\u201026b suppressed the mRNA expression levels of ANF, \u03b2MHC, and ACTA1 and reduced the cell surface area in cardiomyocytes. We confirmed that miR\u201026b targets the 3\u2032 untranslated region (3\u2032UTR) of GATA4 and canonical transient receptor potential channel (TRPC) 3. Conversely, silencing of the endogenous miR\u201026b family enhanced the expression levels of TRPC3 and GATA4. On the other hand, overexpression of SCP1 induced the mRNA expression of ANF and \u03b2MHC and increased the cell surface area in cardiomyocytes. Next, we compared the effect of overexpression of SCP1 with its introns and SCP1 cDNA to observe the net function of SCP1 expression on cardiac hypertrophy. When the expression levels of SCP1 were the same, the overexpression of SCP1 cDNA had a greater effect at inducing cardiac hypertrophy than SCP1 cDNA with its intron. In conclusion, SCP1 itself has the potential to induce cardiac hypertrophy; however, the effect is suppressed by intronic miR\u201026b in cardiomyocytes. miR\u201026b has an antagonistic effect on its host gene SCP1. J. Cell. Biochem. 113: 3455\u20133465, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24222","type":"journal-article","created":{"date-parts":[[2012,6,7]],"date-time":"2012-06-07T15:07:24Z","timestamp":1339081644000},"page":"3455-3465","source":"Crossref","is-referenced-by-count":18,"title":["MicroRNA 26b encoded by the intron of small CTD phosphatase (SCP) 1 has an antagonistic effect on its host 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