OR01-2 Cardiac calcium channel expression in heart-specific GH receptor gene disrupted mice

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: OR01-Cell Specific GH & IGF-1 Signaling
Saturday, June 15, 2013: 11:30 AM-1:00 PM
Presentation Start Time: 11:45 AM
Room 134 (Moscone Center)
Xingbo Liu*, Adam Jara, Edward Owen List, Darlene E Berryman and John Joseph Kopchick
Ohio University, Athens, OH
Heart failure occurs when the heart cannot pump enough blood and oxygen to support other organs. It is the primary cause of more than 55,000 deaths each year in US, and the five year survival rate is less than 50%. There is accumulating evidence correlating GH deficiency with heart failure. GH has been shown to play roles in cardiac growth, myocardial contractility and vascular function. To better understand the mechanism by which GH affects cardiac function, we explored cardiac calcium channel gene expression in tamoxifen-inducible, cardiac-specific GHR disrupted (iC-GHRKO) mice. iC-GHRKO mice and controls (n=5) were injected with tamoxifen (80mg/kg) at four months of age. Two weeks after injection, hearts were dissected and total RNA was isolated. Using quantitative PCR, we evaluated RNA transcript levels of four key calcium channels involved in normal cardiac contraction: ATPase calcium transporting, slow twitch 2 (ATP2A2); cardiac specific sodium/calcium exchange (NCX1); cardiac ryanodine receptor 2 (RYR2); and voltage-dependent, L type calcium channel (CACNA1C). Compared to controls, levels of RYR2 were significantly reduced by 14%, ATP2A2 levels were significantly reduced by 35%, and NCX1 levels were significantly increased by 17% in iC-GHRKO mice. Levels of CACNA1C in iC-GHRKO mice were similar to controls. These changes are similar to what is observed in the failing heart and suggest that GH may be an important factor in cardiac calcium homeostasis. Future studies will focus on confirming these results at the protein level.

Nothing to Disclose: XL, AJ, EOL, DEB, JJK

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: AJ is supported by a graduate GMS fellowship from the Bill and Melinda Gates Foundation and by a student enhancement award from Ohio University. EOL, DEB, and JJK are supported by funds from NIA (AG031736), NIDDK (DK075436) and by the Diabetes Institute at Ohio University. JJK also is supported the State of Ohio’s Eminent Scholar Program that includes a gift from Milton and Lawrence Goll and by the AMVETS.