Cardiac resistance to growth hormone in uremia

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Presentation transcript:

Cardiac resistance to growth hormone in uremia Zhilan Zheng, Di Fei Sun, Padmaja Tummala, Ralph Rabkin Kidney International Volume 67, Issue 3, Pages 858-866 (March 2005) DOI: 10.1111/j.1523-1755.2005.00150.x Copyright © 2005 International Society of Nephrology Terms and Conditions

Figure 1 (A) Cardiac growth hormone receptor (GHR), Janus kinase (JAK2), signal transducers and activators of transcription (STAT5a and STAT5b) protein levels are unchanged in chronic renal failure (CRF). Protein levels were determined with Western immunoblots of cardiac lysates from CRF and pair-fed control rats treated with growth hormone or vehicle 15 minutes before sacrifice. (B) Tyrosine phosphorylation of STAT5a/b in response to growth hormone is impaired in the heart in CRF. STAT5 and phosphorylated STAT5 levels were assayed by Western immunoblots with antibodies that recognizes both STAT5a and STAT5b or both tyrosine phosphorylated STATs. Hearts were collected from CRF and control rats 15 minutes after an intravenous bolus of vehicle or bovine growth hormone, 30 ug/kg. Kidney International 2005 67, 858-866DOI: (10.1111/j.1523-1755.2005.00150.x) Copyright © 2005 International Society of Nephrology Terms and Conditions

Figure 2 Nuclear levels of signal transducer and activator of transcription 5b (STAT5b) and phosphorylated STAT5a/b are lower in chronic renal failure (CRF) rats compared to controls 15 minutes after growth hormone (GH) administration, while levels of STAT5a are unchanged. Growth hormone, 3 μg/100 g, or vehicle was given intravenously as a bolus to growth hormone–deficient CRF and control rats. Western immunoblots of nuclear protein extracts were performed using antibodies against p-STAT5a/b and STAT5a and STAT5b. Kidney International 2005 67, 858-866DOI: (10.1111/j.1523-1755.2005.00150.x) Copyright © 2005 International Society of Nephrology Terms and Conditions

Figure 3 Signal transducers and activators of transcription (STAT5) phosphorylation following high dose growth hormone (GH) treatment. Chronic renal failure (CRF) and pair-fed control growth hormone–deficient rats were given an intravenous bolus of growth hormone, 25 μg/100 g and the heart was collected 10 minutes later. Kidney International 2005 67, 858-866DOI: (10.1111/j.1523-1755.2005.00150.x) Copyright © 2005 International Society of Nephrology Terms and Conditions

Figure 4 Growth hormone receptor (GHR), Janus kinase (JAK2), and signal transducers and activators of transcription (STAT5) protein levels are unchanged in the heart of Sprague-Dawley rats with chronic renal failure (CRF), but growth hormone–induced protein tyrosine phosphorylation of these proteins is impaired. (A) Western immunoblots of GHR, JAK2, and STAT5 protein levels in lysates prepared from the heart of CRF and control pair-fed rats obtained 10 minutes after an intravenous bolus of growth hormone, 250 μg/kg, or vehicle. Samples from vehicle treated animals were pooled for this immunoblot. (B) Tyrosine-phosphorylated GHR, JAK2, and STAT5 levels in the same samples as shown in Figure 3a. The phospho-GHR and phospho-JAK2 were detected in immunoblots of GHR and JAK2 immunoprecipitates with ant-phosphotyrosine antibody (clone 4G10). Phospho-STAT5 was detected without immunoprecipitation using a phospho-STAT5 specific antibody (six rats/group). (C) Relative phosphorylation of GHR, JAK2, and STAT5 proteins 10 minutes after bovine growth hormone bolus in CRF and control animals. *P < 0.05. Phospho-protein signals were corrected for the specific protein levels and the ratios were normalized to the pair-fed control mean, which was assigned a value of 100. Bars indicate mean ± SEM. Kidney International 2005 67, 858-866DOI: (10.1111/j.1523-1755.2005.00150.x) Copyright © 2005 International Society of Nephrology Terms and Conditions