Table 2. Summary of effects of the leptin receptor antagonist SHLA on leptin induced JAK2/STAT3 activation increased gene and protein expression of p110CUX1 and cathepsin L and the hypertrophic response as determined by cell surface area and gene expression of ANP and β-MHC.

Parameter	Control	SHLA	Leptin	Leptin+SHLA
JAK2/18S	0.32±0.04	0.39±0.04	1.07±0.16*	0.34±0.03
JAK2/β-actin	0.63±0.07	0.59±0.06	1.38±0.13*	0.67±0.07
STAT3/18S	0.83±0.06	0.85±0.07	2.38±0.31*	0.94±0.10
p-STAT3/STAT3	0.12±0.02	0.14±0.03	0.29±0.04*	0.11±0.02
p110CUX1/β-actin	0.61±0.11	0.67±0.08	1.08±0.16*	0.62±0.07
Cathepsin L/18S	2.43±0.27	2.36±0.19	4.39±0.41*	2.48±0.33
Cathepsin L/β-actin	0.12±0.04	0.14±0.03	0.31±0.04*	0.12±0.05
CSA (µm2)	2178±183	2219±214	3094±314*	2339±346
ANP/18S	0.27±0.03	0.26±0.04	0.68±0.04*	0.30±0.05
β-MHC/18S	0.26±0.05	0.25±0.03	0.77±0.08*	0.28±0.04

The table summarizes the effect of the leptin receptor antagonist SHLA on various parameters including gene expression of JAK2, STAT3, cathepsin L, ANP and β-MHC (all indicated as ratios to 18S gene expression), protein levels of JAK2, p110CUX, cathepsin L (as ratios to β-actin) and P-STAT3 (as ratio to total STAT3) as well as cell surface area (CSA). SHLA completely abolished all responses to leptin. *P<0.05 from all other groups. N = 4.