A poor maternal environment is known to predispose offspring to non-communicable diseases in later life, including asthma (Martino & Prescott, 2011). Bronchial hyperresponsiveness (BHR) is a feature of asthma, which has been linked to alterations in the RhoA pathway (Chiba et al., 1999). We have recently demonstrated BHR in the male offspring of protein restricted dams (Davis et al., 2012) and the aim of the current study was to investigate the role of the RhoA pathway in this response. Pregnant Wistar rats were fed either a control diet (C, 18% casein) or a protein restricted diet (PR, 9% casein) from conception to term. At term, dams and pups were returned to standard chow. At 150 days male offspring were sacrificed by cervical dislocation and bronchi were dissected and snap frozen in liquid nitrogen. mRNA was extracted from bronchi and reverse transcribed to cDNA. mRNA levels of genes RhoA, ROCK-1 and ROCK-2 were quantified using qPCR. Data is expressed as mean ± SEM and was analysed by student’s t-test. Significance was accepted at p<0.05. In bronchial segments from 150 day old offspring of control and PR dams, mRNA levels of RhoA were similar between the groups (C, 0.59 ± 0.03, n=5; PR 0.60 ± 0.02, n=4 p=0.75). Similarly, mRNA levels of ROCK-1 and ROCK-2 were also not different between the two groups (ROCK-1; C, 0.62 ± 0.11, n=5, PR, 0.65 ± 0.05, n=4, p=0.84; ROCK-2, C, 0.78 ± 0.04, n=5, PR, 0.94 ± 0.13, n=4, p=0.24). Increased mRNA levels of RhoA or ROCK does not appear to be responsible for the BHR in this model as the results showed that there was not a significant difference between the control and PR bronchi. However, this does not rule out whether post-translational modification may be responsible for the previously reported BHR.