Pulmonary hypertension is characterized by structural and functional changes in the lung including proliferation of vascular smooth muscle cells (VSMCs) and excessive collagen synthesis. Although CTGF is known to promote cell proliferation, migration, adhesion, and extracellular matrix formation in various tissues, the study on CTGF in experimental pulmonary hypertension has been limited. Here, we examined the expression of CTGF in lung of the rat treated with monocrotaline (MCT). PBS or MCT (60 mg/kg) was injected subcutaneously into 6-week-old Sprague Dawley rats followed by molecular and histochemical analyses of the lung tissue. Establishment of pulmonary hypertension was verified by the significantly increased RVSP and RV/LV weight ratio in the MCT-treated rats. The MCT-treated rats also exhibited indications of pulmonary hypertension such as medial hypertrophy and perivascular fibrosis of pulmonary arteries. RT-PCR analysis of the lung at 5 weeks showed significantly increased expression of CTGF in the MCT-treated group. In situ hybridization studies also confirmed abundant CTGF mRNA expression in cells like VSMCs of the artery, clustered pneumocytes (alveolar epithelial cells), and the infiltrated macrophages. Interestingly, CTGF mRNA was not detected in SMCs of vein or bronchiole. In PBS-injected control, basal expression of CTGF was seen in bronchial epithelial cells, alveolar lining cells, and endothelial cells. Taken together, our results suggest that monocrotaline-induced pulmonary hypertension leads to CTGF upregulation in the lung and that CTGF might play an important role in pulmonary hypertension. Our findings have implication for the development of novel therapy aimed at reducing CTGF or antagonizing the role of CTGF for the treatment of pulmonary hypertension.