You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["Variant", "Disease", "Species", "CellLine", "Chemical", "Gene"].

Please return the output as a JSON object of the format: {"CellLine": ["hRPTEC", ...], "Chemical": ["Glucose", ...], "Disease": ["Diabetes", ...], "Gene": ["HNF-6", ...], "Species": ["Patients", ...], "Variant": ["Pro75Ala", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

Sildenafil attenuates hypoxic pulmonary remodelling by inhibiting bone marrow progenitor cells. The recruitment of bone marrow (BM)-derived progenitor cells to the lung is related to pulmonary remodelling and the pathogenesis of pulmonary hypertension (PH). Although sildenafil is a known target in PH treatment, the underlying molecular mechanism is still elusive. To test the hypothesis that the therapeutic effect of sildenafil is linked to the reduced recruitment of BM-derived progenitor cells, we induced pulmonary remodelling in rats by two-week exposure to chronic hypoxia (CH, 10% oxygen), a trigger of BM-derived progenitor cells. Rats were treated with either placebo (saline) or sildenafil (1.4 mg/kg/day ip) during CH. Control rats were kept in room air (21% oxygen) with no treatment. As expected, sildenafil attenuated the CH-induced increase in right ventricular systolic pressure and right ventricular hypertrophy. However, sildenafil suppressed the CH-induced increase in c-kit(+) cells in the adventitia of pulmonary arteries. Moreover, sildenafil reduced the number of c-kit(+) cells that colocalize with tyrosine kinase receptor 2 (VEGF-R2) and CD68 (a marker for macrophages), indicating a positive effect on moderating hypoxia-induced smooth muscle cell proliferation and inflammation without affecting the pulmonary levels of hypoxia-inducible factor (HIF)-1a. Furthermore, sildenafil depressed the number of CXCR4(+) cells. Collectively, these findings indicate that the improvement in pulmonary haemodynamic by sildenafil is linked to decreased recruitment of BM-derived c-kit(+) cells in the pulmonary tissue. The attenuation of the recruitment of BM-derived c-kit(+) cells by sildenafil may provide novel therapeutic insights into the control of pulmonary remodelling.
{"CellLine": [], "Chemical": ["sildenafil", "oxygen", "Sildenafil"], "Disease": ["pulmonary remodelling", "hypoxic pulmonary remodelling", "inflammation", "hypoxia", "pulmonary hypertension", "CH", "right ventricular hypertrophy", "PH"], "Gene": ["c-kit", "hypoxia-inducible factor (HIF)-1a", "tyrosine kinase receptor 2", "CXCR4", "VEGF-R2", "CD68"], "Species": ["Rats", "rats"], "Variant": []}