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Hemin upregulats the expression of the platelet derived growth factor-B gene in the lung of hypoxic rat

Zhen Guo

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Abstract

AIM To investigate the effect of Hemin on the production of endogenous CO and the expression of PDGF B gene in rat lung tissue, and discuss the mechanism by which Hemin decreases the right ventricular systolic pressure (RVSP) and ameliorated the vascular remodeling of pulmonary artery in the hypoxic pulmonary hypertension rats. METHODS The rat model of hypoxic pulmonary hypertension were recreated by intermittent normal pressure hypoxia (10% O 2). Right ventricular systolic pressure was measured by right ventricular catheter. The quantity of carbon monoxide hemoglobin (COHb) in rat arterial blood was examined by double wavelength spectrophotometry. Expression of PDGF B and PCNA protein were determined by immunohistochemistry staining. PDGF B mRNA was examined by in situ hybridization. RESULTS ① The in situ hybridization and immunohistochemistry staining in the wall of intra acinar pulmonary arteries (IAPA) of normal rats were negative, but positive in hypoxic rats. The quantity of COHb in the arterial blood of hypoxic rats was higher than that of normal rats( P 0 01). ②After treated with Hemin, the quantity of COHb in arterial blood increased( P 0 05). Compared with the hypoxic rats, the level of PDGF B mRNA and the expression of PDGF B, PCNA proteins were decreased( P 0 01, or P 0 05). CONCLUSION Hemin can induce the production of endogenous CO, and suppress the hypoxic remodeling of pulmonary artery by inhibiting the expression of PDGF B gene.

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AIM To investigate the effect of Hemin on the production of endogenous CO and the expression of PDGF B gene in rat lung tissue, and discuss the mechanism by which Hemin decreases the right ventricular systolic pressure (RVSP) and ameliorated the vascular remodeling of pulmonary artery in the hypoxic pulmonary hypertension rats. METHODS The rat model of hypoxic pulmonary hypertension were recreated by intermittent normal pressure hypoxia (10% O 2). Right ventricular systolic pressure was measured by right ventricular catheter. The quantity of carbon monoxide hemoglobin (COHb) in rat arterial blood was examined by double wavelength spectrophotometry. Expression of PDGF B and PCNA protein were determined by immunohistochemistry staining. PDGF B mRNA was examined by in situ hybridization. RESULTS ① The in situ hybridization and immunohistochemistry staining in the wall of intra acinar pulmonary arteries (IAPA) of normal rats were negative, but positive in hypoxic rats. The quantity of COHb in the arterial blood of hypoxic rats was higher than that of normal rats( P 0 01). ②After treated with Hemin, the quantity of COHb in arterial blood increased( P 0 05). Compared with the hypoxic rats, the level of PDGF B mRNA and the expression of PDGF B, PCNA proteins were decreased( P 0 01, or P 0 05). CONCLUSION Hemin can induce the production of endogenous CO, and suppress the hypoxic remodeling of pulmonary artery by inhibiting the expression of PDGF B gene.

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Available abstract

AIM To investigate the effect of Hemin on the production of endogenous CO and the expression of PDGF B gene in rat lung tissue, and discuss the mechanism by which Hemin decreases the right ventricular systolic pressure (RVSP) and ameliorated the vascular remodeling of pulmonary artery in the hypoxic pulmonary hypertension rats. METHODS The rat model of hypoxic pulmonary hypertension were recreated by intermittent normal pressure hypoxia (10% O 2). Right ventricular systolic pressure was measured by right ventricular catheter. The quantity of carbon monoxide hemoglobin (COHb) in rat arterial blood was examined by double wavelength spectrophotometry. Expression of PDGF B and PCNA protein were determined by immunohistochemistry staining. PDGF B mRNA was examined by in situ hybridization. RESULTS ① The in situ hybridization and immunohistochemistry staining in the wall of intra acinar pulmonary arteries (IAPA) of normal rats were negative, but positive in hypoxic rats. The quantity of COHb in the arterial blood of hypoxic rats was higher than that of normal rats( P 0 01). ②After treated with Hemin, the quantity of COHb in arterial blood increased( P 0 05). Compared with the hypoxic rats, the level of PDGF B mRNA and the expression of PDGF B, PCNA proteins were decreased( P 0 01, or P 0 05). CONCLUSION Hemin can induce the production of endogenous CO, and suppress the hypoxic remodeling of pulmonary artery by inhibiting the expression of PDGF B gene.

Key concepts: Hemin, Immunohistochemistry, In situ hybridization, Lung, Hypoxia (environmental), Platelet-derived growth factor receptor, Pulmonary artery, Pulmonary hypertension

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