Pulmonary Arterial Hypertension KnowledgeBase (PAHKB)
PAHKB
Pulmonary Arterial Hypertension KnowledgeBase
General information | Literature | Expression | Regulation | Mutation | Interaction

Basic Information

Gene ID

10911

Name

UTS2

Synonymous

PRO1068|U-II|UCN2|UII;urotensin 2;UTS2;urotensin 2

Definition

prepro U-II|urotensin II|urotensin-2

Position

1p36

Gene type

protein-coding

Source

Count: Uts2; 29180

Sentence

Abstract

The expression of U II and Uts2R in right ventricle arteries and right ventricle myocytes increases significantly during the formation of pulmonary hypertension and right ventricle hypertrophy in rats chronically exposed to hypoxia-hypercapnia.

AIM: To observe the expression of Urotensin II (U II) and its receptor (UT) on right ventricle in rats with chronic pulmonary hypertension induced by hypoxia and hypercapnia. METHODS: Twenty male SD rats were randomly divided into normal control group (NC) and hypoxia-hypercapnia 4-week group(HH). Mean pulmonary arterial pressure(MPAP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+ S) were calculated separately. U II in plasma was measured using radioimmunoassay. The expression of U II was observed in right ventricle myocytes and right ventricle arteries by immunohistochemistry. The expression of U II mRNA and UT mRNA were observed in right ventricle myocytes and right ventricle arteries by in situ hybridization. RESULTS: (1) The MPAP and RV/LV + S of HH group were higher respectively than those of NC group (P < 0.01, respectively). (2) The plasma U II content of HH group did not increased obviously than that of NC group. (3) The expression score of U II, U II mRNA, UT mRNA by right ventricle myocytes in HH group were higher significantly than those of NC group (P < 0.01 respectively). (4) The average value of integral light density (LD) of U II, U II mRNA, UT mRNA by right cardial arteries in HH group were higher significantly than those of NC group (P < 0.01, respectively). CONCLUSION: The expression of U II in right ventricle arteries and right ventricle myocytes increase significantly during the formation of pulmonary hypertension and right ventricle hypertrophy in rats chronically exposed to hypoxia-hypercapnia. These changes indicate that U II might be involved in right ventricle remodeling, which promotes proliferation of cardiac muscle cells.

Urotensin II was expressed in the lung of pulmonary hypertension patients with congenital heart disease.

OBJECTIVE: To observe the expression of urotensin II (UII) on the lung of patients with pulmonary hypertension (PH) with congenital heart disease and investigate the meaning of this phenomenon. METHOD: Thirty eight patients with CHD were divided into three groups according to pulmonary arterial systolic pressure (PASP) measured in cardiac catheterization and surgery: normal pulmonary pressure group (N group, PASP < 30 mm Hg, n = 10), mild PH group (M group, PASP >/= 30 mm Hg, n = 15), severe or moderate PH group (S group, PASP >/= 50 mm Hg, n = 13). The expression of UII protein and UII mRNA in pulmonary arterioles were measured separately by immunohistochemical (IHC) analysis and in situ hybridization (ISH) analysis. RESULT: (1) The results of UIIIHC staining: The UII protein expression of group M was higher than that of group N (20.22 +/- 3.58 vs. 14.34 +/- 2.18, P < 0.01), but less than group S (20.22 +/- 3.58 vs. 28.92 +/- 3.22, P < 0.05). (2) The results of UIIISH mRNA staining were similar to IHC staining, the A value of group M was higher than group N (12.51 +/- 2.02 vs. 8.85 +/- 1.41, P < 0.05), less than that of group S(12.51 +/- 2.02 vs. 25.35 +/- 4.33, P < 0.01). (3) Correlation study: there was a positive correlation between the A values of UIIIHC and pulmonary hypertension (r = 0.64, P < 0.01, n = 38), a positive correlation between the A values of UIIISH and pulmonary hypertension (r = 0.58, P < 0.01, n = 38). CONCLUSION: There was the expression of Urotensin II protein and mRNA in the lung of pulmonary hypertension patients with congenital heart disease, and these expression may involve the formation of pulmonary hypertension of congenital heart disease.

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