Publications by authors named "Jiao-Jie Xue"

3 Publications

  • Page 1 of 1

Dehydroepiandrosterone attenuates pulmonary artery and right ventricular remodeling in a rat model of pulmonary hypertension due to left heart failure.

Life Sci 2019 Feb 31;219:82-89. Epub 2018 Dec 31.

Cardiovascular Department of the Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong Province, China. Electronic address:

Aim: Pulmonary hypertension due to left heart failure (PH-LHF) is the most common cause of pulmonary hypertension. However, therapies for PH-LHF are lacking. Therefore, we investigated the effects and potential mechanism of dehydroepiandrosterone (DHEA) treatment in an experimental model of PH-LHF.

Main Method: PH-LHF was induced in rats via ascending aortic banding. The rats then received daily DHEA from Day 1 to Day 63 for the prevention protocol or from Day 49 to Day 63 for the reversal protocol. Other ascending aortic banding rats were left untreated to allow development of PH and right ventricular (RV) failure. Sham ascending aortic banding rats served as controls.

Key Finding: Significant increases in mean pulmonary arterial pressure (mPAP) and right ventricular end-diastolic diameter (RVEDD) were observed in the PH-LHF group. Therapy with DHEA prevented LHF-induced PH and RV failure by preserving mPAP and preventing RV hypertrophy and pulmonary artery remodeling. In preexisting severe PH, DHEA attenuated most lung and RV abnormalities. The beneficial effects of DHEA in PH-LHF seem to result from depression of the STAT3 signaling pathway in the lung.

Significant: DHEA not only prevents the development of PH-LHF and RV failure but also rescues severe preexisting PH-LHF.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.lfs.2018.12.056DOI Listing
February 2019

The Effects and Mechanism of Atorvastatin on Pulmonary Hypertension Due to Left Heart Disease.

PLoS One 2016 7;11(7):e0157171. Epub 2016 Jul 7.

Department of Cardiology, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.

Background: Pulmonary hypertension due to left heart disease (PH-LHD) is one of the most common forms of PH, termed group 2 PH. Atorvastatin exerts beneficial effects on the structural remodeling of the lung in ischemic heart failure. However, few studies have investigated the effects of atorvastatin on PH due to left heart failure induced by overload.

Methods: Group 2 PH was induced in animals by aortic banding. Rats (n = 20) were randomly divided into four groups: a control group (C), an aortic banding group (AOB63), an atorvastatin prevention group (AOB63/ATOR63) and an atorvastatin reversal group (AOB63/ATOR50-63). Atorvastatin was administered for 63 days after banding to the rats in the AOB63/ATOR63 group and from days 50 to 63 to the rats in the AOB63/ATOR50-63 group.

Results: Compared with the controls, significant increases in the mean pulmonary arterial pressure, pulmonary arteriolar medial thickening, biventricular cardiac hypertrophy, wet and dry weights of the right middle lung, percentage of PCNA-positive vascular smooth muscle cells, inflammatory infiltration and expression of RhoA and Rho-kinase II were observed in the AOB63 group, and these changes concomitant with significant decreases in the percentage of TUNEL-positive vascular smooth muscle cells. Treatment of the rats in the AOB63/ATOR63 group with atorvastatin at a dose of 10 mg/kg/day significantly decreased the mean pulmonary arterial pressure, right ventricular hypertrophy, pulmonary arteriolar medial thickness, inflammatory infiltration, percentage of PCNA-positive cells and pulmonary expression of RhoA and Rho-kinase II and significantly augmented the percentage of TUNEL-positive cells compared with the AOB63 group. However, only a trend of improvement in pulmonary vascular remodeling was detected in the AOB63/ATOR50-63 group.

Conclusions: Atorvastatin prevents pulmonary vascular remodeling in the PH-LHD model by down-regulating the expression of RhoA/Rho kinase, by inhibiting the proliferation and increasing the apoptosis of pulmonary arterial smooth muscle cells, and by attenuating the inflammation of pulmonary arteries.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0157171PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936674PMC
July 2017

[Effects of a recombinant adenovirus expressing human hypoxia-inducible factor 1α double-mutant on the in vitro differentiation of bone marrow mesenchymal stem cells to cardiomyocytes].

Zhonghua Xin Xue Guan Bing Za Zhi 2010 Jul;38(7):638-43

Department of Cardiology, Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China.

Objective: To observe the effects of mutant hypoxia-inducible factor-1α (HIF-1α) adenovirus (Adeno-HIF-1α-Ala402-Ala564) on cardiomyocytes (CMCs) differentiation from the mesenchymal stem cells (MSCs) co-cultured with CMCs.

Methods: Following groups were studied: HIF-1α group (MSCs + CMCs + Ad-HIF-1α), LacZ group (MSCs + CMCs + Ad-LacZ), Sham group (MSCs + CMCs + PBS) and MSC + HIF-1α Group (MSCs + Ad-HIF-1α). MSCs were co-cultured with myocardial cells in proportion of MSCs:CMCs 1:2, after 24 hours, cells were infect with virus (MOI = 100) or treated with PBS, cardiac troponin (cTnT) expression in MSCs was detected 7 days post infection by immunochemical analysis, mRNA expression of HIF-1α, TGF-β(1), Smad4, NKx2.5, GATA-4 was also detected by RT-PCR.

Results: HIF-1α increased MSCs differentiation to myocardial cells (differentiation rate 32.68% ± 6.52% vs. 8.28% ± 0.09% in the LacZ group and 10.25% ± 2.20% in the Sham group and 0.32% ± 0.05% in the MSC group (all P < 0.05 vs. HIF-1α group). mRNA expression of HIF, TGF-β(1), Smad4, NKx2.5 and GATA-4 was also significantly upregulated in HIF-1α group all P < 0.05 vs. Sham group).

Conclusion: HIF-1α promoted MSCs, co-cultured with myocardial cells, differentiating to cardiomyocytes via upregulating TGF-β(1)/Smad4 signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
July 2010
-->