Title:Mesenchymal Stromal Cell-derived Exosomes Attenuate Experimental Pulmonary Arterial Hypertension
Volume: 22
Issue: 12
Author(s): LiLi Ge, Wen Jiang, Shanshan Zhang, Jue Wang, Qian Xin, Chao Sun, Kailin Li, Tonggang Qi and Yun Luan*
Affiliation:
- Central Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, No. 247, Beiyuan Dajie, Jinan, 250033,China
Keywords:
Pulmonary arterial hypertension, pulmonary vascular remodeling, exosomes, MSC-EXO, right ventricular hypertrophy,
EndMT.
Abstract:
Background: Pulmonary arterial Hypertension (PH) is a chronic disease that ultimately
progresses to right ventricular failure and death. Until now, there is still a lack of effective treatment
applied. The purpose of the present study was to observe the protective effect of Mesenchymal
Stromal Cell-Derived Exosomes (MSC-EXO) against experimental Pulmonary arterial Hypertension
(PH) and right ventricular failure.
Methods: All the experimental rats received an intraperitoneal injection of 50 mg/kg monocrotaline
to induce PH model. Three weeks after the model was successfully established, the cell Culture Media
(CM) or MSC-EXO derived from human umbilical cord was administered daily via the tail vein.
All animals were randomly divided into 4 groups: Control (saline-treated), MCT-PH, MCT-CM and
MCT-EXO groups. Post-operation, hemodynamic data and index of right ventricular hypertrophy
(RVHI) were recorded to evaluate the inhibition of MSC-EXO on MCT-induced PH. Histology,
immunohistochemistry and western blot were used to analyze the effect of MSC-EXO against vascular
remodeling and further reveal the mechanism.
Results: In the present study, our results showed that MSC-EXO administration could significantly
reduce the Right Ventricular Systolic Pressure (RVSP) and RVHI, suppress the pulmonary vascular
remodeling and The Endothelial-Mesenchymal Transition (EndMT) process.
Conclusion: Our results provided the firm information for a new method in the treatment of PH; the
mechanism may be related to the inhibition of vascular remodeling and EndMT.
