What is the clinical evidence from this study?

Study design: Other. Population: Hypertension. Intervention: WKY-EVs-mediated miR155-5p transfer vs. SHR-EVs. Primary outcome: Vascular smooth muscle cell proliferation and vascular remodelling.

December 2, 2019Journal of Extracellular VesiclesOpen Access

MiR155‐5p in adventitial fibroblasts‐derived extracellular vesicles inhibits vascular smooth muscle cell proliferation via suppressing angiotensin‐converting enzyme expression

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Key result

WKY-EVs-mediated miR155-5p transfer attenuated vascular smooth muscle cell proliferation and vascular remodelling in spontaneously hypertensive rats via suppressing ACE expression.

Why the study?

Vascular smooth muscle cell proliferation drives vascular remodelling and stiffening in hypertension, but the role of adventitial fibroblasts-derived extracellular vesicles in this process remained unclear.

Does WKY-EVs-mediated miR155-5p transfer inhibit VSMC proliferation and vascular remodeling in spontaneously hypertensive rats?

Population

Normotensive Wistar-Kyoto rats and spontaneously hypertensive rats

Comparison

WKY-derived extracellular vesicles vs SHR-derived extracellular vesicles

Design

Preclinical animal and in vitro mechanistic study

Authors

XRXingsheng RenNorthwestern University YTYing TongWuXi AppTec (China)YQYun QiuNanjing University of Chinese Medicine

Discussion

Member takes

Implication

miR155-5p delivery via EVs may modulate hypertensive remodeling; leaves open translation to human therapy.

Structured PICO

Does WKY-EVs-mediated miR155-5p transfer inhibit VSMC proliferation and vascular remodeling in spontaneously hypertensive rats?

Population

Normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (an animal model of human essential hypertension), including isolated aortic adventitial fibroblasts and vascular smooth muscle cells (VSMCs).

Intervention

Extracellular vesicles (EVs) derived from WKY or SHR aortic adventitial fibroblasts, miR155-5p mimic/inhibitor/overexpression, captopril, losartan, and ACE knockdown.

Comparator

Untreated controls or respective opposite strain EVs.

Outcome

Vascular smooth muscle cell (VSMC) proliferation, vascular remodeling, blood pressure, and angiotensin-converting enzyme (ACE) expression.surrogate

Adventitial fibroblast-derived EVs from normotensive rats transfer miR155-5p to suppress ACE expression, thereby inhibiting VSMC proliferation and vascular remodeling in a hypertensive rat model.

Cite This Study

Ren et al. (2019) studied Hypertension. WKY-EVs-mediated miR155-5p transfer vs. SHR-EVs was evaluated on Vascular smooth muscle cell proliferation and vascular remodelling. WKY-EVs-mediated miR155-5p transfer attenuated vascular smooth muscle cell proliferation and vascular remodelling in spontaneously hypertensive rats via suppressing ACE expression.

synapsesocial.com/papers/6a96185a7fcc09ac6bee7067 https://doi.org/10.1080/20013078.2019.1698795

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MiR155‐5p in adventitial fibroblasts‐derived extracellular vesicles inhibits vascular smooth muscle cell proliferation via suppressing angiotensin‐converting enzyme expression

Discussion

Member takes

Implication

Structured PICO

Cite This Study

MiR155‐5p in adventitial fibroblasts‐derived extracellular vesicles inhibits vascular smooth muscle cell proliferation via suppressing angiotensin‐converting enzyme expression

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

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